HCoLL Flashcards

1
Q

Advanced Directives / Advanced decision to refuse treatment

A

Made when the patient has capacity for when they lose capacity.

Pt can set out the treatment they do not want and in which circumstances.

Cannot demand treatment or refuse basic care

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2
Q

Can a patient with an ADRT be treated when detained under the mental health act?

A

yes

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3
Q

What are things to consider when thinking about DNACPR?

A
  • Survival chances
  • QoL after resuscitation – hypoxic brain damage/pain/broken ribs/etc
  • Will ITU be able to support this patient post-arrest
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4
Q

DNACPR

A

Only covers CPR and not any other treatments.

= A medical decision but should be discussed with the patient and family.

Needs a medical reason other than age to be valid (e.g. not fit for ITU post-arrest/frailty/terminal/etc).

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5
Q

ReSPECT form

A

= personalised recommendations for clinical care in a future emergency, where the patient is unable to make or express decisions.

A more holistic summary of end-of-life care than DNACPR

Relevant for people with complex health needs/nearing end of life/at risk of sudden deterioration.

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6
Q

What is mental capacity?

A

= a person’s ability to make their own decisions and choices.

Judged according to a specific decision and at the time at which the decision is being made.

Capacity can be regained (e.g. acute confusion/delirium)

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7
Q

5 principles of capacity

A
  1. Assume capacity unless proven otherwise.
  2. Individuals should be supported to make their own decisions where possible.
  3. Unwise decisions must still be respected.
  4. If someone lacks capacity, you must act in their best interests.
    => Consider person’s wishes, feelings, beliefs, values.
    => Consider the views of close friends/family (but if they are not acting in best interests, can refer to court of protection).
    => Consider whether they will regain capacity.
  5. If someone lacks capacity, you must choose the least restrictive option.
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8
Q

Lasting Power of Attorney

A

A person is appointed to make decisions about a specific area of a patient’s life when they lose capacity (e.g. finances, health and well-being).

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9
Q

How do you assess capacity?

A

Stage 1: Does the person have an impairment of the mind or brain?

If no, there is no reason to question capacity.

Stage 2: can the person…
•	Understand information?
•	Retain information?
•	Weigh up consequences?
•	Communicate the decision? 

If they cannot demonstrate these criteria, this indicates that they LACK capacity for this particular decision

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10
Q

What is elder abuse?

A

= a single or repeated act or lack of appropriate action, occurring within any relationship where there is an expectation of trust, which causes harm or distress to an older person.

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11
Q

Types of elder abuse

A
  • Financial
  • Emotional/psychological
  • Physical
  • Sexual
  • Neglect/abandonment (not always intentional – passive neglect).
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12
Q

What should be done if elder abuse is suspected?

A

If you are concerned you MUST TAKE ACTION.

=> Document concerns and escalate to someone more senior.
=> Consider adults safeguarding referral

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13
Q

What is the difference between euthanasia and assisted suicide, and what are the laws in the UK surrounding these?

A

Euthanasia = the act of deliberately ending a person’s life to relieve suffering

Assisted-suicide = deliberately assisting another person to kill themselves

Both are illegal in UK law.
Euthanasia is considered manslaughter/murder.

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14
Q

Who is required for a MHA assessment?

A

2 doctors (who are deemed able to complete the assessment)

A specialist social worker.

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15
Q

what needs to be considered in a mental health act assessment?

A

Consider:

the previous nature of the illness, 
progression, 
the current severity of illness, 
risks to themselves/others, 
compliance with medication, 
engagement with healthcare professionals
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16
Q

Mental Health Act

A

Guides compulsory inpatient admission for assessment and treatment of people of and disorder/disability of the mind.

A last resort – the most restrictive way to take someone into hospital, does deprive the patient of their liberty.

Usually comes into play when a person is at risk of harming themselves/others/their own health and safety

ONLY applies to psychiatric disorders

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17
Q

What aspects of cognitive function are important for driving?

A

spatial awareness,
attention,
concentration

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18
Q

Deprivation of Liberty Safeguards (DOLS)

A

Used when it is necessary to deprive a patient of their liberty when they lack capacity to consent to their care and treatment, in order to keep them safe from harm.

If all of the following are true, you need to apply for a deprivation of liberty:

  1. Patient is deemed to lack capacity for self-discharge.
  2. Person is subject to continuous supervision and control
  3. If the person wishes to leave and you wouldn’t be happy with them doing so.
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19
Q

What is delirium?

A

a common clinical syndrome characterised by disturbed consciousness/attention, cognitive function or perception, which has ACUTE ONSET and FLUCTUATING COURSE

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20
Q

Causes of Delirium?

A
Drugs / dehydration
Electrolyte disturbances
Level of pain / lack of analgesia
Infection / inflammation 
Respiratory failure
Impaction of faeces / Intracranial
Urinary retention
Metabolism / MI
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21
Q

Risk factors for developing delirium

A
  • Having dementia (~50% of delirium cases occur in patients with prior dementia)
  • Over 65
  • Frailty
  • Multiple comorbidities
  • Poor hearing/vision
  • Polypharmacy
  • Recent surgery
  • Terminal illness
  • Previous Hx of delirium
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22
Q

What are the types of delirium?

A

Hyperactive
Hypoactive
Mixed

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23
Q

Delirium - Sx

A

HYPERACTIVE
Abnormally alert, Agitation/restlessness, disorientation, hallucinations, aggression, wandering, inappropriate behaviour.

HYPOACTIVE:
Often unrecognised, presents similar to depression.

Withdrawn, not eating/drinking, drowsy, disorganised

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24
Q

?delirium - assessment

A

“Is the patient more confused than normal?”

CAM = Confusion Assessment Methods

  1. More confused than normal
  2. Inattentive
    3a. Disorganised thinking
    3b. Altered state of consciousness

If yes to 1 AND 2 AND 3a or 3b, then is the course acute and fluctuating?

If yes => DELIRIUM.

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25
Q

1st Line Investigations for Confusion

A
  • Collateral Hx (establish baseline cognition).
  • Physical examination (conscious level, ?infection, neurology).
  • Confusion Bloods
  • Urinalysis
  • CXR, ECG, CT/MRI
  • Assess nutritional status
  • Medication review
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26
Q

What are “confusion bloods”?

A

FBC, CRP, U&Es, LFTs, TFTs, glucose, Ca, B12, folate

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27
Q

Delirium - Management

A

TREAT UNDERLYING CAUSE (if ignored => high mortality).

Reduce medications – avoid opiates, anticholinergics.

Reassure and keep orientated, active, hydrated, nourished.

Optimise senses and promote good sleep hygiene.

Only use drugs if other interventions have failed and patient is a risk to themselves or others.
=> Haloperidol 0.5mg = 1st line
=> Lorazepam 0.5mg (if haloperidol is contraindicated – Parkinson’s, LB dementia).
=> Only use short-term (usually 1 week or less).

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28
Q

What is the 1st line drug in management of delirium?

What are some contraindications of this drug?

A

Haloperidol 0.5mg

CIs - Parkinson’s, LB dementia

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29
Q

Delirium vs Dementia

A
DELIRIUM
Develops over hours/days
Fluctuating course
Altered consciousness
Usually reversible 
Psychomotor changes – increased/decreased
Impaired attention

DEMENTIA
Develops over years/months
Progressive
Consciousness usually clear
Irreversible
No psychomotor changes (until late disease)
Often good attention (until late disease)

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30
Q

What is dementia?

A

Dementia is a PROGRESSIVE and IRREVERSIBLE syndrome describing a set of symptoms due to degenerative changes in the brain.

It causes impaired function with no other medical explanation

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31
Q

Dementia - symptoms

A
  1. Memory Loss
  2. Difficulties with higher cognitive processes (at least 1 of):
    - Impaired executive function (e.g. problem solving, emotions).
    - Apraxia (difficulty motor planning)
    - Agnosia (difficulty recognising objects)
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32
Q

How long must the symptoms have been going on for a possibility of a diagnosis of dementia?

A

At least 6 months

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33
Q

How common is dementia?

A

~7% of people aged >65 have dementia

Affects F>M

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34
Q

What are the different types of dementia?

How common are they?

A
  1. Alzheimer’s Disease – 2/3rd
  2. Vascular Dementia – 20%
  3. Lewy Body Dementia – 5%
  4. Frontotemporal Dementia – 2%
  5. Other rarer causes
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35
Q

What are the other rarer causes of dementia?

A
  • Wernicke-Korsakoff Syndrome
  • Down’s Syndrome
  • Huntington’s
  • Multiple Sclerosis
  • Parkinson’s Disease Dementia
  • Creuzfeldt-Jakob disease
  • Pugilistic Dementia (repetitive head trauma).
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36
Q

What is the most common type of dementia?

A

Alzheimer’s Disease

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37
Q

Alzheimer’s - Pathophysiology

A
  • Characteristic beta-amyloid plaques and neurofibrillary tangles.
  • Brain atrophy, particularly the hippocampus.
  • Enlarged ventricles
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38
Q

Alzheimer’s - Symptoms

A

= Progressive memory loss that affects function.

Later on - Problems finding words, Mood/behaviour problems

There tends to be a gradual, progressive decline.

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39
Q

Cause of Alzheimer’s

A

Cause is unknown.

Early onset (<65) there is some familial risk
Association with APO-E gene
Association with CVD risk factors.

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40
Q

What is the average life expectancy of someone diagnosed with Alzheimer’s

A

7 years

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41
Q

Vascular Dementia - cause

A

Caused by reduced blood supply to the brain (due to diseased blood vessels)

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42
Q

Vascular Dementia - symptoms

A

Usually stepwise progression - stable and then sudden decline

Symptoms = problems with memory, thinking and reasoning.

Often overlaps with symptoms of Alzheimer’s.

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43
Q

Risk factors for vascular dementia

A

HTN, cholesterol, alcohol, smoking, DM, male, etc

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44
Q

Lewy body Dementia - pathophysiology

A

Characterised by alpha-synuclein deposits in the brain

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45
Q

Lewy body Dementia - early and late symptoms

A

Early stages – hallucinations and delusions, mood swings/ short tempered, short attention span, fluctuating alertness.

Late stages – Motor deterioration, similar to Parkinson’s.

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46
Q

Lewy body Dementia - differentials

A

Parkinson’s (but here the motor problems develop before cognitive decline.

Alzheimer’s

Schizophrenia – hallucinations/delusions

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47
Q

Fronto-temporal Dementia - pathophysiology

A

Involves damage to upper and middle frontal lobe and temporal lobe

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48
Q

Fronto-temporal Dementia - variants

A

Behavioural (2/3)
Progressive non-fluent aphasia
Semantic dementia

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49
Q

Fronto-temporal Dementia - symptoms of behavioural variant

A

Loss of inhibition – rude and compulsive

Personality changes – loss of interest in people, loss of sympapthy/empathy

Crave food – often sweet/fatty, eat until vomit.

Speech, language difficulties

(A cognitive deficit is not so obvious).

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50
Q

Dementia - investigations/diagnosis

A
Detailed History (often collateral) 
=>	Duration of Sx, effects on ADLs

Physical examination
=> CNS/PNS, gait, CVS, thyroid.

Blood tests +/- lumbar puncture

Medication Review
=> Look for any correlation of medications and duration of symptoms

Cognitive tests

CT/MRI
=> To exclude other causes.

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51
Q

Dementia - differentials

A
  • Delirium
  • Other mental illness (e.g. depression)
  • Substance misuse
  • Traumatic brain injury
  • Metabolic (hypothyroidism, B12 deficiency).
  • Medications (steroids, anti-depressants).
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52
Q

Dementia - management

A

There is NO CURE – eventually progresses to dependence and palliative care.

  1. Referral to Memory Clinic / RRLP
  2. Pharmacological – alleviate symptoms/slow progression
  3. Non-pharmacological
    => Social services care plan – home help, equipment, meals on wheels, day care.
    => Consider capacity – organise ADs/LPAs/DNACPRs while the patient still has capacity.
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53
Q

Dementia - pharmacological options

A

Cholinesterase Inhibitors – e.g. donepezil, rivastigmine, galantamine.
=> Alzheimer’s, LBD and Parkinson’s (mild-moderate disease).

NMDA Receptor Antagonists – e.g. Memantine
=> Alzheimer’s only (moderate-severe disease).

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54
Q

What is the pharmacological treatment for vascular dementia?

A

There isn’t one

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55
Q

What is the pharmacological treatment for FT dementia?

A

There isn’t one

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56
Q

What is the pharmacological treatment for Alzheimer’s disease?

A

Cholinesterase Inhibitors

NMDA Receptor Antagonists

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57
Q

What are the components of a mini-ACE ?

A

Patient Demographics - include occupation, handedness, age at leaving full-time education

Orientation - day, date, month, year

Memory - address

Fluency – Animals

Visuo-spatial – Clock drawing

Memory Recall - address

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58
Q

What is the mini-ACE?

A

A cognitive assessment

Used as a SCREENING TOOL to identify cognitive impairment.

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59
Q

What are the cut-off scores in the mini-ACE?

A

<25 - likely to have come from a dementia patient

<21 - almost certainly a score to have come from a dementia patient

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60
Q

Charles-Bonnet Syndrome

A

= Hallucinations

Often associated with diminished eyesight (e.g. macular degeneration), due to overcompensation of the brain.

Patients will mostly still have insight into these hallucinations

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61
Q

Old Age Psych History components

A

Demographics + reason for referral

PC and HPC
=> Onset – insidious vs. rapid.
=> Non-cognitive symptoms.
=> Impact on ADLs

Hx of psychiatric illness

PMHx
=> Pre-morbid personality.
=> Hx of delirium?
=> Vascular risk factors – stroke, TIA, MI, peripheral vascular disease, HTN, diabetes, falls.

DHx

FHx

SHx
=>	Current living arrangements
=>	Amount of care – family/friends or district nurses/day care?
=>	Drugs/smoking/alcohol/benzodiazepines
=>	Driving – concerns, incidents?
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62
Q

What are the things to assess in a Mental State Examination ?

A

Appearance and Behaviour

Speech

Emotion
=> Mood/affect

Perception
=> auditory/visual/olfactory hallucinations

Thoughts
=> content and expression

Insight

Cognitive Function
=> mini-ACE

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63
Q

How common is later life depression?

A

affects 1 in 5 in the community (more common in nursing homes)

affects F > M.

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64
Q

“monoamine hypothesis” of depression

A

Depression results as a deficiency of one or more of Dopamine, Noradrenalin and Serotonin.

=> Anti-depressants increase the levels of these neurotransmitters

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65
Q

Risk factors for later life depression

A
  • Chronic Pain/Long-term conditions
  • Loss – spouse/job/independence
  • Isolation
  • PMHx or FHx of depression/anxiety
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66
Q

ICD-10 Diagnostic Criteria for Depression - core and other Sx

A

CORE SYMPTOMS

  1. Low Mood - worse in the morning
  2. Anhedonia
  3. Fatigue
OTHER SYMPTOMS
•	Guilt/hopelessness
•	Suicidal thoughts/self-harm
•	Psychosis (hallucinations/delusions)
•	Sleep disturbance/poor memory
•	Change in appetite
•	Agitation
•	Psychosomatic (pain/GI complaints, excessive concern over physical health)
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67
Q

Severity of depression by ICD-10 criteria

A

Mild – 2 core and 2 other Sx.
Moderate – 2/3 core and 3 other Sx.
Severe – 3 core and 5 other Sx.

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68
Q

Agitation as a Sx of depression

A

Usually depression presents as slowing of everything (speech, movement, thinking, etc.) but, in the elderly, agitation is often seen (inability to relax).

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69
Q

Psychosis as a Sx of depression

A

If the mood symptoms start before the psychosis, then it can be considered depression.

If the psychotic symptoms start first, then it’s more likely to be a psychotic disorder

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70
Q

Geriatric Depression Scale

A

= 15 yes/no questions to help screen for, assess severity of and monitor clinical depression in an older person.

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71
Q

DDx for depression

A

Endocrine/metabolic

  • Hypothyroidism
  • Anaemia
  • Hypercalcaemia
  • Malignancy

Dementia

Parkinson’s Disease

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72
Q

What are important things to assess when assessing for suicide risk?

A
Risk to self
Risk to others
Non-compliance with medication 
Self-neglect
Exploitation/vulnerability
Driving 
Physical Health/Falls
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73
Q

Suicide assessment - risk to self

A

Previous Hx or attempted self-harm/suicide

FHx of suicide

Current episode – ongoing thoughts (frequency, severity, intrusiveness), planning, final acts, the future

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74
Q

Suicide assessment - risk to others

A

Verbal/physical threats of harm to others

Thoughts or attempted harm

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75
Q

What can cause non-compliance with medications?

A

Memory issues, side effects, lack of insight, stigma

76
Q

Management of Depression

A

BIOLOGICAL:
- Antidepressants – SSRIs are 1st line
=> Wait 2-4 weeks, if no improvement then change to another.
- Anxiolytics – BZDs (short-term use)
- Hypnotics – Z-drugs (e.g. Zopiclone, etc.)
- ECT

PSYCHOLOGICAL:
- CBT

SOCIAL:

  • Support networks/groups
  • Social services referral
  • Lifestyle – limit alcohol, increase exercise, meaningful activity, etc.
77
Q

What is pseudo-dementia?

A

Temporary dementia-like symptoms (attention and memory deficit) secondary to depression.

78
Q

What are the main differences between dementia and pseudo-dementia?

A

Pseudodementia does not cause actual degeneration of the brain, while dementia does.

Hx of disturbance in pseudodementia is often short and abrupt onset, while dementia is more often insidious.

79
Q

What is useful to establish in the Hx to help differentiate between dementia and pseudo-dementia ?

A

if the changes in mood preceded any changes in cognition

80
Q

Pseudo-dementia and cognitive assessments

A

Often people with pseudodementia can perceive their changes in cognition, but actually perform quite well on cognitive assessments (often the opposite with dementia)

81
Q

What is total bladder volume?

When is the first desire to void normally?

A

~600mL total volume

~250mL = desire to void

82
Q

How is continence maintained?

A

co-ordinated interaction of the bladder, urethra, pelvic floor muscles and the nervous system.

=> Maintained so long as the urethral pressure exceeds the bladder pressure

83
Q

Nervous input to micturition

A

Frontal Cortex – provides voluntary control of micturition.

Parasympathetic NS – initiates micturition reflex (contraction of detrusor muscle in bladder – S2-S4)

Sympathetic NS – inhibits micturition reflex, allows bladder filling (contraction of smooth muscle sphincter and proximal urethra – T11 – L2)

84
Q

What is required for normal bladder function?

A
  • Intact nerve pathways
  • Normal muscle tone – in detrusors, sphincters and pelvic floor
  • Absence of any outflow obstruction
  • Normal cognition
  • Absence of environmental/psychological factors which may inhibit micturition
85
Q

Causes of faecal incontinence

A
  • Diarrhoea
  • Faecal impaction
  • Nerve damage (spinal cord injury, MS, DM)
  • Anal damage (e.g. post-radiotherapy)
  • Cognitive (dementia, stroke)
  • Other causes – IBD, malignancy, poor diet/fluid intake.
86
Q

Urinary incontinence

A

= the complaint of any involuntary leakage of urine sufficient to be a health or social problem.

Prevalence increases with age – VERY common in the elderly (30% at home, 50% in care homes).

More common in women

87
Q

Causes of established urinary incontinence

A

Outlet incompetence (childbirth, prostatectomy)
Outlet obstruction (BPH, strictures, etc.)
Detrusor overactivity
Detrusor underactivity (neurological)
Cognitive (dementia)

88
Q

Causes of acute urinary incontinence

A
Delirium
Infection (UTI)
Atrophic urethritis/vaginitis
Drugs
Psychiatric disorders (especially depression)
Polyuria (DM, excess intake)
Restricted mobility
89
Q

What drugs can cause urinary incontinence?

How?

A

CCBs, antidepressants, antipsychotics – decreased detrusor activity

Alpha blockers – relax urinary sphincter

ACEIs – cough worsens stress incontinence

Sedatives – reduce awareness of full bladder

Diuretics – increase urine output (including alcohol and caffeine)

90
Q

Types of urinary incontinence

A
  1. Urge incontinence
  2. Stress/Pressure Incontinence
  3. Overflow Incontinence
  4. Functional Incontinence
91
Q

What is the most common type of incontinence in the elderly?

A

= urge incontinence

92
Q

Functional Incontinence

A

due to a cognitive failure to inhibit reflex (e.g. dementia, stroke)

Risk factors – immobility, sedation, unfamiliar surroundings

93
Q

Investigations for urinary incontinence

A

History + Examination

Urinalysis
Bloods - FBC, U&E, creatinine, glucose

Frequency/Volume Charts

Pre- and Post-void Bladder Scan
Uroflowmetry

94
Q

What volume of urine in 24 hours is considered polyuria?

A

> 2000mL / 24h

95
Q

What residual post-void volume in the bladder is considered abnormal?

A

> 100mL = abnormal

96
Q

What are important points to identify in a Hx for incontinence?

A
  • Urgency? Frequency? Dysuria? Nocturia?
  • Hesitancy/dribbling/poor stream?
  • Haematuria? Weight loss?
  • Fevers/rigors/N+V?
  • PMHx/PSHx (also obstetric Hx)
  • DHx
  • Alcohol/caffeine/smoking/fluid intake
97
Q

What examinations are relevant in investigating incontinence?

A

Neurological - Mental status, spinal cord (lower limb weakness), perineal sensation

Abdo - Kidneys and bladder

Pelvic - Organ prolapse/wall weakness

Rectal - Faecal impaction, rectal masses

98
Q

Management of urinary incontinence - Lifestyle

A
  • Smoking cessation, weight loss
  • Restrict fluids (especially in evenings)
  • Reduce alcohol and caffeine
  • Pelvic floor exercises
  • Absorbent pads/commodes
99
Q

Management of urinary incontinence - Medication

A
  • Antibiotics – UTI
  • Tamsulosin/finasteride – BPH
  • Oxybutynin/solifenacin (anticholinergics) – urge incontinence
  • Duloxetine (serotonin/NA reuptake inhibitor) – stress incontinence
100
Q

Incontinence - red flag symptoms

A
  • Haematuria
  • Prolapse beyond vaginal opening
  • Suspicion of prostate cancer
  • Abnormal neurology
  • Saddle anaesthesia
  • Recent back trauma
  • Recent pelvic surgery
101
Q

What is osteoporosis?

A

= reduced bone mineral density with altered microarchitecture causing the bones to be weak and fragile.

Caused by osteoclast (bone resorption) activity being greater than osteoblast (bone formation activity).

102
Q

Result of osteoporosis

A

Gradual bone weakening – especially hip, spine, wrist.

Increased risk of fracture – e.g. from standing height/low trauma

Back pain/kyphosis/loss of height

103
Q

Osteoporosis - Risk Factors

A

Primary:

  • Age / female gender
  • Genetics
  • Low BMI
  • Calcium/VitD deficiency
  • Previous low trauma fracture

Secondary:

  • Chronic inflammation (RA, malignancy)
  • Hyperthyroidism/hyperparathyroidism
  • Malabsorption of Calcium
  • Premature menopause
  • Steroid use
  • Smoking
  • Alcohol excess (>3 units per day)
104
Q

FRAX Score

A

= 10-year risk of osteoporosis and hip fractures

FRAX Score Parameters:

  • Age, gender, BMI
  • Smoking/alcohol Hx
  • Steroid use
  • RA
  • Fracture Hx
105
Q

Osteoporosis - Ix

A

Hx and Examination
=> Calculate FRAX Score

U&E, bone profile, Vit D, TFTs, PTH, ESR, sex hormones

X-Ray

DEXA Scan
=> Measures bone mineral density
=> Gold standard Ix if intermediate/high FRAX risk

106
Q

what DEXA Scan results indicate osteoporosis?

A

Osteoporosis = T-score >2.5 s.d. below average.

Osteopenia = T-score 1-2.5 s.d. below average.

107
Q

DEXA scan - T-score

A

= s.d.s below average for young adult male.

108
Q

DEXA scan - Z-score

A

= s.d.s below average for age-matched control.

109
Q

Osteoporosis - Management

A
  1. Lifestyle:
    - Improve calcium intake
    - Exercise (especially weight-bearing)
    - Smoking cessation/reduced alcohol consumption.
  2. Physio/OT => Reduce falls risk
  3. Medication:
    - VitD and Calcium supplements.
    - Bisphosphonates
    - Medication review – ?stop steroids
110
Q

What is important counselling information when prescribing bisphosphonates?

A

• Can cause GI upset/oeseophageal ulcers and rarely jaw necrosis

  • Tablets/injections once per week
  • Swallow with water and sit upright for 30 mins after
111
Q

Definition of malnutrition

A

= a state of nutrition in which a DEFICIENCY or EXCESS of energy, protein and other nutrients causes measurable adverse effects on tissue/body form (shape, size, composition) and function to affect clinical outcome.

112
Q

Malnutrition - symptoms

A
  • Loss of appetite
  • Weight loss
  • Tiredness/loss of energy
  • Reduced physical performance
  • Altered mood
  • Poor concentration
113
Q

Risk factors for malnutrition

A

Cognitive:

  • Unable to vocalise desires
  • Misinterpret sensation of hunger
  • Reduced appetite/early satiety
  • Depression/bereavement
  • Dementia/delirium

Social:

  • Access to food
  • Isolation/loneliness (don’t eat socially)
  • Finances

Physical:

  • Dental problems
  • GI/swallowing problems
  • Medications
  • Poor mobility/reduced dexterity
  • Reduced sense of smell/taste
114
Q

Why is there an increased risk of malnutrition in hospitals?

A
  • Unpleasant environment (smell, sights, sounds, etc.)
  • Limited time for eating
  • Can’t access food
  • Limited provision for religious/dietary needs
  • NBM or missed meals (e.g. while undergoing tests)
  • Increased nutritional requirements due to illness
115
Q

Malnutrition Universal Screening Tool (MUST)

A

= a 5-step tool to screen for malnourishment/risk of malnourishment.

Done within 24 hours of admission and repeat weekly (or sooner if the patient’s condition changes).

0 = low risk
=> Repeat screening weekly/situation changes

1 = medium risk
=> Document intake for 3 days
=> Decide if further intervention is needed

≥2 = high risk
=> Dietetic support to improve intake
=> Close monitoring.

116
Q

Malnutrition - Management

A

Always try food first!

1st LINE
Dietary Alterations
e.g. little and often, full-fat options, nourishing drinks, multivitamins

2nd LINE
Oral Nutritional Supplements
e.g. Fortisips

3rd LINE
Enteral Nutrition
e.g. NG, PEG, RIG Tube

117
Q

Indications for Enteral Nutrition

A

Inability to take sufficient nutrition orally

Functioning gastrointestinal tract

118
Q

Definition of TIA

A

= acute focal neurological deficit of cerebrovascular cause, lasting <24 hours.

Usually resolves in minutes

119
Q

Definition of stroke

A

= acute focal neurological deficit of cerebrovascular cause lasting >24 hours/results in death.

120
Q

Types and subtypes of stroke

A

Ischaemic stroke (85%)

  • Thrombotic
  • Embolic

Haemorrhagic stroke (15%)

  • Intracerebral
  • Subarachnoid
121
Q

Ischaemic Stroke - Sx

A

Motor – unilateral weakness, slurred speech

Sensation – numbness

Coordination problems

Higher cognitive dysfunction – dysphasia, agnosia, apraxia, inattention, memory loss.

Vision – amaurosis fugax, homonymous hemianopia

122
Q

Ischaemic Stroke - Risk Factors

A

Modifiable:

  • HTN
  • Alcohol/smoking
  • Obesity/DM
  • Lack of exercise
  • Hyperlipidaemia

Non-modifiable:

  • Age, male
  • FHx
  • Previous stroke/TIA
  • AF
123
Q

Amaurosis fugax - what is it and how is it managed?

A

= transient loss of vision in one eye.

90% due to atherosclerotic disease in carotid artery.

Mx – aspirin 300mg PO and refer to TIA clinic

124
Q

Presentation of haemorrhagic stroke

A
  1. Intracerebral Haemorrhage:
    • Focal neurological deficits
    • Reduced consciousness
    • Headache, nausea, vomiting.
  2. Subarachnoid Haemorrhage
    • Sudden thunderclap headache.
    • Reduced consciousness
    • Meningism – photophobia, stiff neck, vomiting.
125
Q

Risk factors for haemorrhagic stroke

A
Berry aneurysms (SAH)
Charcot-Bouchard microaneurysms (intracranial haemorrhage)

AVMs

Uncontrolled HTN

Alcohol/cocaine/smoking

Anticoagulants, coagulopathies

126
Q

Bamford Classification of stroke - TACS

A

= Total anterior circulation stroke

A large cortical stroke affecting the areas of the brain supplied by both the middle and anterior cerebral arteries.
All 3 of:
• Higher cerebral dysfunction
• Homonymous hemianopia
• Contralateral hemiparesis/hemisensory loss (at least 2 of face, arm, leg)

127
Q

Bamford Classification of stroke - PACS

A

= Partial anterior circulation stroke

Involves small branches of the MCA and ACA – i.e. only part of the anterior circulation is compromised.

2/3 of the criteria for TACS
OR isolated higher dysfunction.

128
Q

Bamford Classification of stroke - POCS

A

= Posterior circulation syndrome

Involves damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem).

1 of:
• CN palsy, PLUS contralateral motor/sensory loss.
• Bilateral motor/sensory deficit.
• Isolated homonymous hemianopia.
• Cerebellar dysfunction (nystagmus, uncoordinated).

129
Q

Bamford Classification of stroke - LACS

A

= Lacunar stroke

A subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions (e.g. dysphasia).

1 of:
• Pure unilateral hemiparesis OR hemisensory loss.
• Pure unilateral hemi-sensorimotor loss.
• Ataxic hemiparesis.

130
Q

Stroke - Assessment

A

ABCDE

History:
- Onset, duration, symptoms, etc.

Examination:
- GCS, Neurological, General SR (especially CVS)

Recognition of stroke screening tool / NIHSS severity assessment.

131
Q

Investigations in ischaemic stroke

A

Bloods – FBC, U&Es, CRP/ESR, lipids, glucose, clotting, TFT

ECG – check for AF/evidence of MI

Brain Imaging
=> CT – exclude haemorrhage
=> MRI – usually done later if diagnostic uncertainty remains.

Carotid artery doppler – detect ICA stenosis

Other tests to determine cause
=> ECHO, CXR, antibody screen, thrombophilia screen.

132
Q

Indications for urgent CT in ?stroke

A
  • Anticoagulated
  • Known bleeding disorder
  • Decreased GCS
  • Papilloedema/stiff neck
  • Severe headache
  • Being considered for thrombolysis
133
Q

Investigations in Haemorrhagic Stroke

A
  • Bloods
  • ECG
  • IMAGING – CT
  • Lumbar Puncture – xanthochromia (yellow discolouration) confirms SAH.
134
Q

Ischaemic Stroke - Mx

A
  1. Antiplatelets:
    => Aspirin – 300mg PO o.d. for 2 weeks.
    => Clopidogrel – 75mg PO o.d. for life.
  2. Thrombolysis – if within 4.5 hours of onset.
    => Alteplase (unless contraindicated)
  3. Statins
    => Atorvastatin 80mg PO
  4. Surgery
    => Carotid endarterectomy considered if ICA stenosis >50%
  5. Address Risk Factors - BP, AF, Smoking, alcohol, diet, exercise, DM
  6. Rehabilitation = key in stroke management
    => MDT input – physio/OT, SALT, optometry
135
Q

Contraindications of thrombolysis in ischaemic stroke

A
ABSOLUTE – 
Hx of IC haemorrhage/seizure/neoplasm, 
Pregnancy, 
Stroke in last 3/12, 
GI bleed in last 3 weeks, 
BP >180/110, 
Clotting disorder, 
Sx suggesting SAH. 
RELATIVE –
Anticoagulated, 
Cancer, 
>75 years, 
Major surgery in past 2 weeks.
136
Q

Haemorrhagic stroke - Mx

A

STOP ANTIPLATELETS/ANTICOAGULANTS

Reverse anticoagulants

  • Vit K for warfarin
  • Protamine sulphate for heparins

BP control

Discuss with neurosurgeons

Monitor obs and neurological signs.

137
Q

Driving Advice following stroke

A

Not able to drive for a minimum of 4 weeks after a stroke or TIA.

Do necessarily need to inform DVLA unless:

  • Seizures
  • LGV or passenger-carrying vehicle driver.
  • Brain surgery
  • If driving is still affected 1 month after stroke/TIA.
  • More than one stroke in 3 months
  • SAH
138
Q

What is a pressure ulcer?

A

localised damage to the skin and/or underlying tissue,

usually over a bony prominence, resulting from sustained pressure

139
Q

Who are most at risk of pressure ulcers?

A
  • Reduced mobility/immobility.
  • Vascular disease.
  • Sensory impairment.
  • Extremes of age (poor circulation)
  • Previous Hx of pressure damage (weak skin)
  • Malnutrition / dehydration
  • Significant cognitive impairment
140
Q

Common locations of pressure ulcers

A

Heels, elbows, hips and base of the spine.

Can also be related to a medical device (e.g. NG-tube).

141
Q

Categories of Pressure Ulcer

A

Category I – non-blanchable erythema.

  • People with pale skin tend to get red patches
  • People with darker skin get purple/blue-ish patches rather than red.

Category II – partial thickness skin loss.

Category III – full thickness skin loss.
- Bone, tendon or muscle are not exposed.

Category IV – full thickness tissue loss.

Deep tissue injury (DTI) – depth unknown.

Unstageable (US) ulcer – depth unknown

142
Q

When is osteomyelitis likely due to pressure ulcer?

A

A category IV ulcer where there is full thickness tissue loss and the bone is exposed.

143
Q

Pressure Ulcer risk assessment

A

Carry out and document a pressure ulcer risk assessment WITHIN 2 HOURS of admission

High risk (<10-12 Braden score) => red skin bundle

Medium risk (13-14 Braden score) => amber skin bundle

Low risk (>15 Braden score)

144
Q

Skin assessment for identification of pressure ulcers

A

The skin should be checked for:

  • Skin integrity in areas of pressure
  • Colour changes or discolouration
  • Variations in heat, firmness and moisture (for example, because of incontinence, oedema, dry or inflamed skin).

BLANCH TEST

145
Q

Pressure ulcer blanch test

A

Use finger palpation or diascopy to determine whether erythema or discolouration (identified by skin assessment) is blanchable.

  • Press on the skin for 10 secs
  • Check for blanching and re-filling.
  • If the skin doesn’t blanch, this indicated damage has already occurred.
146
Q

Pressure Ulcer Assessment

A

Assess and document:

  • Location
  • Cause of ulcer
  • Dimensions of ulcer (Surface Area, estimate of depth)
  • Category of ulcer
  • Exudate and signs of local infection
  • Pain/odour
  • Photo of ulcer
147
Q

Pressure Ulcer - Mx

A

Care to the wound - dressing, cleaning, debridement

Prevent worsening - SSKIN bundle

  • Support surface
  • Skin assessment
  • Keep moving (change position frequently, at least every 4-6 hours)
  • Incontinence/moisture monitoring (consider barrier creams)
  • Nutrition management

Antibiotics if any evidence of:

  • Systemic sepsis
  • Spreading cellulitis
  • Underlying osteomyelitis
148
Q

Risk factors for falling

A
INTRINSIC
Cardiovascular (arrythmias, syncope, postural hypotension).
Balance and gait
Visual impairment
Cognitive impairment/confusion
Incontinence
Malnourishment
Medications
EXTRINSIC
Poorly fitting footwear
Inappropriate walking aid
Insufficient equipment
Insufficient lighting
Unfamiliar environment
Trip hazards
Medications
BEHAVIOURAL
Alcohol 
Risky behaviour (lifting, bending)
Rushing to answer phone, etc.
Poor diet/fluid intake
Non-compliance with advice
Fear of falling
Lack of exercise
149
Q

Which medications are more likely to cause falls in the elderly?

A

Antihypertensives (incl. diuretics & vasodilators & anti-arrythmics)

Sedatives/opioids/hypnotics,

Antidepressants.

150
Q

What investigations must be done in ALL fall patients?

A

Hx and Examination – gait (GALS), heart sounds, neurological, vision

ECG

Lying and Standing BP

151
Q

What L/S BP drop indicates postural hypotension?

A

A drop in SBP >20mmHg or DBP >10mmHg indicated orthostatic/postural hypotension.

152
Q

What other investigations may be useful in fall patients?

A
  • FBC, U&E, TFTs
  • CRP
  • CK – if a long lie (rhabdomyolysis)
  • Bone biochemistry – for osteoporosis
  • Echo/24-hour tape – if ECG abnormal/CV symptoms
  • CT – if head injury
153
Q

Falls - management

A
  1. Patient Education:
    - e.g. getting up slowly, using aids, etc.
  2. Physiotherapy:
    - Strength and balance training
  3. Occupational Therapy:
    - Home hazards assessment
  4. Medical Review:
    - Analgesia
    - Medication review
    - Diagnose any new medical conditions
    - Optimise comorbidities
    - Cognitive Screen
    - Bone health assessment
154
Q

Falls prevention

A

RISK ASSESSMENT - All patients should be considered high risk of falls and need assessment if:

  • > 65 years
  • 50-64 years with medical conditions predisposing to falls.

MOBILITY - Encouraging mobility is key!
=> Sedentary behaviour contributes to deconditioning and functional loss.

155
Q

What is Parkinson’s disease?

A

= a neurodegenerative disorder caused by a loss of the dopamine producing cells in the Substantia Nigra.

(Dopamine is a neurotransmitter chemical particularly associated with control of movement by the basal ganglia)

156
Q

Parkinson’s disease - Risk factors

A

MOST CASES ARE IDIOPATHIC

RFs:
- Age, male sex, FHx/identical twin affected

  • (Possible – herbicides/pesticides, heavy metal/industrial work, farming community, repeated head trauma)
157
Q

Parkinson’s - Criteria for Diagnosis

A

Criteria for Diagnosis:

  • Rigidity and Bradykinesia
  • +/- postural instability
  • +/- resting tremor (4-6 Hz)
158
Q

How long does it take motor symptoms to manifest in Parkinson’s disease?

A

Motor symptoms often don’t manifest clinically until ~80% of dopamine producing cells are lost.

Often non-motor symptoms precede motor symptoms and also have a greater impact on life.

159
Q

Motor Symptoms of Parkinson’s

A
  • Bradykinesia
  • Rigidity
  • Postural instability

• Resting tremor
=> Worse if anxious/angry/excited
=> Better with activity

• Freezing
=> Narrow/confined spaces, when changing direction

• Dystonia (painful cramping in feet/legs)
=> Worse at night

  • Dysphagia
  • “Classic Parkinson’s Gait” – shuffling/small steps, stooped over, reduced arm swings.
160
Q

Non-motor Sx of parkinson’s

A
  • Masked face
  • Hypophonia (deep, soft, monotonous voice)
  • Micrographia (progressively smaller handwriting)
  • Depression/ Anxiety/ Psychosis
  • Anosmia
  • Insomnia/REM sleep disorder/restless legs
  • Fatigue
  • Constipation/urinary incontinence
  • Seborrhoeic dermatitis
  • Cognitive impairment
161
Q

“on-off” phenomena of Parkinson’s

A

There is a massive fluctuation in Sx – unpredictable “on-off” phenomena.

Sudden switch from mobility (“on”) to immobility (“off”) in seconds or minutes.

162
Q

Parkinson’s disease - cognitive problems

A
  1. Mild Cognitive Impairment (MCI)
    • In 25% of those newly diagnosed with PD.
    • Possible risk factor for developing PDD.
  2. Parkinson’s Disease Dementia (PDD)
    • A dementia syndrome with insidious onset and slow progression within the context of established PD.
163
Q

How to differentiate between PDD and LBD

A

If dementia occurs before PD symptoms, then LB dementia.

164
Q

Falls in Parkinson’s Disease

A

very common

Risk Factors:

  • More advanced PD
  • Cognitive impairment/dementia
  • Depression/anxiety
  • Prior fall Hx
  • Postural Hypotension
  • Postural Instability/freezing
  • Reduced lower extremity strength
  • Dyskinesia
  • Polypharmacy
165
Q

Suggestive features of Idiopathic PD

A

Unilateral Onset + persistent asymmetry
Upper limb predominance
Presents with bradykinesia

Treatment responsive (to L-dopa)

166
Q

Suggestive features of Vascular PD

A

Bilateral onset
Lower limb predominance (upper limbs spared)
Presents with falls/gait problems
Hx of atherosclerosis/strokes

Stepwise progression
Will have a poor response to Levodopa.

167
Q

Suggestive features of Essential Tremor

A

Bilateral
FHx in 50%

Stable – doesn’t progress.

Improves with alcohol
Treat with beta-blockers (Propranolol)

168
Q

Suggestive features of Drug-induced Parkinsonism

A

History of antipsychotics (olanzapine, risperidone, quetiapine, etc.) or metoclopramide.

169
Q

Parkinson’s disease - Investigations

A

History

Examination (PD focused)

  • Bradykinesia – finger thumb pinching.
  • Rigidity – tone when resting
  • Resting tremor
  • Postural instability – gait assessment/shoulder-tug test.
  • Speech, face (masked?), writing (small)

Confusion bloods – r/o acute/reversible causes

CT/MRI – r/o other cause

Levodopa test
=> If responsive, suggests idiopathic PD.

PET/SPECT (DAT) scan
=> To detect decreased dopaminergic activity in basal ganglia.

Medication review – antipsychotics.

170
Q

Prognosis of Parkinson’s

A

Prognosis varies and depends on age, genetics, and comorbidities/frailty.

There is no cure.

171
Q

Management of Parkinson’s Disease

A
  1. Levodopa Monotherapy
  2. Dopamine Receptor Agonists
  3. Levodopa Dual Therapy – Dopamine Metabolism inhibitors
4.	Non-pharmacological
=> Patient education – advice to minimize “freezing”
=>	Comprehensive Geriatric Assessment
=>	Social support
=>	Physio/OT
  1. Treatment of Non-motor Symptoms
172
Q

Advice to minimise “freezing” in parkinson’s

A
  • Avoid multitasking while walking

* Use cues to help overcome freeze

173
Q

What is Levodopa?

What is the usual dose per day?

When might there be complications?

A

= a dopamine precursor (dopamine itself cannot cross the BBB).

=> Increases synaptic dopamine.

Combined with carbidopa to prevent peripheral metabolism to dopamine (but cannot cross the BBB so allows action of L-dopa in the CNS).

Usual maximum dose 600-1000mg / day

Complications may arise after 4-6 years and efficacy reduces (narrowed therapeutic window).

174
Q

Side effects of Levodopa

A

SEs – dyskinesia (uncontrollable wriggling), confusion, depression, insomnia.

175
Q

Dopamine Receptor Agonists in managing Parkinson’s

A

e.g. Ropinirole, Rotigotine (patch), bromocriptine

Activates post-synaptic receptors.

Used more in early disease or can also be used as a levodopa adjunct in later stages of disease.

SEs – confusion, hallucinations, impulsive control disorder (gambling, hypersexuality).

176
Q

Parkinson’s Follow-up

A

PD medications need regular review.

At follow-up, always ask about:
•	Parkinsonian Sx
•	Hallucinations
•	Fluctuations in motor capabilities
•	Dyskinesias

Also enquire how any symptoms relate to timing of dopaminergic therapy – adjust time and dose accordingly.

177
Q

What medications should always be AVOIDED in parkinson’s patients?

A

Haloperidol, metoclopramide and prochlorperazine

178
Q

Cognitive Stimulation Therapy in Dementia

A

CST = a brief, evidence-based treatment for people with mild to moderate dementia.

Involves 14 themed sessions of structured 45-minute group therapy sessions.

Aims:
=> To actively stimulate and engage people with dementia.
=> Improve confidence and hopefully cognition and memory.
=> Social benefits – relaxing, fun, sociable, opportunities to discuss topics

179
Q

What are the 5 domains of CGA?

A
  1. Medical:
    - Co-morbid conditions and disease severity
    - Medical review
    - Nutritional status
    - Problem list
  2. Psychological:
    - Cognition (e.g. AMT, Mini-ACE)
    - Mood and anxiety (GDS)
    - Fears
  3. Functional:
    - ADLs (Barthel index)
    - Gait and balance
    - Anxiety/exercise status
    - Instrumental activities of daily living.
  4. Social:
    - Informal support from family and friends
    - Social network such as visitors or daytime activities
    - Eligibility for access to care resources
  5. Environmental:
    - Home comfort, facilities, safety
    - Use or potential use of telehealth technology, etc.
    - Transport facilities
    - Accessibility to local resources
180
Q

What are important factors to pay attention to when clerking an older person?

A

Their pre-morbid status (collateral Hx)

Any recent changes – medications, home circumstances, life events.

Social Hx:
=> Who do they live with? Exercise tolerance?

Problem list – medical/ mental/ functional/ social/ environmental issues

Ongoing management
=> Who else has assessed the patient (OT/PT/SALT/Dietician) – what were their conclusions?

181
Q

Timed Up and GO (TUG) Test

A

Involves getting the patient to stand up from a chair, walk 3 metres, turn around and go back to the chair and sit down.

<10 secs is normal, 20 seconds or more indicates they are likely to need outside assistance.

182
Q

Braden Scale

A

Used to judge risk of developing pressure sores

Based on mobility, nutrition, moisture, sensation, activity and friction.

183
Q

Barthel Index

A

An objective standardised tool used to test for “dependency” in ADLs by quantifying the patient’s performance in 10 activities (centred on self-care and mobility).

Measured out of 20 (with 20 being fully independent).

184
Q

National Institute for Health Stroke Scale (NIHSS)

A

Score of stroke severity based on neurological abnormalities on examination.

<5 mild, >20 severe.

185
Q

Abbreviated Mental Test (AMT)

A

A rapid tool to identify cognitive impairment in older people and monitor change in cognitive function.

Limited validity – an abnormal score (<7) needs more detailed cognitive assessment.

Includes:

  • Age
  • Time (nearest hour)
  • Address for recall at end of test (42 West Street)
  • Year
  • Name of this place
  • Identify 2 people
  • Date of birth
  • Year of 1st world war
  • Present Monarch’s name
  • Count backwards from 20
  • Address recall correct?