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Phase 3A > Geriatrics > Flashcards

Geriatrics Flashcards

1
Q

What is delirium?

A

Syndrome of disturbed conciousness accompanied by change in cognition not accounted for by pre- existing dementia

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2
Q

What can delirium be thought of as?

A

Acute brain failure syndrome characterised by impaired conciousness

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3
Q

What causes delirium?

A

Pain
Infection
Medications
Electrolyte and fluid imbalance
Alcohol or drug intoxication
Cardiac, Respiratory or Liver failure
Endocrine dysfunction
Epilepsy
Intracranial pathology

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4
Q

What medications can cause delirium?

A

Anticholinergics
Anxiolytics
Hypnotics
Anticonvulsant
Opiates
Corticosteroids
Lithium
Digoxin
L-dopa

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5
Q

What is the pathophysiology of delirium?

A

Reversible impairment in cerebral oxidative metabolism, neurotransmission abnormalities and cholinergic deficiency

Stress also potentiates response

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6
Q

Why does stress play a role in pathophysiology of delirium?

A

Upregulation of sympathetic activity results in down regulation of parasympathetic tone furthering cholinergic deficiency.

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7
Q

Why are older patients at higher risk of delirium?

A

More vunerable to reduced cholinergic transmission

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8
Q

How is delirium classified?

A

Hyperactive, hypoactive and mixed

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9
Q

What are the risk factors for delirium?

A

Increasing age
Medical condition or taking regular medication
Poor hearing or vision
Infection
Poor dietary intake

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10
Q

What are the features of hyperactive delirium?

A

Restless and agitated
Aggression
Unusually vigilant

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11
Q

What is the presentation of hypoactive delirium?

A

Withdrawn, feeling lethargic and tired
Drowsy
Unusually sleepy
Unable to stay focused when awake

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12
Q

What is the presentation of mixed delirium?

A

Symptoms of both hypoactive and hyperactive delirium

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13
Q

What are the features of delirium?

A

Acute or subacute onset
Reversible
Diurnal or hour to hour fluctuation
Disturbance to circadian rhythm
Elements of hallucinations or misinterpretation
Behaviours of fear, agitation and aggression
Disturbed psychomotor behaviour
Poor short and long term memory
Poor insight

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14
Q

What investigations are performed to diagnose delirium?

A

MSE
Assess cognition
Urine dip to rule out UTI
FBC, CRP, LFT, glucose, U+E
Blood culture
Blood gas
Chest X-ray
Lumbar puncture
CT/ MRI

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15
Q

What is the management for delirium?

A

Treat the cause

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16
Q

How should delirium be managed in an unknown cause?

A

Supportive measures
Continually reassess and consider other tests

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17
Q

What medication can be given for symptom management in delirium?

A

Haloperidol

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18
Q

What are the complications of delirium?

A

Weakness
Malnutrition
Permanent cognitive decline

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19
Q

What is benign paroxysmal positional vertigo?

A

Peripheral vestibular disorder manifesting as a sudden, short lived episode of vertigo elicited by specific head movements

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20
Q

At what age is BPPV more likely to affect patient?

A

50 and 70 years

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21
Q

What is the cause of BPPV?

A

Primary/ idiopathic

Head trauma
Labyrinthitis
Vestibular neuronitis
Meniere’s disease
Migraines
Iatrogenic; Otological/ nonotological surgery, repositioning manoeuvres

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22
Q

What is the pathophysiology of BPPV?

A

Abnormal signals arising from semicircular canals leads to misinterpretation of movement
Mechanisms involve Canalithiasis, Cupuloithasis

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23
Q

What are the risk factors for BPPV?

A

Increasing age
Female sex
Head trauma
Vestibular neuronitis
Labyrinthitis
Migraines
Inner ear disease
Meniere’s disease
Otitis media
Osteoporosis

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24
Q

What is the clinical presentation of BPPV?

A

Head movements provoke symptoms
Brief duration of sudden onset episodic vertigo lasting less than 30 seconds
Nausea, imbalance, lightheadedness
Positive Dix- Hallpike manoeuvre
Normal neurological and otological examination

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25
Q

What investigations are used to diagnose BPPV?

A

Dix- Hallpike manoeuvre
Supine lateral head turns
Audiogram
Brain MRI

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26
Q

What are differentials for BPPV?

A

Meniere’s disease
Vestibular neuronitis
Labyrinthitis
Perilymphatic fistula
CNS disorders

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27
Q

What is the management for BPPV?

A

Patient education and reassurance
Repositioning manoeuvre
Vestibular rehabilitation exercise
Vestibular suppressant medication (Benzodiazepines, Antihistamines)
Surgery

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28
Q

What is the monitoring need for BPPV?

A

Follow up few weeks post surgery
Repeat Dix- Hallpike manoeuvre

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29
Q

What are the complications of BPPV?

A

Peri or post manoeuvre related BPPV
Autonomic dysfunction
Accident at work or home
Hearing loss

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30
Q

What is the prognosis of BPPV?

A

Highly treatable

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31
Q

What are the differentials for delirium?

A

Depression
Dementia
Mental illness
Hypothyroidism

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32
Q

What is a hip fracture?

A

Fracture of distal femur to the femoral head and proximal toa level few centimetres below lesser trochanter

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33
Q

What is the epidemiology of hip fractures?

A

More common in those over 65 years
Average age is 83 years
If below 40 years trauma is most likely to cause fracture

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34
Q

What are the causes of hip fractures?

A

Fall from standing height
Osteopenia
Osteoporosis
High energy trauma

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35
Q

What is the pathophysiology of hip fracture?

A

Cortical disruption, periosteal damage, damage to intramedullary and cancellous architecture
Cortical thinning and decrease in trabecular bone mass results in low bone quality
Results in decreased mechanical strength resulting in fracture

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36
Q

How are hip fractures classified?

A

Intracapsular
Extracapsular

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37
Q

What is the potential complication of intracapsular fracture?

A

Avascular necrosis due to cdamage to retinacular vessels

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38
Q

What are risk factors for hip fracture?

A

Osteoporosis
Osteopenia
Falls
Low BMI
Female sex
High energy trauma

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39
Q

What is the clinical presentation of a hip fracture?

A

History of trauma or fall
Pain in affected hip, groin, thigh
Inability to bear weight on affected hip
Shortened, externally rotated hip

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40
Q

Investigations used to diagnose hip fracture?

A

X-ray
Blood screen
ECG

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41
Q

What is seen on X-ray radiograph in a hip fracture?

A

AP view; interruption of shenton’s line
Lateral view; anterior displacement of femoral shaft/ neck relative to head

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42
Q

Differentials for hip fracture?

A

Acetabular fracture
Pubic rami fracture
Femoral shaft or subtrochanteric femur fracture
Femoral head fracture
Septic hip

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43
Q

What is the management of a hip fracture?

A

ABCDE
Consider urgent trauma call
Primary survey of patient
Analgesia and nerve block
Surgical management

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44
Q

What is the management for hip fracture if patient cannot tolerate surgery?

A

Analgesia, nerve block
Bed rest
Continue to monitor and reassess suitability for surgery
Consider palliative care

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45
Q

What are the complications of a hip fracture?

A

Thromboembolic events
Avascular necrosis
Non uniform/ failure of fixation

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46
Q

What is the prognosis of hip fracture?

A

30% mortality at 1 year
Majority of patients do not regain pre_fracture level of function
Extracapsular fractures have a better prognosis

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47
Q

What is frailty?

A

Distinctive health state related to ageing process in which multiple body systems gradually lose their built in reserves

Long term condition but not an inevitable part of ageing

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48
Q

What is the epidemiology of frailty?

A

10% of people over 65
25-50% of people over 85 years

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49
Q

What are the features of frailty?

A

Varies in severity
Not static, can improve or decline
Causes serious, adverse outcomes for patient

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50
Q

What is the pathophysiology of frailty?

A

Certain aspects of patients health or lifestyle lead to active inflammation in the system which becomes chronic
Inflammatory mediators and response leads to pathological changes in muscle, endocrine system, the blood and heart
All leads to signs and symptoms of frailty

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51
Q

Risk factors for frailty?

A

Advancing age
Genetic
Lifestyle; smoking. poor nutrition
Environment

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52
Q

What is the clinical presentation of frailty?

A

Weakness
Weightloss
Exhaustion
Low activity
Slowed performance

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53
Q

What investigations are used to assess frailty?

A

Clinical frailty score

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54
Q

What are the complications of frailty?

A

Falls
Disability
Dependancy for ADL
Surgery risks
Death

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55
Q

What is Parkinson’s disease?

A

Chronic progressive neurodegenerative disorder characterised by bradykinesia, resting tremor, rigidity

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56
Q

What is the epidemiology of Parkinsons disease?

A

Mean age of onset is 65 years
Increasing prevalance with increasing age
Greater incidence in men
More common in white ethnicity

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57
Q

What is the pathophysiology of Parkinson’s disease?

A

Mitochondrial dysfunction and oxidative stress results in degeneration of dopaminergic neurones from pars compacta
Results in reduced striatal dopamine meaning thalamus is inhibited resulting in bradykinesia

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58
Q

What is the cause of Parkinson’s disease?

A

Mitochondrial dysfunction
Chronic heavy metal exposure
Oxidative damage by free radicals
Pesticides
MPTP found in illegal opiates

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59
Q

How is Parkinson’s classified?

A

According to age of onset
Juvenile parkinsonism; under 21 years
Young onset; between 21 and 40 years

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60
Q

Risk factors for Parkinson’s?

A

Increasing age
Family history
Mutations in gene encoding Glucocerebrosidase
MPTP exposure
Male sex
Head injury
Chronic metal exposure
Higher educational status

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61
Q

What is the clinical presentation of Parkinson’s?

A

Asymmetrical
Bradykinesia
Resting tremor
Cogwheel rigidity
Parkinsonian gait
Postural instability
Micrographia
Fatigue
Depression and anxiety
Sleep disorder
Urinary problems

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62
Q

How is parkinsonian gait described?

A

Stooped posture, small shuffling gait, reduced arm swing, narrow base

Difficultly initiating movement

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63
Q

What investigations are used to diagnose Parkinson’s?

A

Clinical presentation and history
Dopaminergic agent trial; improved symptoms
MRI head

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64
Q

What is seen in a head MRI?

A

Brain atrophy
Lewy bodies

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65
Q

What are the differentials for Parkinson’s?

A

Essential tremor
Dementia
Drug induced parkinsonism
Metabolic abnormalities
Corticobasal degeneration

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66
Q

What is the non medical management for parkinsons?

A

Physiotherapy, Occupational therapy, Speech therapy
Gait specific training

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67
Q

What is the medical management of Parkinson’s?

A

Levodopa
Decarboxylbase inhibitor e.g Co-careldopa
Dopamine agonist e.g Ropinirole
MOAB inhibitors e.g Selegiline
COMT inhibitors e.g Entacapone

Surgical ablation

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68
Q

Complications of Parkinsons ?

A

Levodopa induced dyskinesia
Motor fluctuations
Dementia
Constipation, bladder dysfunction
Depression, psychosis, anxiety

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69
Q

What is the prognosis of Parkinson’s disease?

A

Symptom control as there is no curative or disease modifying medication
Eventual cognitive dysfunction

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70
Q

What factors predict a poorer prognosis for Parkinson’s disease?

A

Older age at symptom onset
Rigidity, hypokinasia as presenting symptoms
Decreased response to dopaminergic medications

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71
Q

What is dementia?

A

Syndrome characterised by deterioration in cognition resulting in impairment in ADL

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72
Q

What are the main types of dementias?

A

Alzheimer’s dementia
Vascular dementia
Fronto temporal dementia
Lewy body dementia

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73
Q

What is alzheimer’s dementia?

A

Primary chronic neurodegenerative disease with insidious onset, progressive and slow decline

74
Q

What is the epidemiology of Alzheimers disease?

A

Most common type of dementia
More common in women, black and hispanic people
Incidence rises with increasing age

75
Q

Aetiology of Alzheimers dementia?

A

Build up of interneuronal amyloid peptides
Autosomal dominant variant

76
Q

What is the pathophysiology of Alzheimers dementia?

A

Overproduction or diminished clearance of beta amyloid protein leads to build up and formation of dense extracellular amyloid oligomers which are deposited as diffuse plaques

Plaques lead to inflammatory process causing neuritic plaque formation resulting in cell and synaptic death

Tau protein’s accumulate in intraneural spaces as neurofibrillary tangles causing dystrophic neunites

77
Q

What is a neurofibrillary tangle?

A

Intracellular aggregation of tau proteins

78
Q

What are the risk factors for Alzheimers dementia?

A

Advancing age, family history
Genetics; Down’s syndrome, PSEN 1, PSEN2, Amyloid precursor protien
Female sex
Below secondary school education, Unemployment
Lifestyle; smoking, midlife obesity, alcohol, T2DM

79
Q

What is the clinical presentation of Alzheimer’s dementia?

A

Memory loss
Disorientation to time and place
Dysphasia
Apathy
Change in personality
Poor abstract thinking
Constructional dyspraxia

80
Q

What is seen on MRI scan in Alzheimer’s dementia?

A

Generalised cerebral atrophy
Predominance in medial temporal lobe and lateral parietal lobe

81
Q

Investigations to diagnose and rule out differentials for dementia?

A

Bedside cognitive test ; MOCA, MMSE
Bloods ; FBC, U+E, LFT, TFT, B12, Vitamin D, folate
Urine drug screen
CT Head

82
Q

Differentials for dementia?

A

Delirium
Depression
Parkinsons disease
Hypothyroidism
B12, folate deficiency
Bipolar disorder
Major depression
Substance misuse
Normal pressure hydrocephalus
HIV associated dementia

83
Q

What medications can be used in Alzheimer’s dementia?

A

Cholinesterase inhibitors e.g Donepezil, rivastigmine, galantamine

NMDA receptor antagonist e.g Memantine

Insomnia management ; Trazodone

84
Q

What are the monitoring requirements for Alzheimers?

A

Every 6 months to evaluate functional and cognitive change, issues with medication, new signs and symptoms and review management

85
Q

What are the complications of Alzheimers dementia?

A

Pneumonia
institutionalisation
Urinary tract infection
Falls
Weight loss
Elderly abuse

86
Q

What is frontotemporal dementia?

A

Primary neurodegenerative brain disease resulting in personality change, disruption in social conduct and language

87
Q

What are the types of frontotemporal dementia?

A

Behavioural variant
Primary progressive aphasia
Movement disorders

88
Q

What is the epidemiology of Frontotemporal dementia?

A

Midlife onset typically between 45 and 65 years
Peak prevalance in 7th decade of life
Male predominance

89
Q

Aetiology of frontotemporal dementia?

A

Autosomal dominant mutations in microtubule associated genes
Environmental causes; TBI, lifestyle factors

90
Q

What is the pathophysiology of Frontotemporal dementia?

A

Neuronal loss, gliosis and microvascular changes in frontal lobes, anterior cingulate cortex and and insular cortex

Abnormal intracellular accumulation of hyperphosphorylated tau proteins leads to abnormal neuronal communication

91
Q

Risk factors for frontotemporal dementia?

A

Mutations in MAPT gene (FTD with parkinsonism phenotype)
Mutations in GRN gene (FTD with behavioural phenotype)
Traumatic brain injury

92
Q

What in the clinical presentation of Frontotemporal dementia?

A

Disregard to social conventions
Impatience and irritability
Slovenly appearance
Child like impulsive actions
Poor emotional processing
Progressive loss of language fluency or comprehension
Memory impairment, disorientation
Progressive self neglect, abandonment of work, activities and social contacts

93
Q

What is seen on Brain MRI in frontotemporal dementia?

A

Focal atrophy in frontal and anterior temporal lobe
Assymmetry between left and right side

94
Q

What is the management of frontotemporal dementia

A

Supportive care and therapy
Antidepressants and Antipsychotics

Amantadine

95
Q

What kind of supportive care is needed in frontotemporal dementia?

A

Home modification
Occupational therapy
Speech and language therapy
Physiotherapy
Behavioural management
Will creation while cognition is still intact

96
Q

What are the monitoring requirements for Frontotemporal dementia?

A

Comprehensive cognitive and behavioural evaluation every 6-12 months
Assess driving status every 6 months

97
Q

Complications of frontotemporal dementia?

A

Financial crisis
Dangerous driving
Problems with relationships
Falls
Legal crisis

98
Q

What is the prognosis of frontotemporal dementia?

A

Shorter survival and faster rate of cognitive and functional decline than Alzheimers dementia

99
Q

What is vascular dementia?

A

Chronic progressive impairment of cognitive function predominantly caused by vascular problems

100
Q

Epidemiology of vascular dementia?

A

Second most common type of dementia
More common in men

101
Q

Aetiology of vascular dementia?

A

Infarction
Leukoaraiosis
Haemorrhage

102
Q

What is the pathophysiology of vascular dementia when infarction is the cause?

A

Large infarct will exhaust compensatory mechanisms leading to widespread neuronal damage and dementia

Small infarct affecting basal ganglia and thalamus lead to dementia

103
Q

What is the pathophysiology of vascular dementia when Leukoaraiosis is the cause?

A

Loss of axons, myelin and oligodendrocytes

Perivascular tissue is lost leading to dilation of perivascular space causing damage to capillaries and break down of BBB

Can lead to haemorrhage and infarction

104
Q

Risk factors for vascular dementia?

A

Over 60 years of age
Obesity
Hypertension
Cigarette smoking
Diabetes mellitus
Hypercholesterolemia
Alcohol misuse

105
Q

What is clinical presentation of vascular dementia?

A

History of strokes
Signs of frontal cognitive syndrome
Impaired gait
Focal neurological signs

106
Q

What are signs of frontal cognitive syndrome?

A

Difficulty solving problems
Apathy
Disinhibition
Slowed processing of information
Poor attention
Retrieval memory deficit
Frontal release reflex ; glabella tap, jaw jack, grasp

107
Q

What in the management of vascular dementia?

A

Lifestyle modification
Antiplatelet therapy if atherosclerotic aetiology
Anticoagulation if cardio-embolic aetiology
Carotid endartectomy if stenosis over 70%
Treat co-morbid conditions

108
Q

What are the monitoring requirements for vascular dementia?

A

Every 4-6 months to monitor condition and after treatment
Home safety assessment
Assess driving status every 6 months

109
Q

Complications associated with vascular dementia?

A

Depression
Agitation
Falls
Stroke
Aspiration pneumonia
Decubitis ulceration

110
Q

What is lewy body dementia?

A

Neurodegenerative disorder with parkinsonism, progressive cognitive decline, prominent executive dysfunction

111
Q

What is the least common type of dementia?

A

Lewy body dementia

112
Q

What is the aetiology of lewy body dementia?

A

Toxic protein aggregation
Abnormal phosphorylation
Nitration, oxidative stress, inflammation, lysosomal dysfunction
Genetics; Autosomal dominant

113
Q

What is the pathophysiology of Lewy body dementia?

A

Lewy bodies accumulate in CNS, density and location correlate to symptoms

Cholinergic deficit

114
Q

What is a Lewy body?

A

Alpha synuclein inclusion

115
Q

What other inclusions may be present in Lewy body dementia?

A

Neurofilament light
Ubiquitin

116
Q

What is the clinical presentation of Lewy body dementia?

A

Fluctuation in cognition, attention and arousal
Visual hallucination
Motor symptoms
REM sleep and behavioural disturbance
Depression, anxiety
Delusions and hallucination

117
Q

What is seen on an MRI in Lewy body dementia?

A

Generalised cortical atrophy

118
Q

What is the management for Lewy body dementia?

A

Supportive care
Memantine
Antipsychotics and antidepressants

119
Q

What are the monitoring needs for Lewy body dementia?

A

Individual case
If on cholinesterase inhibitor should be seen every 3-6 months

120
Q

Complications of Lewy body dementia?

A

Pneumonia
Institutionalisation
Dysphagia
Antipsychotic sensitivity
Urinary incontinence
Falls risk
Elderly abuse

121
Q

Prognosis of Lewy body dementia?

A

Progressive disease with steady decline in function, loss of independance and eventual death
Mean survival post diagnosis is 5 years

122
Q

What is mixed dementia?

A

Combination of dementia aetiologies producing a more severe phenotype in patient

123
Q

What is a fall?

A

Fall as a result of chronic impairment in cognition, vision, balance or mobility

124
Q

What isthe epidemiology of a fall?

A

More likely in older adults,
30% over 65 years will have a fall, and 50% over 80 years

125
Q

What is the aetiology of falls?

A

Neuropsychiatric; Visual impairment, peripheral neuropathy, vestibular dysfunction, hearing impairment, gait and balance problems

Cardiovascular; Syncope, orthostatic hypotension, carotid sinus syndrome, post prandial hypotension

Musculoskeletal; Joint instability, mechanical problems, sarcopenia, osteosarcopenia, Sarcopanic deconditioning

Toxic; Medications, Polypharmacy, Substance misuse

Environmental hazards Poor lighting, uneven floor, presence of clutter, lives alone

126
Q

Risk factors for falls?

A

Muscle weakness
Poor balance
Foot deformities
Memory loss, confusion, difficulty with cognition
Syncope
Polypharmacy
Substance misuse
Drinking too much alcohol
Bowel and bladder conditions
MSK disorders

127
Q

What investigations are performed following a fall?

A

Turn 180 test
Time up and go test

128
Q

What should be done after a fall?

A

Assess severity of fall
Perform a risk assessment
Educate on fall prevention

129
Q

What emergencies can arise following a fall?

A

Sudden onset change in conciousness
New head trauma
Fractures

130
Q

What is a pressure sore?

A

Localised damage to skin and underlying soft tissue usually cover bony prominence or around medical/ non medical device

131
Q

Epidemiology of pressure sores?

A

Incidence increases with age
Upto 2/3 in over 70 year olds
1 in 4 spinal injuries patients

132
Q

Aetiology of pressure sore?

A

Pressure
Shear
Moisure
Friction

133
Q

What is the pathophysiology of pressure sore?

A

Deformation of cells from pressure and shear forces disrupts all structure resulting in death
Compression of blood vessels causes transient ischaemia
Blockage of lymphatics causes accumulation of toxic waste

Can have some reperfusion injury and inflammatory response

134
Q

Risk factors for pressure sores?

A

Immobility
Sensory impairment
Older age
Surgery
Intensive care stay
Malnourishment
History of pressure ulcer
Environmental causes; surface and position
Diabetes and peripheral vascular disease

135
Q

How is a pressure sore graded?

A

Graded between stage 1 and 4 based on skin changes

136
Q

How is a stage 1 pressure sore described?

A

Non blanching erythema, purple or maroon localised area of decoloursed intact skin

137
Q

How is a stage 2 pressure ulcer described?

A

Shallow open wound or loss of fissue on area subject to pressure

138
Q

How is a stage 3 pressure ulcer described?

A

Full thickness wound on areas subjected to pressure with or without underming

139
Q

How is a stage 4 pressure sore described?

A

Full thickness wound with involvement of major tissues with/ without underming

Exposed bone, tendon, muscle

140
Q

What in the clinical presentation of a pressure sore?

A

Localised tenderness or erythema

Increased exudate/ foul odour

141
Q

What investigations are performed to diagnose a pressure sore?

A

Clinical diagnosis
Swab wound to rule out infection
Deep tissue biopsy

142
Q

Why is it important to take pictures of pressure sores?

A

Monitor progression and compare to previous presentation

143
Q

Differentials for pressure sore?

A

Moisture associated dermatitis
Venous ulcer
Arterial ulcer
Diabetic neuropathy
Pyoderma gangrenesum
Osteomyelitis

144
Q

What is the management of pressure sores?

A

Pressure reducing aids
Reposition patient
Hygiene and cleansing with dressings
Analgesia

For stage 3/4 ulcers consider antibiotic therapy or surgery

145
Q

What are the monitoring requirements of pressure sores?

A

Assess risk routinely
Regular repositioning of patient
Swab sore for infection
Regular dressings

146
Q

Complication of pressure sores?

A

Sepsis
Cellulitis
Osteomyelitis
Mortality

147
Q

What in the prognosis of pressure sores?

A

High risk of recurrence especially in spinal injuries patients

148
Q

What is elderly abuse?

A

Intentional act or failure to act that causes harm or creates risk to an older adult

149
Q

What is the frequency of elder abuse?

A

Reported cases of 2.6%
For every reported case upto 24 go unreported

150
Q

Aetiology of elder abuse?

A

Physical and cognitive decline
Psychosocial abnormalities in alouser
Carer stress
Environmental factors

151
Q

Types of elder abuse?

A

Physical injuries
Mental abuse
Financial abuse
Sexual abuse
Neglect

152
Q

Risk factors for elderly abuse?

A

Age over 75 years
Cognitive impairment
Dependance on carer for personal carer
Depression /other mental illness
Substance misuse in carer
Financial dependance of older adult

153
Q

Presentation of elder abuse?

A

Self report abuse
Inconsistent history from carer and patient
Agitated state
Social isolation
Physical injuries
Malnutrition
Improper medication use
Carer dominance
Pressure ulcers
Shabby appearance

154
Q

Differentials for elderly abuse?

A

Dementia
Falls in elderly
Medicine non adherence
Substance abuse
Depression

155
Q

Investigations for elderly abuse?

A

Clinical photographs
X-ray, CT head, abdomen
Serum drug and toxicology screen

156
Q

Management of elderly abuse?

A

Treat injuries
Involve social services
Report incidents to authorities

157
Q

Complications of elderly abuse?

A

Pressure ulcer
Fractures; Hip, ankle, wrist, rib, spinal compression fracture
Brain injury
Depression
Delirium
PTSD
Death

158
Q

What is polypharmacy?

A

Prescribing of medications no longer clinically indicated, appropriate or optimised for that person

Combination of medications has potential to cause harm

Practicalities of using medicines prescribed is unmanageable, causing harm or distress

159
Q

Benefits to patient for tackling polypharmacy?

A

Fewer adverse drug reactions

Fewer hospital admissions

Improved patient outcome

Shared decision making leading to greater commitment to treatment

Improved relationship between patient and healthcare proffesional, education and managemencent of wider health issues

160
Q

Benefits to healthcare system for management of polypharmacy?

A

Reduced burden on repeat prescribing systems

Reduced waste medication

Better value from funded medication
Fewer avoidable hospital admissions

161
Q

How common is constipation in elderly?

A

Affects over 1/3 of patients over 60 years

162
Q

What is the aetiology/ risk factors for constipation?

A

Female sex
Older age
Inactivity
Low calorie intake
Low fibre diet
Polypharmacy
Low income

163
Q

What is the clinical presentation of constipation?

A

Straining while opening bowels
Difficulty passing stool
Incomplete evacuation
Hard stool
Abdominal pain

164
Q

What is the management of constipation?

A

Lifestyle changes; increased physical activity, adequate dietary fibre intake and fluids, reduce coffee, tea and alcohol

Bowel training

Provide laxative

Enemas

165
Q

Complications of constipation?

A

Syncope
Anorexia
Nausea
Pain
Ulcer which can perforate

166
Q

What is urinary incontinence?

A

Involuntary accidental leakage of urine

167
Q

What is the aetiology of urinary incontinence?

A

Weak bladder or pelvic floor muscles
Overactive detrusor muscle
Damage to nerves innerrating bladder
Arthritis and mobility problems can delay reaching toilet
Pelvic organ prolapse
Injury during surgery

168
Q

What are the types of urinary incontinence?

A

Stress incontinence
Urge incontinence
Overflow incontinence
Functional incontinence

169
Q

What are treatment options for incontinence?

A

Bladder control exercises
Mediation
Pessary
Catheter
Electrical nerve stimulation
Surgery

170
Q

What is malnutrition?

A

Deficiency or excessive nutrient intake, imbalance of essential nutrient utilisation leading to poor health and growth
Affects all systems of the body, increasing vulnerability to illness

171
Q

Epidemiology of malnutrition?

A

1 in 20 adults in UK are affected
Costing NHS £20 billion per year

172
Q

What in the aetiology of malnutrition?

A

Mental health condition
Change in mental state; bereavement
Low intake of food
Social and mobility issues
Digestive tract disorder; malabsorption, inflammatory bowel disease, IBS, dysphagia
Dementia
Alcohol use

173
Q

Risk factors for malabsorption?

A

Increasing age
Social isolation
Low income
Serious illness

174
Q

Clinical presentation of Malnutrition?

A

Tiredness and low energy
Loss of appetite
Unintentional weightloss
Clothes become lose
Loss of fat, muscle mass and tissue
Longer healing after cuts/ infection
Dizziness / headache
Difficulty keeping warm

175
Q

Investigations for malnutrition?

A

MUST screening tool
History + examination
Blood texts to rule out organic cause

176
Q

Management of malnutrition?

A

Involve dietician to start nutrition
Monitor for re-feeding syndrome

177
Q

Complications of malnutrition?

A

Re-feeding syndrome
Fatigue and lethargy
Falls
Difficulty coughing
Heart failure
Anxiety, depression, psychosocial problem
Reduced ability to fight infection

178
Q

What is a DOLS?

A

Procedure described in law where it is necessary to deprive a patient or resident of their liberty who lacks capacity to consent to care/ treatment

179
Q

Where is DOLS applicable?

A

Nursing home or hospital in England or Wales

180
Q

What is a DNACPR?

A

In a situation in which patients heart stops beating or they stop breaking the healthcare team will not perform CPR

Phase 3A (7 decks)

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