Elderly Flashcards

1
Q

What is dementia?

A

Irreversible, chronic and progressive cognitive impairment which is sufficient to impair ADLs
Problems present for 6/12
Only proven post mortem with histological evidence

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2
Q

Differentials for dementia

A

Delirium
‘Reversible dementia’: present with cognitive impairment that may resolve if treated e.g subcutaneous haematoma, hypothyroidism and vitamin deficiency
Pseudodementia: memory problems in severe depression can resemble dementia
HIV-related cognitive impairment/dementia
MCI

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3
Q

Investigations for dementia

A

Bloods: FBC (infection/anaemia), U&Es (dehydration, renal failure, hyponatraemia)
Glucose
TFTs (hypothyroidism), LFTs (alcohol misuse)
MMSE
Collateral Hx
Septic screen: MSU, CXR, blood cultures, wound swabs, sputum/stool samples
CT head/MRI

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4
Q

Mx for dementia

A

Adaptations for patients: dosset boxes/blister packs to help medication compliance, reality orientation (visible clocks)
Social support: personal care, meal prep or med prompting
Support carers
Treat sensory impairment: glasses/hearing aids
Psychological therapies
Psychotropic meds

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5
Q

What psychotropic medications can be used in dementia?

A

Start low and go slow is golden rule
Acetylcholinesterase inhibitors (donepezil/rovastigimine) prevent acetylcholinesterase destroying acetylcholine - increasing neurotransmitter levels in synapses and compensating for overall cholinergic loss - not curative but slow process in AD and DLB
Sodium valproate and low dose BDZs or antipsychotics can also be used as a last resort if behavioural management

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6
Q

Aetiology of alzheimers

A

age is main risk factor
amyloid plaques and neurofibrillary tangles
accumulation of these leads to reduction in information and eventually death of brain cells
Genetics can cause early onset: autosomal dominant - Presenelin 1 (chromosome 14), Presenelin 2 gene (chromosome 1), beta-amyloid precursor protein (APP) gene (chromosome 21)

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7
Q

Pathology of Alzheimer’s

A

Atrophy: due to neuronal loss, hippocampus affected early, then temporal and parietal lobes, on CT sulci and ventricles may be enlarged (can be normal)

Plaque formation: APP can be abnormally cleaned into beta-amyloid which aggregates into insoluble lumps

Intracellular neurofibrillary tangles (NFTs)
Cholinergic loss

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8
Q

Risk factors for vascular dementia

A

older age
male sex
smoking
HTN
DM
Hypercholesterolaemia
AF

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9
Q

Pathology of vascular dementia

A

atherosclerosis, cortical ischaemia and infarction
Infarcts appear in CT as multiple lucencies

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10
Q

Presentation of vascular dementia

A

stepwise progression with each step representing a sudden deterioration as an infarct occurs
Many tiny infarcts causes a smoother more subtle deterioration
Sx reflect sites of lesions and may be ‘patchy’ and some areas of cognition spared
Neurological signs: hemiparesis or aphasia, episodes of confusion especially at night

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11
Q

Lewy Body dementia pathology

A

Lewy bodies are eosinophilic intracytoplasmic neuronal structures
Made of alpha-synuclein with uniquitin
PD found in brainstem but in DLB also seen in cingukate gurus and neocortex

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12
Q

Presentation of Lewy Body dementia

A

Fluctuating confusion with marked variation in levels of alertness
Vivid visual hallucinations
Spontaneous parkinsonism
Falls, syncope and TLOC
Short term memory is less affected
Can resemble delirium but don’t prescribe antipsychotics as extreme antipsychotic sensitivity in DLB can result in death

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13
Q

Aetiology of frontotemporal dementia

A

Neuron damage and death occurs in frontal and temporal lobes
Atrophy occurs due to deposition of abnormal proteins (often tau protein) within lobes

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14
Q

Clinical features of lewy body dementia

A

altered emotional responsiveness, apathy, disinhibition, impulsivity
progressive decline noted in interpersonal skills
changes on food preference, more childlike amusements
obsessions and rituals may be noted
progressive breakdown in output of language
speech takes effort and is not-fluent, apraxia or disorders of speech sound
impaired comprehension of sentences and impact on literacy skills

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15
Q

What is normal pressure hydrocephalus?

A

Occurs due to abnormal build up of cerebrospinal fluid in ventricles causing increased pressure, producing symptoms of cognitive impairment
Occur at any age

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16
Q

Risk factors for normal pressure hydrocephalus

A

head trauma
infection or inflammation of brain
tumours
subarachnoid haemorrhage

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17
Q

Sx of normal pressure hydrocephalus

A

progressively worsening memory lapses
personality and mood disturbances
difficulties with walking
dementia
urinary incontinence

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18
Q

Mx of normal pressure hydrocephalus

A

Ventriculoperitoneal (VP) shunt is used to drain excess CSF into abdomen, relieved pressure on brain

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19
Q

Prion protein diseases (CJD)

A

Infectious prion proteins cause diseases such as Creutzfeldt-Jakob disorder
can be sporadic or variant
sporadic CJD tends to affect under 40s
Variant CJD is caused by eating meat infected by bovine springform encephalopathy through infected cattle meat

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20
Q

Presentation of CJD

A

Initially minor memory lapses, mood disturbances and loss of interest
Progresses over weeks to unsteadiness and physical clumsiness
Then to stiffness, jerking movements, incontinence and aphasia
Death occurs within 6m of symptom presentation

21
Q

Delirium

A

Acute transient state of global dysfunction with clouding of consciousness
Patient not aware of their environment
Sign of physical illness need to treat underlying cause

22
Q

Risk factors for delirium

A

old age
pre-existing physical/mental illness
substance misuse
polypharmacy
malnutrition

23
Q

Causes of delirium

A

Trauma: head injury, burns
hypoxia
infective
metabolic: electrolyte disturbances, end organ failure
hypoglycaemia
nutritional: Wernickes encephalopathy
raised ICP
Drugs and alcohol: intoxication/withdrawal
Medications: anticholinergics/opiates

24
Q

Clinical presentation of delirium

A

sudden onset
fluctuating symptoms
often worse in evenings/night
usually disorientated and has poor attention/short term memory
mood changes
illusions and hallucinations
disorganised thinking and pressured/rambling speech
hypoactivity or hyperactivity

25
Q

physiological changes of ageing

A

cardiac: CO decreases, BP increases, development of arteriosclerosis
Resp: impaired gas exchange, decrease in vital capacity, slower expiratory flow rates
Renal: decreased creatinine clearance, serum creatinine stays constant due to proportionate age-related decrease in creatinine production
Altered hepatic drug metabolism
Osteoporosis
Epidermal atrophy in skin
Decline in lean body mass
Degenerative joint changes and loss of muscle mass

26
Q

Methods of assessing frailty

A

Electronic frailty index (EFI) automated tool which uses GP health records to assess frailty - used to identify patients >65 with moderate-severe frailty - higher score = increased level of frailty
Gait speed: taking >5s to cover 4m suggests frailty
Timed up and go test: taking >10s to get up from chair, walk 3m, turn and sit down suggest frailty
Rockwood clinical frailty score
PRISMA 7 questionnaire: score of >/= 3 suggests frailty

27
Q

What are frailty syndromes?

A

Increase chance of being frail
- falls
- immobility/sudden change in mobility “off legs”
- delirium/acute confusion or worsening of pre-existing memory loss
- new or worsening incontinence
- susceptibility to side effects of meds

28
Q

What is frailty?

A

clinically recognised state of increased vulnerability resulting from ageing and a decline in physical and physiological reserves
More common in those with multi-morbidity, low SES, poor diet and sedentary lifestyle

29
Q

Management and prevention of frailty

A

Comprehensive review of medical, functional, psychological and social needs
Med reviews
Falls reviews
Management and personalised care programmes (respect form)
Mid-life lifestyle changes to help delay or onset of dementia and frailty

30
Q

STOPP START criteria

A

STOPP (screening tool of older persons potentially inappropraite perscription) aims to reduce incidence of medicines-related adverse effects from potentially inappropriate prescribing polypharmacy
START (screening tool to alert to right treatment) can be used to prevent omissions of indicated, appropriate medicines in older people with specific conditions

31
Q

What is a geriatric assessment

A

Shown to improve outcomes for older people including improved physical and cognitive function, reduced mortality and readmissions
5 categories:
Physical health - problem list, comorbidities, medications, nutritional assessment
Mental health - cognitive status, assessment of mood
Functional status - basic ADLs, instrumentals ADLs, gait and balance assessment, exercise/activity assessment
Social functioning - informal social support
Environmental assessment - care resource eligibility/financial assessment, home safety, access to transport facilities
Focus on factors which patient has identified as priorities and main needs - develop a long-term plan to manage needs

32
Q

Impact of frailty

A

Increased risk of adverse outcomes: falls, hospitalisation, mortality
Increased healthcare use and costs
Suboptimal care: due to fragmented delivery of appropriate treatments and services (every organ system treated by different specialists)
Poorer QoL: more hospital attendances, more hospital admissions, decreased independence and increased reliance on others

33
Q

Nutrition in elderly patients

A

Energy requirements tend to fall with advancing age due to a decrease in basal metabolic rate and decreased physical activity
Ability to synthesise vit D in skin decreases with age - 10mcg of vit D daily - eat fortified foods such as oily fish and fortified cereal

34
Q

Risk factors for falls

A

History of falls
Conditions that affect mobility or balance: arthritis, DM, incontinence, stroke, syncope or PD
Muscle weakness
poor balance
visual/auditory/cognitive impairment
depression
alcohol misuse
polypharmacy/use of psychoactive drugs/anti-HTN - BDZs, anti-HTN increase risk of postural hypoT
Environmental hazards: loose rugs or mats, poor lighting, uneven surfaces, wet surfaces, loose fittings (hand rails) and poor footwear

35
Q

Causes of falls

A

lower limb weakness
gait/balance problems
visual impairment
arthritis of lower limb joints
postural hypotension (drugs, dehydration, anaemia, sepsis, prolonged bedrest, adrenal insufficiency)
Polypharmacy
cognitive impairment
Drugs: nitrates, anti-HTNs, anti-depressants, antipsychotics, opiates, anticholinergics, BDZs
Neurological conditions: previous stroke, PD, MS
DM
PVD

36
Q

Physical consequences of falls

A

fractures
open wounds
bruises
extravasation of blood
sprains
joint dislocations
brain injuries
strained muscles
long lie syndrome and rhabdomyolysis
functional decline

37
Q

Psychological consequences of falls

A

reduction in social and physical activities
reduced independence due to new difficulties with ADLs
depression and anxiety
fear of falling again - lead to avoidance of some activities, may stay in house
reduced contact with family or friends
reduced support to family and friends
increased concern from family - reduced independence

38
Q

What is osteoporosis

A

bone mineral density of 2.5/+ SD from mean peak mass measured by DEXA scan applied to femoral neck reported as a T-score
Increase in bone fragility and susceptibility to fracture
Primary = age-related
Secondary = due to other conditions/drugs

39
Q

What do different T-scores mean?

A

Normal = >-1
Osteopenia = -1 to -2.5
Osteoporosis = <-2.5
Severe osteoporosis <-2.5 + fracture

40
Q

Risk factors for oesteoporosis

A

Older age
Post menopausal women - HRT is protective (tamoxifen, raloxifene)
Reduced mobility and activity
Low BMI
Low calcium/vit D intake
Alcohol and smoking
personal or FH of fractures
Chronic disease (CKD, hyperthyroidism and RA)
Long-term corticosteroids (>7.5mg of prednisolone daily for >3m)
Certain meds: SSRIs, anti-epilpetics and anti-oestrogens

41
Q

Who is at high risk of fragility fracture?

A

All women 65/+
All men 75/+
All women 50-64 and men 50-74 with any risk factors
People <50 with any of:
-current or frequent use of oral steroids
- untreated premature menopause
- previous fragility fracture
People <40 with any of:
- current or recent use of high-dose oral steroids >7.5mg pred for 3m
Previous fragility fracture of spine, hip, forearm or humerus
Hx of multiple fragility fractures

42
Q

What can be used to calculate the risk of hip fracture and major osteoporotic fracture?

A

QFracture and FRAX assessment tools

43
Q

FRAX and QFracture

A

Estimates 10-year probability of a major osteoporotic fracture or hip fracture
10y risk of 10% is threshold for ordering DEXA
Clinical RF: age, sex, weight, height, smoking, alcohol use and previous fractures as well as BMD

44
Q

Non-osteoporotic causes of fractures

A

metastatic bone disease
multiple myeloma
osteomalacia
Paget’s disease

45
Q

Investigations for osteoporosis

A

XR: low sensitivity/specificity - often after fracture
DEXA scan: calculate BMD (T score: >2.5 SD below average = osteoporosis
Bloods: calcium, phosphate, ALP - normal in osteoporosis

46
Q

Mx of osteoporosis

A
  • lifestyle advice: weight bearing exercise may increase BMD, calcium and vit D rich diet
  • Bisphosphonates - 1st line = alendronic acid, 2nd = etidonate (not licensed for use in men) /risedronate
  • Calcium and vitamin D - offer if deficient
  • HRT - can prevent in postmenopausal women
  • Raloxifene
  • Teriparatide - if suffer further fractures despite treatment with other agents
  • Calcitonin - reduce pain after vertebral fracture
  • Denosumab: mon
47
Q

Mx if high risk of fragility fracture

A

Offer DEXA scan
Start treatment if BMD T-score -2.5 or less
If >-2.5 modify RF and repeat DEXA

48
Q

Mx if intermediate risk of fragility fracture

A
  • arrange DEXA scan for those whose fracture risk is close to threshold
  • offer drug treatment
  • no DEXA scan
  • Offer lifestyle advice and follow-up <5y