Geriatrics Flashcards
Delirium (acute confusional state)
clinical syndrome with acute onset, fluctuating change in mental status with inattention, disorganised thinking & altered levels of consciousness usually seen in >65y/o hospitalised pts
Characterised by high morbidity & mortality
Epidemiology of delirium
most common complication of hospitalisation in the elderly & high incidence in those with pre-existing cognitive impairment
↑ incidence with age
usually seen in those >65 y/o
Risk factors for delirium
age >65 yrs male sex pre-existing cognitive deficit e.g. dementia severe comorbidity previous delirium current severe illness/hip fracture ↑ pain drug use/dependence / substance misuse visual/hearing impairment poor mobility social isolation terminal illness ICU admission
Aetiology of delirium
Acute infections especially UTIs prescribed drugs e.g. benzos, analgesia (morphine), steroids, antiparkinson meds surgery/trauma urinary retention constipation sleep deprivation pain dehydration toxic substances (drugs/alcohol) neoplasia/malignancy
Subtypes of delirium
Hypoactive:
↓ psychomotor activity, apathy & quiet confusion
mostly seen in elderly pts
Hyperactive:
↑ psychomotor activity, agitation, delusions & disorientation
usually seen with substance abuse/withdrawal
Mixed delirium:
fluctuating psychomotor activity between hyper/hypoactive states
most common in general population
Presentation of delirium
usually acute presentation
fluctuating course throughout day
may be worse in evening (sundowning)
disorganised thinking, hallucinations (usually visual), cognitive deficits, impaired memory, emotional lability,, agitation, combativeness, disorientation, poor concentration, psychotic ideas (short duration & simple content)
Investigating delirium
Full physical examination Bloods (FBC/U&Es/LFTs/TFTs/Mg2+/Ca2+/creatinine/glucose) ECG Urine dip + MC&S CXR blood cultures ABG imagine/investigations for suspected cause
Management of delirium
treatment of underlying condition
Supportive care:
clear communication, reminders of day/time/location, familiar objects from home, involve family & carers
Environmental:
side room, control noise/lighting/temp
adequate nutrition
attention to continence / help with constipation
stop offending medication (e.g. benzos, morphine, warfarin, furosemide, lithium, TCAs, steroids)
Alzheimers dementia (AD)
a chronic neurodegenerative disease wait insidious onset & progressive but slow decline, may occur commonly with other types of dementia e.g. vascular
most common type of dementia
Characteristics of Alzheimer dementia (AD)
widespread cortical atrophy
extracellular senile/amyloid plaques made from beta amyloid
intracellular neurofibrillary tangles made from hyperposphorylated Tau
↓cholinergic function (acetylcholine deficiency)
Risk factors for Alzheimer dementia (AD)
caucasian heritage ↑ age hyperlipidaemia diabetes HTN smoking alcohol misuse Down's syndrome Genetics
Presentation of Alzheimer dementia (AD)
insidious onset & slow progression
short term memory impairment (episodic memory affected first)
disorientation (in time & place, subtle at first e.g. misplacing items/getting lost)
Presentation of Alzheimer dementia (AD)
insidious onset & slow progression
short term memory impairment (episodic memory affected first)
disorientation (in time & place, subtle at first e.g. misplacing items/getting lost)
nominal dysphasia
apathy
impaired ADLs
personality change / mood change
poor abstract thinking & judgement
psychiatric symptoms
agitation & irritability
impaired executive function (later on in disease)
Investigations for Alzheimer dementia (AD)
Bedside cognitive assessment (MMSE, MoCA, AMTS)
CT/MRI head (cortical atrophy)
Management of Alzheimer dementia (AD)
Person centred MDT care (memory assessment, memory enhancement strategies, therapies e.g. aroma/music therapy)
Pharmacological:
1st line: AChE inhibitors e.g. donepezil, galantamine, rivastigmine (for moderate AD)
2nd line: NMDA receptor antagonist e.g. memantine (if AChE contraindicated/as add on to AChE)
SSRIs as depression
Genetics of Alzheimer dementia (AD)
Amyloid precursor protein (APP)
Presenilin 1
Presenilin 2
ApoE4 (late onset)
NB ApoE3 = neutral & ApoE2 = portective
Vascular dementia (VD)
also know as multi infarct dementia, is a chronic progressive cognitive impairment caused by cerebrovascular disease leading to ischaemia / haemorrhage
2nd most common type of dementia
Sybtype of vascular dementia (VD)
its a spectrum of disease called vascular cognitive impairment of which vascular dementia is the worst
stroke related VD - multi/single infarct
subcortical VD - small vessel disease
mixed dementia - presence of both VD & AD
Inherited form of Vascular dementia
inherited as CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
RARE
Risk factors for vascular dementia (VD)
↑ age history of stroke/TIA AF HTN Diabetes smoking obesity CHD
Investigation/Assessment of vascular dementia (VD)
cognitive impairment screening
MRI/CT (may show infarcts / white matter changes)
NINDS-AIREN for diagnosis of probably VD (presence of cognitive decline interfering with ADLs, presence of CVD, relationship between the 2 suspected)
Management of vascular dementia (VD)
Individualised person centred care (cognitive stimulation programmes, therapies, multi sensory stimulation)
consider AChE inhibitors or memantine if comorbid Alzheimers
Frontotemporal dementia
progressive neurodegenerative disease of the frontal and/or temporal lobe generally due to mutations of proteins leading to lobar atrophy
3rd most common type of dementia
Onset of Frontotemporal dementia
usually age <65yrs
i.e. earlier than other dementias
Presentation of Frontotemporal dementia
insidious onset relatively preserved memory & visuospatial skills personality change social conduct problems disinhibition inappropriate social behaviour loss of empathy/sympathy lack of insight may have difficulties with speech (hesitant, loss of vocabulary, ↓fluency)
Investigations/Assessment of Frontotemporal dementia
formal cognitive testing & dementia screen
MRI (atrophy of frontal and/or temporal lobe)
Management of Frontotemporal dementia
patient centred care (SALT, therapies, supportive therapy)
SSRIs = 1st line to modify behavioural symptoms
atypical antipsychotics = 2nd line
Hallmarks of the subtypes of frontotemporal lobar degeneration
Chronic progressive aphasia:
Non fluent speech with meaning
Semantic dementia:
fluent but empty speech
Pick’s disease (frontotemporal dementia)
personality change, disinhibition & inappropriate social conduct
Lewy body dementia (LBD)
clinical syndrome of progressive conginitve decline characterised by pathological alpha-synuclein cytoplasmic inclusion (Lewy bodies) in the substantial migration, paralimbic & neo cortical areas
~20% of all dementia
Lewy body dementia vs Parkinsons dementia
LBD:
onset of cognitive & motor symptoms within 1 year of each other
Parkinsons dementia:
if cognitive symptoms occur >1 year after onset of motor symptoms
Presentation of Lewy body dementia (LBD)
progressive cognitive impairment in contrast to Alzheimer’s, early impairments in attention and executive function
cognition may be fluctuating, in contrast to other forms of dementia
parkinsonism
visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
Presentation of Lewy body dementia (LBD)
progressive cognitive impairment (memory loss, decline in problem solving ability, spatial awareness difficulties, impairment of executive function & attention)
conginiton may be fluctuation (fluctuating levels of attention & awareness)
Mild parkinsonism (tremor, rigidity poverty of facial expression, bradykinesia)
visual hallucinations
frequent falls
REM sleep disturbances
NB unlike AD there is early impairment of executive function & attention rather than just memory
Management of Lewy body dementia (LBD)
patient centred care (care plans, therapies, cognitive stimulation programmes)
Pharmacological:
AChE inhibitors & memantine can be used as in AD
Medication to avoid in Lewy body dementia (LBD)
Its very sensitive to antipsychotics
may cause them to develop irreversible parkinsonism & worsen the dementia
Osteoporosis
progressive systemic skeletal disease characterised by ↓ bone mass & micro-architectural deterioration of bone tissue leading to ↑ fragility of the bone & ↑ susceptibility to fractures
more common in women
↑incidence with age
Bone density assessment
Bone density is expressed as standard deviation in relation to a reference population
A Z-score compares bone density of an individual to normal at that age, with a score of -2 indicating bone density below the normal for that age
A T-score compares bone density of an individual to that of a young healthy population
Characterising bone density assessment
Normal:
T-score ≥ -1
Osteopenia:
T-score < -1 but > -2.5
Osteoporosis:
T-score ≤ -2.5
Severe osteoporosis:
T-score ≤ -2.5 + a fracture
Risk factors for osteoporosis
female sex ↑ age low BMI smoking alcohol misues prolonged immobilisation corticosteroid use menopause medications (PPIs, L-thyroxine, anticonvulsants, heparin, steroids) family history of osteoporosis / fragility fractures
Management of osteoporosis
For everyone: Vit D & Calcium supplementation
1st line: Bisphosphonates e.g. Alendronate (1st line) or risendronate (2nd line)
2nd line: denusomab (has increasing role as 2nd line), Raloxifene, strontium ranelate
NB if alendronate not tolerated try risendronate before moving onto 2nd line medication e.g. denusomab
Management of osteoporosis
For everyone: Vit D & Calcium supplementation
1st line: Bisphosphonates e.g. Alendronate (1st line) or risendronate (2nd line)
2nd line: denusomab (has increasing role as 2nd line), Raloxifene, strontium ranelate
NB if alendronate not tolerated try risendronate before moving onto 2nd line medication e.g. denusomab
Investigation / Assessment of osteoporosis
DEXA scan /plain X-rays
FRAX or Q-fracture scores to assess 10yr rick of pt developing frailty fracture
Ca2+ / Phosphate / PTH / Alkaline phosphatase (all normal)
How to take Bisposphonates
How to take:
take 30 min before meal in morning & evening with plenty of water & standing up/keep upright for 30 min after
Adverse effects of Bisposphonates
Adverse effects:
oesophageal reactions: oesophagitis, oesophageal ulcers (especially alendronate)
osteonecrosis of the jaw (presents as jaw pain)
↑ risk of atypical stress fractures of the proximal femoral shaft in patients taking alendronate
Pressure sores / ulcers
A focal area of unrelieved pressure resulting in ischaemia, cell death & necrosis of the epidermis & soft tissue, which typically develop over bony prominences
Pressure sores / ulcers
A focal area of unrelieved pressure resulting in ischaemia, cell death & necrosis of the epidermis & soft tissue, which typically develop over bony prominences
generally develop in its unable to move parts of their bodies due to illness / paralysis / age
Risk factors for developing Pressure sores / ulcers
malnourishment incontinence lack of mobility ↑ age surgery previous pressure ulcers sensory impairment diabetes dementia critical care pts
Score used for risk assessment of Pressure sores / ulcers
Waterlow score
includes a number of factors including body mass index, nutritional status, skin type, mobility and continence.
Grade 1 Pressure sores / ulcers
non blanching erythema of intact skin / discolouration of skin
warmth/oedema/induration/hardness may be used as indicators especially in those with darker skin where it may appear blue/purple
Grade 2 Pressure sores / ulcers
partial thickness skin loss involving epidermis / dermis or both, the ulcer is superficial & presents clinically as an abrasion or blister
surrounding skin may be red / purple
Grade 3 Pressure sores / ulcers
full thickness skin loss involving damage to / encores of subcutaneous tissue that ma extend down to but not through the underlying fascia
Grade 4 Pressure sores / ulcers
extensive destruction / tissue necrosis / damage to muscle/bone/supporting structures with or without full thickness skin loss
extremely difficult to heal & predisposes to potentially fatal infection
Unstageable Pressure sores / ulcers
full thickness tissue loss in which the base is covered by slough and/or eschar in the wound resulting in inability to determine true depth
Typical locations of Pressure sores / ulcers
Sacrum
Heels
others include elbows, lateral malleolus, greater trochanter
Secondary infections of decubitus ulcers
very common
especially with staph aureus & pseudomonas
Investigations of Pressure sores / ulcers
generally clinical diagnosis
may want to consider wound swab
Management of Pressure sores / ulcers
often difficult to heal
pressure relief e.g. alternating pressure mattresses, reposition (every 2h), mobilising pt
adequate nutrition, treat underlying condition, adequate pain relief
infection control (clean, senile dressing) + Abs (if indicated)
dressings & debridement
Time between admission and assessment of pressure ulcer risk
<6h
pressure sores can develop within hours in an immobilised individual
Pathological / fragility fractures
fractures that result from mechanical forces that would not ordinarily result in a fracture, known as low energy trauma e.g. forces equivalent to a fall from standing height or less
Aetiology of Pathological / fragility fractures
Metastatic tumours:
breast, lung, thyroid, renal, prostate
Bone disease: osteogenesis imperfecta (brittle bone disease), osteoporosis, metabolic bone disease, Paget's disease
Local benign conditions:
chronic osteomyelitis, solitary bone cysts
Primary malignant tumours:
chondrosarcoma, osteosarcoma, Ewing’s sarcoma
Presentation of Pathological / fragility fractures
common sites include vertebrae (compression), hip fracture distal radius (Colles)
other sited include ribs, pelvis, arm, shoulder
NB vertebral compression fractures may often go unrecognised & cause worsening back pain
Assessment of Pathological / fragility fractures
FRAX score / Q-fracture score (used to assess risk of fragility fracture in the next 10yrs)
± a DEXA scan
Prognosis of Pathological / fragility fractures
often result in ↓QoL, pain, disability & loss of independence
Falls in the elderly
falls are a major threat to older peoples QoL often causing ↓ in self care ability & participation in physical & social activities
fear of falling can often lead to further decline in activity
Risk factors for falling
lower limb muscle weakness vision problems incontinence age >65 fear of falling polypharmacy (>4 meds) depression postural hypotension psychoactive drugs cognitive impairment arthritis balance/gait disturbances low weight history of falls alcohol misuse confusion inappropriate footwear environmental factors malnutrition
Risk of injury from falls
weak bones (e.g. osteoporosis, osteomalacia, pagets) poor self protection (lack of subcutaneous fat, neurological problems)
Investigations for falls
Full history (including risk assessment & medication review) & examination
BP, LSBP, bloods glucose, urine dip, ECG
FBC/U&Es/LFTs/bone profile/Vit B12/TFTs
CXR/X-ray of injured limb, CT head, echo
Prevention of falls
Environmental: home assessment & modification
Power & balance: exercise
Alcohol: ↓intake
Neurological issues: treat underlying disease & PT/OT/SALT input
visual disturbance: e.g. cataracts (can be managed)
Medication: should be reviewed, with STOPP-START guide
Falls assessment tests
Turn 180° test
timed up and go test
Medications that commonly cause falls
Meds causing postural hypotension:
nitrates, diuretics, anticholinergics, beta blockers, L-Dopa, antidepressants, ACE-Is
Other meds causing falls:
benzos, antipsychotics, opiates, codeine, digoxin, anticonvulsants, sedatives
STOPP-START guide
A screening tool in older people to recognise medicine safety concerns: STOPP identifies medications where the risk outweighs the therapeutic benefits in certain conditions and START suggests medications that may provide additional benefits ie proton pump inhibitors for gastroprotection in patients on medications increasing bleeding risk
Incontinence
lack of voluntary control over urination or defecation
associated with loss of dignity & social isolation
related issues include moisture, pressure sores, skin breakdown & infection
Urinary incontinence
common problem affecting 4-5% of the population, but grossly underreported (affectes 30-40% of people aged >65yrs)
especially common in elderly females
Risk factors for urinary incontinence
pregnancy childbirth ↑ age high BMI Family history hysterectomy UTIs cognitive impairment neurological disorders
Stress incontinence
involuntary leakage of urine on effort/exertion e.g. coughing or laughing
due to weak/incompetent sphincters e.g. due to obesity/pelvic trauma/post prostate surgery
or secondary to weak pelvic floor muscles e.g. due to childbirth or genitourinary prolapse
positive bladder stress test i.e. urine leakage on ↑ intraabdominal pressure
Functional incontinence
does not involve lower urinary tract but rather due to environmental / psychological / cognitive / physical impairement
e.g. pts unable to make it to toilet in time due to poor mobility
Urge incontinence
aka overactive bladder
strong sudden sense of urgency followed by involuntary leakage of urine i.e. a compelling desire to urinate that cannot be deterred
due to detrusor instability / hyperreflexia leading to involuntary detrusor contraction
often idiopathic or may be secondary to PD/MD/dementia etc
Overflow incontinence
frequent & involuntary intermittent/constant dribbling of urine in absence of the urge to urinate
due to impaired/weak detrusor e.g. in MS with neurogenic bladder leading to incomplete voiding
or a bladder outflow obstruction e.g. BPH
Mixed incontinence
mixture of urge & stress incontinence
Investigating urinary incontinence
history & examination urine dipstick & culture post void bladder scan urodynamics study FBC/U&Es/LFTs
General management of incontinence
temporary containment products e.g. pads / collecting devices to achieve social continence
lifestyle changes e.g. change fluid intake, regular toileting
Management of stress incontinence
1st line: pelvic floor exercises
2nd line: duloxetine / surgery (e.g. mid urethral tape)
Management fo urge incontinence
1st line: bladder retraining
2nd line: bladder stabilising drugs e.g. antimuscarinics including oxybutynin/tolterodine
if worried about anticholinergic effects in frail elderly pts consider mirabegron
NB avoid oxybutynin in frail older women
Management of mixed incontinence
1st line: bladder retraining & pelvic floor exercises
Management of overflow incontinence
relieve obstruction e.g. finasteride/tamsulosin for BPH
intermittent self catheterisation
Faecal incontinence
inability to control / involuntary discharge of stool / gas
Risk factors for faecal incontinence
↑ age diarrhoea urinary incontinence constipation multiple child births
Aetiology of faecal incontinence
- childbirth (especially if associated with obstetric trauma)
- surgery (e.g. haemorrhoidectomy / anal tissue repair)
- degeneration of internal anal sphincter (↓resting pressure)
- neurological disease (post stroke, cerebral tumours, MS, dementia)
- constipation (faecal impaction can lead to overflow incontinence)
- medication (e.g. laxative abuse/overuse)
Investigations for faecal incontinence
change in bowel habit warrants investigation
FBC/ferritin/U&Es/bone profiel/TFTs
stool sample
faecal occult blood
Management of faecal incontinence
diet & nutrition, optimise hydration
bower training & regular timing of going to bathroom
medication (consider alternative to meds that may contribute to incontinence e.g. loperamide)
skin protection
NB if pts with faecal loading/impaction = rectal bowel clearance with enemas or potent oral laxatives
Multimorbidity
defined as the presence of ≥ 2 long term health conditions including defined physical / mental health conditions, learning disabilities, symptom complexes such as chronic pain, sensory impairments & alcohol / substance misuse
Risk factors for multimorbidity
↑ age female sex low socio-economic status smoking alcohol misuse lack of physical activity poor nutrition obesity
Assessment of frailty
Rockwood frailty score
PRISMA-7 questionnaire
establish extent of disease burden
assess pain management
Colon cancer
3rd most common cancer in the UK, 2nd leading cause of cancer death
Screened for via faecal occult test every 2yrs for all those aged 60-74 in England & offered a colonoscopy if abnormal
presents with weight loss, night sweats, fever, fatigue, abdo discomfort, change in bowel habits, blood in stool
staged with Duke’s classification on colonoscopy / CT + measure CEA (carcinoembryonig antigen)
managed with surgery ±radio/chemo
Breast cancer
most common cancer in females, with invasive ductal carcinoma being the most common
screening is a 3 yearly mammogram for all those aged 50-70 yrs
presents with palpable mass, retraction, skin dimpling, nipple inversion, bloody discharge, lymphadenopathy
Breast cancer
most common cancer in females, with invasive ductal carcinoma being the most common
screening is a 3 yearly mammogram for all those aged 50-70 yrs
presents with palpable mass, retraction, skin dimpling, nipple inversion, bloody discharge, lymphadenopathy
investigated with mammography, USS, fine needle aspiration / core needle biopsy
managed with mastectomy / wide local excision ± sentinel node biopsy ± radio/chemo
Prostate cancer
very common cancer in men (95% are adenocarcinoma)
presents with lower urinary tract symptoms e.g. hesitancy, polyuria, nocturia, retention, haematuria but often asymptomatic initially
investigated with PSA, PR exam, transrectal USS, Biopsy (scored using Gleason score) ± MRI/CT
managed with prostatectomy, radiotherapy or goserelin (GnRH agonist)
Pancreatic cancer
commonly adenocarcinoma that tend to be diagnosed late
presents very non specific i.e. weight loss fatigue, epigastric pain, painless jaundice (pancreatic cancer until proven otherwise), pruritic, atypical back pain
investigated with USS & high resolution CT
only ~20% suitable for surgery at diagnosis, Whipples resection (pancreatoduodenectomy)
Stomach cancer
usually seen in those aged 70-80, associated with smoking & H. pylori infections
presents with dyspepsia, N&V, anorexia, weight loss, dysphagia
investigated with endoscopy & biopsy + CT for staging
Managed with subtotal/total gastrectomy + chemo
Lung cancer
leading cause of cancer death world wide, 90% are attributable to smoking
presents with haemoptysis, persistent cough, dyspnoea, weight loss, chest pain, hoarseness, wheezing
investigated with CXR, CT & bronchoscopy
managed with surgical resection ± chemo, or radiotherapy if inoperable
Oesophageal cancer
most commonly adenocarcinoma, often relayed to GORD/Barretts oesophagus or smoking
presents with dysphagia, weight loss, vomiting, hoarseness, odynophagia
investigated with upper GI endoscopy, contrast swallow & CT
managed with oesophagectomy ± adjuvant chemo
Chronic lymphocytic leukaemia (CLL)
monoclonal proliferation of well differentiated lymphocytes, usually B-cells (99% of cases)
usually asymptomatic, but may present with weight loss, anorexia, infections, lymphadenopathy
investigated with FBC, blood film and immunophenotyping
managed with close observation if asymptomatic otherwise chemo & rituximab/ibrutinib
Myeloma
characterised by plasma cell proliferation usually seen round the age 70
presents with hypercalcaemia (constipation, nausea, confusion), renal impairment, anaemia, bleeding/bruising, bone pain, fragility fractures & infections
investigated with blood film, serum/urine electrophoresis (↑ monoclonal IgG/IgM), Ca2+ (↑), FBC (anaemia) & MRI (lytic bone lesions)
managed with Thalidomide + an Alkylating agent + Dexamethasone as old people unlikely to be suitable for stem cell transplant
Basal cell carcinoma (BBC)
most common type of skin cancer & cancer in the western world
presents on sun exposed areas e.g. head/neck as rodent ulcers which grow very slowly, often initally a pearly white coloured papule with telangiectasia
managed with surgical excision with histopathology ± radiotherapy
Squamous cell carcinoma (SCC)
common skin cancer, 2nd most common after BCC
presents initially as plaque like nodular papillomatous rash which then ulcerates usually with red inverted edges, the floor of the ulcer bleeds easily
found on face/neck especially lower lip/ear/hands
managed with surgical excision + margins with histopathology after
