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HEALTHC ARE OF THE ELDERLYRevision Session
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TOPICS
Dementia
Delirium
Depression
Fragile bones & Fractures Falls
Parkinson’s & Movement Disorders
Cerebrovascular Disease, TIA & Stroke
Malignancy
Cardiology
Respiratory
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DEMENTIA
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DEFINITION
Needs to meet the following ALL three criteria:
An acquired decline in memory & other cognitive
functions
In an alert person
Sufficiently severe to affect daily life
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PREVALENCE & TYPES
1% Age 60-65
5% >65 years
>30% Over 85s
Dementia of AD (60%)
Vascular Dementia (30%)
Mixed
Neurodegenerative dementias (15%)
Reversible dementias (
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EXAMPLES OF NEURODEGENERATIVE D
Dementia with Lewy Bodies
Parkinson’s disease with Dementia
Frontotemporal Dementia (Pick’s disease)
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EXAMPLES OF REVERSIBLE DEMENTIAS
Drugs
Metabolic
Subdural haemorrhage
Normal Pressure Hydrocephalus
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THEY C AN’T BE L ABELLED AS DEMENTIA
Deaf
Dysphasic
Delirious
Depressed Under influence of drugs
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TRIGGERS FOR THINKING & DX DEMENTIA
Patient presents with delirium – common in
patients with already having dementia
After spouse’s death – poor cognition is seen
Social withdrawal Requests for help from social services
Poor concordance with prescribed drug therapy
Domestic crisis (e.g. fire (cook), Road traffic
accident) Spouse/family more control or speaking for
patient
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Including
delusional
beliefs,
disorientation in
time, place &
person,
comprehension &
language
impairment
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DEMENTIA A SSESSMENT - HISTORY
PC
HPC
PMHx
FMHX See lecture notes for complete list
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DEMENTIA A SSESSMENT - HISTORY
Typical story of dementia:
Progressive decline in cognitive function over several
years
Ending with complete dependency and death due to:
Dehydration
Malnutrition
+/- Sepsis
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DEMENTIA A SSESSMENT - HISTORY
When Deterioration (DDx type of Dementia):
If
Insidious (slowwwwwwwww) & Gradual AD
Stepwise Stroke/vascular aetiology
Abrupt after a single critical stroke
Rapid over weeks/months think drug, metabolic or
structural cause (e.g. tumour, subdural)
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DEMENTIA A SSESSMENT - HISTORY
Abnormalities arise in following:
7. Ability to self-care
E.g. grooming, bathing, dressing, continence/toileting
8. Ability to recognise familiar objects, people and
places (agnosia)
9. Ability to carry out complex, co-ordinated
movements (apraxia)
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DEMENTIA A SSESSMENT – PHYSICAL EX
Look for reversible factors and underlying cause
of cognitive impairment e.g.think risk factors
Vascular disease e.g. CVD, PVD. Cerebrovascular
Parkinsonism
Stage of dementia:
E.g. in advanced dementia (of any type), may observe:
Primitive reflexes (grasp, suckling, palmar-mental)
Global hyperreflexia +/- extensor planters
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DEMENTIA A SSESSMENT – MENTAL EX
Use of CAM to exclude delirium (agitation,
restlessness, poor attention and flucuating
conscious level)
Use of Geriatric Depression Scale to exclude
depression
Use of MOCA
to measure cognitive function
Check lecture
Aim is to check if any anxiety, depression or
hallucinations
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CONTINUED….
Require full neuropsychological assessment!
To ddx between dementia & depression
Differentiate subtypes
AAMI vs Early dementia Differentiating between focal impairments &
dementias
Measuring progression & response to treatment
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DEMENTIA INVESTIGATIONS
Aiming to treat reversible causes:
Blood tests
FBC & ESR & CRP
U,C&E, Calcium
LFTs, TFTs Random BM
Syphilis and HIV (if atypical features or special risks)
ECG
CXR
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DEMENTIA INVESTIGATIONS
Aiming to treat reversible causes:
Neuroimaging criteria (CT/MRI)
Early onset (
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DEMENTIA OF ALZHEIMER’S TYPE
Most common
Typical history
Insidious (slowwww) onset With slow progression over years
Early – short term memory loss
Progresses to broad global cognitive dysfunction,
behavioural change and functional impairment
Behavioural problems common Eso with mild and moderate dementia
Can occur before obvious (overt) cognitive impairment
Labile mood
Memory loss
Slow progression of Sx
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DEMENTIA OF ALZHEIMER’S TYPE
Typical Physical Ex:
NORMAL
Investigations
Neuroimaging:
Only problem: MEDIAL TEMPORAL LOBE ATROPHY
Ventricular enlargement
EEG
A slow wave activity (not the case for pseudodementia)
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DEMENTIA OF ALZHEIMER’S TYPE
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VASCULAR DEMENTIA
Second most common (25% of all dementias)
Typical history
Vascular Risk factors
DM
HTN
Smoking
Other vascular pathology including previously with Ix
evidence
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VASCULAR DEMENTIA
Typical history
Presentation
Patchy cognitive impairment (not uniform like AD)
Onset associated with stroke
Deterioration – abrupt or stepwise
Features of:
Extra-pyramidal, pseudobulbar features & emotional
lability
Urinary incontinence of no other reason – early sign
Other features can either be:
Cortical mimicking AD
Subcortical e.g. apathy, depression
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VASCULAR DEMENTIA
Typical Physical Ex:
If stroke or diffuse Cerebrovascular disease will
see focal neurology e.g.:
Abnormal gait
Hyperreflexia Extensor Plantars
Etc...
Other evidence of vascular pathology:
AF
PVD
Investigations
Neuroimaging:
Only problem: MEDIAL TEMPORAL LOBE ATROPHY
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VASCULAR DEMENTIA
Investigations
Neuroimaging:
Mutliple large vessel infacts
Single critical infarct(e.g. thalamus)
White matter infarcts or periventricular white matterchanges
Microvascular disease
Note too fine to see on imaging however still causing
significant portion of vascular dementia
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VASCULAR DEMENTIA
Investigations
Neuroimaging:
Mutliple large vessel infacts
Single critical infarct(e.g. thalamus)
White matter infarcts or periventricular white matterchanges
Microvascular disease
Note too fine to see on imaging however still causing
significant portion of vascular dementia
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DIFFERENTIATING BETWEEN AD &
VASCULAR DEMENTIA
Vascular risk factors – treat them aggressively
Even if cerebrovascular pathology is not seen on
brain imaging
Also a patient would not be able to appreciate
that they forget easily e.g. short term memorywith AD only with vascular dementia
Can try a trial of acetylcholinesterase inhibitors
to rule out AD as it is not so effective for
vascular dementia
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NEODEGENERATIVE DEMENTIA 1 – LEWY
(3RD MOST COMMON CAUSE)
Overview:
Cognitive and behavioural behaviour before motor
phenomenom.
It will present it to be more severe than the other
neodegenerative dementia
Typical history:
Gradual progressive background dementia
Insidious onset
Short-term flucuations in cognitive function & alertness
Prominent auditory and visual hallucination +/-
paranoia and delusions
Parkinsonism common – less severe form
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NEODEGENERATIVE DEMENTIA 1 - LEWY
Typical history:
Gradual progressive background dementia
Insidious (slowww) onset
Short-term fluctuations in cognitive function &
alertness
Prominent auditory and visual hallucination +/-
paranoia and delusions
Parkinsonism common – less severe form
Triad to rememeber
Cognitive impairment
Visual hallucination
Parkinsonism (e.g. expressionless face)
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NEODEGENERATIVE DEMENTIA 1 - LEWY
Obvious notes:
Typical psychotics are very poorly tolerated
E.g. Haloperidol – worsens confusion or deterioration of
parkinsonism
Use atypicals instead – but with caution E.g. risperiodone and quetiapine
Other drugs that worsen CONFUSION
Levodopa or dopamine agonists
Best to use anti-cholinergics (e.g. rivastigmine) esp
for hallucinations and behavioural disturbance.
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COMPARING BETWEEN DELIRIUM AND
LEWY BODIES DEMENTIA
Same features: Fluctuations
Effect on drugs
Perceptual
Psychotic phenomena
However unique features of Lewy:
Insidious onset
Gradual progression No preciptating illness(e.g. infection) is found
Hallucinations – complex
Delusions
Frequent syncope
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Found in brainstem
and neocortex
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NEURODEGENERATIVE DEMENTIA 2 –
P ARKINSON’S DISEASE WITH DEMENTIA
Commonly seen in patients:
Elderly
Late stages of Parkinson’s disease
Those who become confused on Parkinson’s
medication
Definition
Parkinson’s features needs to precede more than one
year
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NEURODEGENERATIVE DEMENTIA 2 –
P ARKINSON’S DISEASE WITH DEMENTIA
Presentation:
Typical motor features of Parkinson’s (can be severe)
The rest is variable and can overlap with the other
types of dementias
Investigation:
Neuroimaging will show:
Multiple system atrophy
Progressive supranuclear palsy Corticobasal degeneration
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NEURODEGENERATIVE D – 3 –
FRONTOTEMPORAL DEMENTIA
Insidious (slowww) onset Slow (several years) progression
Early Age onset = 35-75yrs
Frontal & Temporal atrophy without AD histology
Chromosome 9
Positive FHx (50%)
Early symptoms: Behavioural or language difficulties
Mild forgetfulness
Insight loss
Difficulties at work (may be first sign)
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NEURODEGENERATIVE D – 3 –
FRONTOTEMPORAL DEMENTIA
Assessment:
Not use MMSE or MOCA – doesn’t test frontal lobe
Will observe behavioural problems
Language dysfunction
Later stages
Primitive reflexes
Broad impairment (similar to AD)
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NEURODEGENERATIVE D – 3 –
FRONTOTEMPORAL DEMENTIA
Investigations
Neuroimaging
Frontal and/or temporal atrophy
For specific conditions of frontotemporal dementia
spectrum: Frontal lobe degeneration
Frontal>Temporal lobe degeneration
Pick’s Disease
Same as above but less common
Will see Pick bodies on postmortem
Motor Neuron Disease with dementia (late stage MND)
Progressive non-fluent aphasia & semantic dementia
Temporal degeneration
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REVERSIBLE DEMENTIA - NPH
Def: also termed symptomatic hydrocephalus, is a
type of brain malfunction caused by excessive
production of cerebrospinal fluid (CSF).
Normal Pressure Hydrocephalus TRIAD:
Gait disturbance (wide-based)
Incontinence of urine
Cognitive impairment
Psychomotor slowing
Apathy
Appear depressed
DDx other causes or have diffuse cerebrovascular disease
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REVERSIBLE DEMENTIA - NPH
Assessment: Physical
Baseline gait (e.g. timed walk)
Cognition (e.g. MOCA)
Neuroimaging
Enlarged ventricles
Lesser extent there may be cerebral atrophy
Lumbar puncture After clinical and imaging evidence of NPH
Opening pressure is normal
Remove 20-30ml of CSF
Check for improvement in gait and cognition after 1-2hrs
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QUESTION
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NPH IN MORE DETAIL
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NPH COMPLICATION
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REVERSIBLE DEMENTIA - NPH
Treatment: Ventriculoperitoneal shunting
Improves gait > cognition
Complications
Infection
Subdural haemtoma
Better prognosis with this treatment if they have:
Short history (days or weeks)
Known cause e.g. trauma or SAH
Normal brain substance on neuroimaging
No significant co-morditities
Benefit from LP and large volume CSF removal
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REVERSIBLE DEMENTIA – DRUGS &
TOXINS
E.g. Alcohol
After many years of chronic drinking
Present with short-term memory impairment
E.g. Psychoactive drugs
Can cause dementia-like syndrome
Reversible
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OTHER DEMENTIAS
Infection 1
Neurosyphilis
Becoming more common – presentation
This should be checked if
atypical presentation of dementia e.g. Seizures Risk of STD e.g. mental illness, history of other STD,
drug/alcohol abuse
Ix
Serological
BEWARE = False positive in Afro-Carribean with a history ofyaws
CSF sample – if highly suspected
Mx Penicillin treatment with microbiology input
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OTHER DEMENTIAS
Infection 2
HIV associated dementia
Occurs late in HIV (or not at all – rare)
Younger people
Infections 3
CJD
Prion-mediated
Causes rapidly progressive cortical dementia
Ex – Myoclonus & psychosis
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OTHER DEMENTIA – V ASCULITIS
Present in many ways
Only suggested with elevated CRP/ESR
without other cause
CT/MRI should not have pathology e.g. periventricular
lesion
Ex – examine for evidence of systemic vasculitis
Ix
Peform serology (ANA)
LP with CSF tests for infection and neoplasm
Mx
Treatable specialist referral
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DEMENTIA – GENERAL M ANAGEMENT
General
Sort out the reversible aggravating factors
E.g. constipation, mild anaemia, drug S/E, low-grade sepsis
Treat depression
SSRI
Social
Be active
OT involved – for safe home environement Carer with care package introduced
Support caregivers
Education patient and families & learning how cope
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DEMENTIA – GENERAL M ANAGEMENT
Practical
Suggest Simple interventions for coping
E.g. lists, calendars, alarms
Simplify medication
E.g. use of MDS Support and educate patient about legal and ethical
issues including
Driving
Report Voluntarily to DVLA – needed to assessed esp if had
critical accidents. OT can also get involved. Use public transport If unsafe, stopped them and support from family - report!
Lasting power of attorney
Will
End-of-life discussion
E.g. clinically assisted nutrition, comfort vs life prolongation
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DEMENTIA – PREVENTION
Lifestyle Interventions
Drugs
Acetylcholinesterase Inhibitors (oldest & first 1997)
Only offers symptomatic relief
Best for AD, DLB and PDD as has the most cholinergicdeficit
Three available
Donepezil 5mg OD (reversible)10mg after 4 weeks
Best for AD (has fewer side effects)
Galantamine 4mg BD 8mg after 2w 12mg after 8w Rivastigmine 1.5mg BD (reversible & non-competitive)
6mg within 12 weeks
If above not tolerated or in severe disease
Memantine (avoid in renal failure) NMDA receptor
antagonist
D A D A G
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DEMENTIA – DEALING WITH
BEHAVIOURAL PROBLEMS
General
Non-Drug
Drug
BZD – for agitation, anxiety & irritability
Citalopram or Trazadone- if depression
Atypical anti-psychotics e.g. quetiapine
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QUESTIONS
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CJD
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QUESTION
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QUESTION
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CJD
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QUESTION
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RETT S YNDROME
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QUESTION
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NEUROS YPHILIS – SEE G YAEN NOTES
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QUESTION
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H YPOTHYROIDISM
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DELIRIUMIncluding Psychosis
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DELIRIUM - DEF & DIAGNOSIS
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DELIRIUM DEF & DIAGNOSIS
Key Features for Diagnosis
A disturbance of consciousness Decrease clarity of awareness of the environment
Decreased ability to focus, shift or sustain attention
Lose thread of conversation and time of day
After recovery, memory for the period will be POOR
Not seen in early dementia or in primary psychotic disorders
Change in cognition
Memory impairment
Disorientation
Language disturbance Perceptual impairment
Illusions & Hallucinations
Acute onset, and fluctuates over hours or few days
Varies during the day – if worse in evening called SUNDOWNING
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OTHER FEATURES – NOT NEEDED FOR DX
Sleep-wake cycle disturbance
Disturbed psychomotor behaviour
Emotional disturbance
Delusions
Poor insight
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C AUSES OF DELIRIUM
Multifactorial – contributory factors: Infections
Chest (Pneumonia), Urine (UTI), Skin
(cellulitis)
Drug intoxication
Anti-cholinergics Anxiolytics/hypnotics
Anticonvulsants
Opiates and opiate like drugs
Disorders of electrolyte/fluid balance
Dehydration Uraemia
Hypercalcaemia
Hypo/Hyper Na+ (can’t be cause alone)
Alcohol or drug withdrawal
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C AUSES OF DELIRIUM
Multifactorial – contributory factors: Organ failure
Cardiac, liver, respiratory
Endocrine –
BM and thyroid (hypo & hyper)
Epileptic
Intracranial pathology
Head injury, space-occupying lesion, raised ICP
NOTE: ACUTE STROKE rarely causes delirium
Pain
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C AUSES OF DELIRIUM
Multifactorial – contributory factors: Recreational Drugs
Alcohol
Marijuana
LSD
Amphetamines
Cocaine
Opiates
Inhalants
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A SSESSMENT OF DELIRIUM
Investigation Simple tests – blood, urine
Baseline
Repeat clinical investigation
More advanced Ix CT/MRI brain
EEG
CSF examination
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DDX DELIRIUM
Anxiety – if agitated (check conscious levels)
Primary mental illness (e.g. schizophrenia)
If there is hallucinations and delusions
TREATMENT OF DELIRIUM
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R O R U
Treating
The underlying cause Competency – in patient’s best interests
Can hold within a ward or hospital if attempt to leave
Temporary physical restraint (e.g. when drug given)
Covert administration of essential drugs
Conservative Quiet environment with orientated features with good light
Same staff and give reassurance repeatedly (give aids glasses)
3M – music, massage and muscle relaxation
Drug Treatment
Criteria - if delirium
Causes significant patient distress
Threatens the safety of patient or others
Interferes with medical treatment (e.g. pulling out if IV
lines, aggression preventing clinical Ex)
PRESCRIBING SEDATING DRUGS IN
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DELIRIUM
Short-acting BZD – lorazepam Typical anti-psychotics – haloperidol
Typical anti-psychotics – olazapine, risperidone
Combination
So typical steps:
When disruptive give either haloperidol or chlorpromazine
(IM or PO) check after 20mins for further doses
NOTE: AVOID CHLORPROMAZINE IN ELDERLY AND IN ALCOHOL WITHDRAWAL
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F ALLS& Funny Turns
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F ALL O VERVIEW
Fall is an event that results in a person non-intentionally coming to rest at a lower level
(usually floor)
Common & Important Resulting in:
Fear
Injury
Dependency
Instutionalisation
Duty
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A SSESSMENT FOLLOWING F ALL
Typical Hx Tripped
Fracture or non-fracture injury
Found on floor
Secondary consequences of falling
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EXAMINING IN F ALLS
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Screening:
Functional
Cardio
Lying & standing BP
Pulse rate & rhythm
Listen for murmurs (esp AS)
Musculoskeletal
Assess footwear (stability & grip)
Remove footwear and examine the feet
Examine the major joints for deformity, instability or
stiffness
Neurological
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F ALLS IX
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MX: REDUCING F ALLS FREQUENCY
MDT Drug review – reduce
Treat Orthostatic hypotension
Physio for strength & balance training
Walking aids Occupational therapists
Vision – glasses or cataract sorted
Reducing stressors
MX: PREVENTING CONSEQUENCES OF F ALLS
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Detect & treat Osteoporosis
Physio – how to stand up Alarms – pendent alarm or pullcords in rooms
Supervision – to check no long lie after post fall
Family, neighbours, carers or voluntary agencies
Change of accomodation Care home
Nursing home
Residential home
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S YNCOPE & PRESYNCOPE
Syncope A sudden, transient loss of consiousness due to
reduced cerebral perfusion
Patient in unresponsive with loss of postural control
(i.e. slumps or falls)
Pre-syncope
Feeling of light-headedness
Would lead to syncope if corrective measures not
taken (e.g. lying or sitting)
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S YNCOPE & PRESYNCOPE
Overview: Major cause of morbidity
Recurrent in 1/3
Risk increases with age and CVD
Cause of serious injuries (fractures) & hospitaladmissions
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S YNCOPE &
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PRESYNCOPE DDX
Seizure Disorder
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S YNCOPE HISTORY
1. Situation Prolonged standing (Orthostatic hypotension)
Exercising (arrthymias or ischaemia)
Sitting or lying down (seizure)
Eating (post-prandial hypotension - within 75mins) Toilet (defecation or micturition syncope)
Coughing (cough syncope)
Pain or frightened (vasovagal syncope)
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S YNCOPE HISTORY
2. Prodrome Any prior warning?
Palpations (arrhythmias)
Sweating with palpations (vasogal syndrome)
Chest pain (ischaemia) Light headedness(any cause of hypotension)
Gustatory or olfactory aura (seizures)
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S YNCOPE HISTORY
3. Was there loss of consciousness? Other terminology fall, blackout, funny turn, collapse
etc.
Syncope
Loss of consciousness
Loss of awareness
Due to cerebral hypoperfusion
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S YNCOPE HISTORY
4. Description of attack Eye Witness
Pale and clammy (systemic & cerebral hypoperfusion)
Ictal features (tongue biting, incontinence, twitching)
NOTE: if prolonged LOC = syncope is UNLIKELY
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S YNCOPE HISTORY
5. Recovery period Observed by eye witness
Rapid recovery = cardiac cause
Prolonged drowsiness & confusion = seizure
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S M
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S YNCOPE M ANAGEMENT
B ALANCE
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For Awareness of position of body in space need:
Peripheral input (dorsal column)
Using peripheral nerves (proprioception) from postural muscles
Mechanoreceptors in joints
Eyes
Visual cues to position
Ears
Info about static head position = otolithic organs (utricle & saccule)
Info about head movement = semicircular canals
Auditory cues – localise with reference to environment
All this info relayed to be assessed by brainstem &
cerebellum (CNS)
B ALANCE & D YSEQUILIBRIUM Problems arising:
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Problems arising:
Peripheral nerves
Neuropathy
Joint Receptors Degenerative joint disease (arthritis)
Postural muscles
Weak – due to inactivity, disease, medication
Reduced muscle mass of ageing
Eyes
Age-related changes decrease visual acuity
Disease e.g. cataracts, glaucoma, etc
Ears Age-related changes in hearing reduced vestibular function
Also with age vulnerable to damage from drugs, trauma, infections & ischaemia
CNS
Age relared slowness
Disease processes – ischaemia, HTN damage,
Dementia, etc
B ALANCE & D YSEQUILIBRIUM
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D
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DIZZINESS
Two main reasons: Reduced sensory inputs
Impairment of integration of sensory input
Types: Light-headedness (Presyncope & syncope)
Dysequilibrium or unsteadiness (Imbalance)
Movement of the patient or room (Vertigo/spinning)
Anxiety Mixed
Other
D D T
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DIAGNOSIS OF DIZZINESS T YPE
Does the room spin, as if you are on a roundabout(vertigo)?
Does it come when you move your head (vertigo)?
Do you feel light-headed, as if you are about to faint(presyncope)?
Does it occur when lying down? (NOT PRESYNCOPE)
Does it come and go? (Chronic, constant symptoms – mixed or psychiatric in origin)
IMBALANCE T YPE DIZZINESS
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Cerebral Ataxia
MS
Vascular
Tumour
Sensory Ataxia
Tabes dorsalis
Neuropathy
Drugs
Anticonvulsants
Hypnotics
Alcohol
Extra-pyramidal
Parkinson’s Disease and others
Normal pressure hydrocephalus
IMBALANCE IX
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IMBALANCE IX
MRI Brain scan Check drug level
Nerve Conduction
Treponema pallidum ELISA
IMBALANCE MX
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IMBALANCE MX
Lower drug intake Levodopa – if extrapyramidal
Steriods (MS)
Surgery
SPINNING VERTIGO TYPE OF DIZZINESS
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SPINNING: VERTIGO – T YPE OF DIZZINESS
Causes: Peripheral
Labyrinthitis
Meniere’s disease
Benign paroxysmal positional vertigo
Central
Basilar insufficiency
MS
VERTIGO IX
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VERTIGO IX
Pure tone audiogram Caloric test
Positional tests
Hallpike manoeuvre
MRI brain
MRA extra-cranial vessels
VERTIGO MX
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VERTIGO MX
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DROP ATTACKS
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Refers to unexplained falls with:
No prodrome No (or very brief) LOC
Rapid recovery
Increases with age
Causes:
Cardiac Arrhythmias
Orthostatic hypotension
Carotid sinus syndrome
Vasovagal syndrome
Vertebrobasilar insufficiency (VBI)
Weak legs (e.g. cauda equina syndrome)
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PRE-SYNCOPE CAUSE:
ORTHOSTATIC (POSTURAL) HYPOTENSION
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ORTHOSTATIC (POSTURAL) H YPOTENSION
Orthostatic hypotension is caused primarily bygravity-induced blood-pooling in the lower
extremities, which in turn compromises venous
return, resulting in decreased cardiac output and
subsequent lowering of arterial pressure.
Diagnostic Criteria
Fall in BP >20mmHg systolic or 10mmHg diastolic on
standing from supine
C AUSES OF ORTHOSTATIC H YPOTENSION
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Drugs
Chronic HTN Volume Depletion
Dehydration, acute haemorrhage
Sepsis
Vasodilatation
Autonomic failure
Pure, diabetic, Parkinson’s
Prolonged bed rest
Adrenal insufficiency
Raised intrathoracic pressure
Bowel or bladder evacuation, cough
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CAROTID SINUS SYNDROME OVERVIEW
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C AROTID SINUS S YNDROME - O VERVIEW
Episodic, symptomatic bradycardia +/-hypotension
Due to hypersensitive carotid baroreceptor reflex
Resulting in syncope or near-syncrope
Common in older patients esp >80yrs
C AROTID SINUS S YNDROME -
PATHOPHYSIOLOGY
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P ATHOPHYSIOLOGY
Normal situation - Reflex Raise in arterial BP
Causes carotid baroreceptors to act via sympathetic NS to
slow and weaken pulse lower BP
This reflex blunts with age
However in CAROTID SINUS SYNDROME
This is exaggerated drop BP even more
C AROTID SINUS S YNDROME –
ASSOCIATIONS & TRIGGERS
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A SSOCIATIONS & TRIGGERS
Associations: Increasing age
Atheroma
Use of drugs affecting SANode
B-blockers
Digoxin
CCB
Typical Triggers
Neck turning (esp looking up or around)
Tight collars
Straining (including cough, micturition & defecation)
Meals
Prolonged standing
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CSS DIAGNOSIS
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CSS DIAGNOSIS
All three factors needed: 1. Unexplained attritutable symptoms
2. Sinus pause >3sec +/- systolic BP fall >50mmHg
When undertaking 5 sec of carotid sinus massage
3. Symptoms are reproduced by carotid sinus
massage
CCS MANAGEMENT
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CCS M ANAGEMENT
Stop aggravating drugs
AV sequential pacing = Cardio-inhibitory Type CSS
Increase circulating volume = Vasodepressor Type CSS
With flucortisome or midodrine
FALLS CLINIC
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F ALLS CLINIC
MDT (health professional led other than doctors) Identifies and reduce syncope and presyncope
Checking drug and carry out Ix
Including CVD – tilt table and arrhythmias
Screen for modifiable risk factors
Referral to geriatrician or GP specialising in this
Referral Criteria
Recurrent (>2) falls
LOC, syncope or near-syncope Injury e.g. fracture or facial injury
Polypharmacy
OSCE STYLE – FROM VIRTUAL PATIENTS
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OSCE STYLE FROM VIRTUAL P ATIENTS
OSCE STYLE – FROM VIRTUAL PATIENTS
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OSCE STYLE FROM VIRTUAL P ATIENTS
OSCE STYLE – FROM VIRTUAL PATIENTS
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OSCE STYLE FROM VIRTUAL P ATIENTS
OSCE STYLE – FROM VIRTUAL PATIENTS
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OSCE STYLE FROM VIRTUAL P ATIENTS
OSCE STYLE – FROM VIRTUAL PATIENTS
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OSCE STYLE FROM VIRTUAL P ATIENTS
URINE DIPSTICK
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ECG
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CG
BLOOD TEST
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CT HEAD
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X-RAY
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A NATOMY
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G ARDEN’S CLASSIFICATION
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G ARDEN’S CLASSIFICATION
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THR
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OSTEOPOROSIS & FRACTURES
O VERVIEW
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Complex skeletal disease characterise by Low bone density
Micro-architectural defects in bone tissue
Resulting in increased bone fragility &susceptibility to fracture
Types
Primary Age related
Secondary
Due to another condition or drugs
EPIDEMIOLOGY
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Facts Fractures in UK & Europe due to osteoporosis occurs
in >50yrs
1 in 2 women
1 in 5 women
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P ATHOPHYSIOLOGY
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Trabecular bone affected: Crush fratucres common
E.g. little old lady being little and having dowager’s hump
Cortical bone affected:
Long bone fractures more common
E.g. femur neck
Biggest cause of death
Account for 80% of fractures in UK in women >50yrs
RISK F ACTORS = PRIMARY
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FHx history Alcohol > 4 units daily
RA
BMI
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Older age (F>60yr, M>65yr)
Female gender
Caucasian
Low BMI
FHx of maternal hip fracture
Postmenopause
Glucocorticoids use
Prior fracture
Secondary amenorrhoea
Smoking
Excessive alcohol use
Vitamin D deficiency
Low calcium intake
Glucocorticoid excess
Corticosteriod use
DX
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CLASSIFICATION OF
OSTEOPOROSIS
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TYPE 1 = POSTMENOPAUSAL
TYPE 2 = SENILE
IDIOPATHIC =
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MOST COMMON order Fractures in OA
MALE FEMALE
1. HIP
FRACTURES
2. COLLE’S
1. VERTEBRAL
FRACTURE 20%
2. HIP FRACTURE
3. COLLE’S
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IX - O VERVIEW
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Imaging X-ray – just good for fracture
DEXA
Bloods Ca, PO4, ALP = all normal
Do specific ones to rule out secondary causes
DEXA
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NEW:
IX
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IX
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C ASE HISTORY
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MX - CONSERVATIVE
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Lifestyle measures:
Quit smoking & reduce alochol
Undertake weight bearing exercise (increased BMD)
Balance exercises e.g. tai chi (e.g reduce risk of falls)
Calcium and vitamin D rich diet
Home-based fall prevention programme
MX - MEDICAL
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Biphosphonate First line = Alendronate
S/E: Photosensitivity, GI upset, oesphageal ulcers, jaw osteonecrosis(Stop if dysphagia or abdo pain)
Alternative = Strontium ranelate
Calcium & Vitamin D
Hormone replacement therapy Prevents osteoporosis in postmenopausal women
Increases CVD and breast cancer risk
Raloxifene (SERM) Less breast cancer risk
Calcitionin Reduces calcium breakdown and increase absorption into bones
MX - MEDICAL
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OTHERS
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MX Denosumab: A monoclonal Ab
t RANK li d
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Recombinant PTHFor those who still
suffer fractures
even if on treatment
Increases risk of
renal malignancy
to RANK ligand
SC twice yearlyReduce
reabsorption
MX
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DDX
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DDX
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VOLUME DEPLETION & DEHYDRATION
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Causes: Multifactorial
Blood loss
Diuretics
Gastrointestinal losses (diarrhoea, NG drainage)
Sequestration of fluid Poor oral intake
Fever
VOLUME DEPLETION & DEHYDRATION
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Symptoms & Signs Thirst (UNCOMMON!)
Malaise, apathy, weakeness
Orthostatic symptoms (lightheadedness or syncope)
Or Postural hypotension
N + V, anorexia and oliguria in severe uraemia
Tachycardia, supine hypotension
Decreased skin turgor, sunken facies, absence of
dependent oedema
Poor urine output
DDX FOR DEHYDRATION
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N A + & H2O
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H YPOVOLAEMIA
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EUVOLAEMIA
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H YPERVOLAEMIA
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DRUGS CAUSING H YPO N A +
Diuretics
SSRI
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SSRI
Carbamezapine
NSAIDs
Combination of Diuretics and SSRI
Others
Opiates
Anti-depressants - MAOI & TCA
Oral Hypoglycaemics (sulphonylureas – ide) PPIs
ACE Inhibitors
Barbiturates
H YPO N A + A SSESSMENT CX
Mild cases
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Subtle or absent S&S
Na+ 115-125mM
Lethargy
Confusion
Altered personality
Na+
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Drugs causing low Na+
Excess water given via NG or IV (rare oral)
Heart failure, liver failure
Thyroid failure, Renal failure
Stress response
E.g. trauma or surgery
Hypoadrenalism
Steroid withdrawal
Addison’s disease
SIADH
Older people multiple causes
HF, diuretics and acute diarrhoea
H YPO N A + IX
Clinical History
E i ti
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Examination
Volume status check
Blood test
Creatinine
Osmolarity
TFTs
LFTs
Glucose
Random cortisol
Spot urine sample for Na & Osmolarity
Synacthen test
Esp if volume depleted and hyperkalaemic
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SIADH
Definition
characterized by excessive release of antidiuretic hormone from
the posterior pituitary gland or another source
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the posterior pituitary gland or another source.
Less than maximally dilute (i.e. inappropiately
concentrated) urine in presence of subclinical excess
body water
Diagnosis HYPOTONIC HYPONATRAEMIA
Na+ 20mM NORMAL VOLUME STATUS
NORMAL RENAL, THYROID, CARDIAC & ADRENAL
FUNCTION
SIADH - CAUSES
Surgical stress
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Neoplasms
Bronchogenic (SMALL LUNG CANCER), pancreatic
CNS Disease Trauma, subdural haematoma, stroke & meningoencephalitis
Lung Disease
Including TB, pneumonia, bronchietasis
Some Drugs causing low Na+
SIADH - IX - SHORT ACTH SIMULATION
TEST (SHORT S YNACTHEN TEST)
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SIADH - TREATMENT
Treat underlying cause
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Treat underlying cause
Mild
Self-correct
Severe +/- symptomatic Restrict water intake to max. 1000ml/day
ELDERLY – 500-800ml/day
Drug treatment
If fluid restriction intolerated
Drug: DEMECLOCYCLINE
Blocks renal tubular effect of ADH
H YPERNATRAEMIA
Causes
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Causes
Dehydration
Poor oral intake or too much water loss Diarrhoea
Vomiting
Diuretics
Uncontrolled DM
Rare Due to salt excess
Due to DI or mineralocorticoids excess
COMMONLY SEEN IN OLDER SEPTIC PEOPLE Increased losses (sweating)
Reduced oral intake
Reduced renal concentrating (water-conserving)
H YPER N A + CX
Clinical features
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Clinical features
Hypotension (supine &/or orthostatic)
Sunken features
Urine scanty and concentrated
Lethargy
Confusion
Coma
Fits
H YPER N A + IX
Na+ = Raised
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Na+ = Raised
PCV = Raised
Urea & Creatinine = High
Hb and albumin = high
K+ low in Conn’s
H YPER N A + MX
Encourage oral fluid
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Encourage oral fluid
IV fluids
Fluid infusion
Not too rapid cause cerebral oedema
NOTE: mild hypernatraemia is clinically
important!
H YPERKALAEMIA
>6 5mmol/L = EMERGENCY!!!!!!!!!!!!!!!!!
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>6.5mmol/L = EMERGENCY!!!!!!!!!!!!!!!!!
Can lead to:
Myocardial hyperexcitability
Causing VF & cardiac arrest
Signs & Symptoms Fast irregular pulse
Chest pain
Palpitations
Light Headedness Weakness
H YPERKALAEMIA C AUSES
Oliguric renal failure
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Oliguric renal failure
K+ sparing diuretics
Rhabdomyolysis
Metabolic acidosis
Excess K+ therapy Addison’s disease
Massive blood transfusion
Burns
Drugs e.g. ACEI, suxamethonium
Artefactual result
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ECG
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H YPERK ALAEMIA MX – NON-URGENT
Treat underlying cause
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Treat underlying cause
Review medications
Polystyrene sulphonate resin (Calcium Resonium
15g/8h PO) Binds K+ in gut preventing absorption and
bringing K+ down over few days
30g enema followed by colonic irrigation 9hrs later If vomiting prevents PO adminstration
H YPERK ALAEMIA - URGENT
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H YPOK ALAEMIA
K+
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K+ 2.5mmol/L Urgent Treatment required
Note: This level cam exacerbate DIGOXIN toxicity
Signs & Symptoms
Muscle weakness
Hypotonia
Hyporeflexia
Cramps
Tetany
Palpitations
Light-headedness (arrhythmias)
Constipation
H YPOK ALAEMIA
ECG signs:
Small or inverted T-waves
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Prominent U-waves (after T waves) Long P-R interval
Depressed ST segments
H YPOK ALAEMIA
Causes:
Diuretics
Indicated by raised HCO3
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Indicated by raised HCO3
Vomiting & Diarrhoea
Pyloric stenosis
Cushing’s syndrome/steroids/ACTH
Conn’s syndrome
[HTN, Hypokalaemic alkalosis – not on diuretics]
Alkalosis
Purgative and liquorice abuse
Renal tubular failure
H YPOK ALAEMIA
Hypokalaemic Periodic Paralysis
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Hypokalaemic Periodic Paralysis
Intermittent weakness lasting upto 72 hours
Due to K+ shifting from extra-to intracellular fluid
H YPOK ALAEMIA TREATMENT
Mild
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>2.5mmol/L – No symptoms
Give oral K+ supplements
Review K+ after 3 days
Severe
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C ALCIUM & PHOSPHATE
PHYSIOLOGY & BLOODS
O VERVIEW OF NORMAL HOMEOSTASIS
PTH
Raises Ca
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Lowers PO4
Triggered when serum ionised Ca drops
Processes activated:
Raised osteoclast activity releasing both from bones
Increased Ca+ & Decreased PO4 reabsorption in kidney Increased renal production of 1,25OH Vitamin D3
O VERVIEW OF NORMAL HOMEOSTASIS
Vitamin D3
Activated version causes
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Absorption from gut for both
Inhibition of PTH release
Enhanced bone turnover
Increased both kidney reabsorption
Calcitonin
Made in C-cells of the thyroid
Causes lowering of both!
Magnesium
Mg prevents PTH release
Causing HYPOCALCAEMIA
RULES
40% bound to albumin
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60% free – active!
Corrected total Ca for albumin
Add 0.1mmol/L to Ca for every 4g/L that albumin isbelow 40g/L
(subtract instead if above 40g/L)
H YPERCALCAEMIA – BONES, STONES, GROANS& PSYCHIC MOANS
S&S
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Abdominal pain Vomiting
Constipation
Polyuria
Polydipsia
Depression, Confusion
Weight loss, Anorexia
Tiredness, weakness
HTN
Pyrexia
Renal Stones, renal failure
Cardiac Arrest
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H YPERC ALCAEMIA - INVESTIGATIONS
Most common causes
Malignancy
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Primary hyperparathyroidism
To differentiate
Malignancy
Low albumin
Low Cl-
Alkalosis
Low K+
Raised PO4
Raised ALP
Primary hyperparathyroidism
Raised PTH
TREATING A CUTE H YPERCALCAEMIA
Esp if >3.5mmol/L & symptomatic
1) Correct dehydration
IV 0.9% saline
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2) Biphosphonates
This prevents bone resorption by inhibiting osteoclast
activity
Use of Single Dose of PAMIDRONATE (max effect 1 wk)
Infuse slowly
S/E: Flu symptoms, reduced PO4, bone pain, myalgia,
nausea, vomiting, headache, lymphocytopaenia, seizures,
drop in Mg and drop in Ca
Other e.g. of biphosphonate
Zoledronic acid
Sodium clodronate
Ibandronic acid
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H YPOC ALCAEMIA
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H YPOC ALCAEMIA
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QUESTION
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H YPERPARATHYROIDISM
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BONE BIOCHEMISTRY
HypercalcaemiaBone Disease - Osteoporosis
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OSTEOPOROSIS OVERVIEW
Prevalence
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F>M (esp >50)
Risk factors
For primary
Age
Parental history of hip fracture
SMOKING
Alcohol >4 units daily
RA
BMI
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Long-term heparin therapy
PPI
Glitazone
Aromatase Inhibitors e.g. anatrozole
IF OSTEOPOROSIS IS GLUCOCORTICOID
INDUCED E.G. ASTHMA DRUGS
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OSTEOPOROSIS PREVENTION
Alendronate is first line
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Vitamin D & Calcium
Raloxifene - SERM