HEALTHCARE OF THE ELDERLY

Revision Session

TOPICS
Dementia
Delirium
Depression
Fragile bones & Fractures
Falls
Parkinsons & Movement Disorders
Cerebrovascular Disease, TIA & Stroke
Malignancy
Cardiology
Respiratory

DEMENTIA

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

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 (<5%)

EXAMPLES OF NEURODEGENERATIVE D
Dementia with Lewy Bodies
Parkinsons disease with Dementia
Frontotemporal Dementia (Picks disease)

EXAMPLES OF REVERSIBLE DEMENTIAS

Drugs
Metabolic
Subdural haemorrhage
Normal Pressure Hydrocephalus

THEY CANT BE LABELLED AS DEMENTIA

Deaf
Dysphasic
Delirious
Depressed
Under influence of drugs

TRIGGERS FOR THINKING & DX DEMENTIA

Patient presents with delirium common in
patients with already having dementia
After spouses 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

DDX FOR CONFUSION IN ELDERLY

DELIRIUM ALONE

DEMENTIA ALONE

DELIRIUM SUPERIMPOSED ON A PREEXISTING DEMENTIA ask When was his

memory last as good as yours?

Determine from history, physical and mental state

examination use of timeline of progression
Useful infro from medical records, carers & family

Including
delusional
beliefs,
disorientation in
time, place &
person,
comprehension &
language
impairment

DEMENTIA ASSESSMENT - HISTORY

PC
HPC
PMHx
FMHX
See lecture notes for complete list

DEMENTIA ASSESSMENT - HISTORY

Typical story of dementia:

Progressive decline in cognitive function over several
years
Ending with complete dependency and death due to:

Dehydration
Malnutrition
+/- Sepsis

DEMENTIA ASSESSMENT - 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)

DEMENTIA ASSESSMENT - HISTORY

Abnormalities arise in following:

Retention of new information (short term memory
loss is often severe with repetitive questioning)

1.

E.g. Appointments, events

Managing complex tasks

2.

E.g. paying bills, cooking a meal for family

Language

3.

Word-finding difficulty, inabilty to hold a conversation

Behaviour

4.

Irritabilty, aggression, poor motivation, WANDERING

Orientation

5.

Getting lost in familiar places

Recognition

6.

Failure to recognise last ones will be partners

DEMENTIA ASSESSMENT - HISTORY

Abnormalities arise in following:

Ability to self-care

7.

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)

DEMENTIA ASSESSMENT 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

DEMENTIA ASSESSMENT 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

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

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

DEMENTIA INVESTIGATIONS

Aiming to treat reversible causes:

Neuroimaging criteria (CT/MRI)

Early onset (<60 years)
Sudden onset or brisk decline
High risk of structural pathology (e.g. known cancer, falls
with head injury)
Focal CNS S&S

When to consider other other types of Ix:

EEG is suspect fronto-temporal dementia or CJD or
seizure activiy
LP if suspect CNS infection
SPECT to differentiate vascular vs AD dementia

DEMENTIA OF ALZHEIMERS TYPE

Most common

Typical history

Labile mood
Memory loss
Slow progression of Sx

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

DEMENTIA OF ALZHEIMERS 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)

DEMENTIA OF ALZHEIMERS TYPE

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

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

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

VASCULAR DEMENTIA

Investigations

Neuroimaging:
Mutliple large vessel infacts
Single critical infarct(e.g. thalamus)
White matter infarcts or periventricular white matter
changes
Microvascular disease
Note too fine to see on imaging however still causing
significant portion of vascular dementia

VASCULAR DEMENTIA

Investigations

Neuroimaging:
Mutliple large vessel infacts
Single critical infarct(e.g. thalamus)
White matter infarcts or periventricular white matter
changes
Microvascular disease
Note too fine to see on imaging however still causing
significant portion of vascular dementia

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 memory
with 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

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

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)

NEODEGENERATIVE DEMENTIA 1 - LEWY

Obvious notes:

Typical psychotics are very poorly tolerated

Use atypicals instead but with caution

E.g. risperiodone and quetiapine

Other drugs that worsen CONFUSION

E.g. Haloperidol worsens confusion or deterioration of

parkinsonism

Levodopa or dopamine agonists

Best to use anti-cholinergics (e.g. rivastigmine) esp

for hallucinations and behavioural disturbance.

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

Found in brainstem
and neocortex

NEURODEGENERATIVE DEMENTIA 2
PARKINSONS DISEASE WITH DEMENTIA

Commonly seen in patients:

Elderly
Late stages of Parkinsons disease
Those who become confused on Parkinsons
medication

Definition

Parkinsons features needs to precede more than one

year

NEURODEGENERATIVE DEMENTIA 2
PARKINSONS DISEASE WITH DEMENTIA

Presentation:
Typical motor features of Parkinsons (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

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)

NEURODEGENERATIVE D 3
FRONTOTEMPORAL DEMENTIA

Signs:

Executive impairment - INATTENTION

Behavioural/personality change - WITHDRAWAL
Early preservation of episodic memory & spatial
orientation
Disinhibition
Hyperorality
Stereotyped behaviour AKINESIA & MUTE
Emotional unconcern APATHY

NEURODEGENERATIVE D 3
FRONTOTEMPORAL DEMENTIA

Assessment:
Not use MMSE or MOCA doesnt test frontal lobe
Will observe behavioural problems
Language dysfunction

Later stages
Primitive reflexes
Broad impairment (similar to AD)

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

Picks 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

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

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

QUESTION

QUESTION

NPH IN MORE DETAIL

NPH COMPLICATION

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

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

OTHER DEMENTIAS

Infection 1

Neurosyphilis

Becoming more common presentation

This should be checked if

Ix

Serological

atypical presentation of dementia e.g. Seizures

Risk of STD e.g. mental illness, history of other STD,
drug/alcohol abuse

BEWARE = False positive in Afro-Carribean with a history of

yaws

CSF sample if highly suspected

Mx Penicillin treatment with microbiology input

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

OTHER DEMENTIA VASCULITIS

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

DEMENTIA GENERAL MANAGEMENT

General

Sort out the reversible aggravating factors

Treat depression

E.g. constipation, mild anaemia, drug S/E, low-grade sepsis

SSRI

Social

Be active
OT involved for safe home environement
Carer with care package introduced
Support caregivers
Education patient and families & learning how cope

DEMENTIA GENERAL MANAGEMENT

Practical

Suggest Simple interventions for coping

Simplify medication

E.g. lists, calendars, alarms

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

DEMENTIA RISK MANAGEMENT

Important
Is there a risk of harm to patient or to others?
How great is the risk, over how long is the patient
exposed to it, how severe are the consequences of the
risk?

Common risks e.g. (see notes)

Falls
Wandering
Aggression by patient to carers or family
Aggression by carers or family
Self neglect (hygiene)
Fire risk (e.g. smoking, gas fires)
Driving
Financial abuse of patient (e.g. theft, fraud, misuse or transfer)

DEMENTIA PREVENTION
Lifestyle Interventions
Drugs

Acetylcholinesterase Inhibitors (oldest & first 1997)

Only offers symptomatic relief
Best for AD, DLB and PDD as has the most cholinergic
deficit
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

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

QUESTIONS

QUESTIONS

CJD

QUESTION

TRANSIENT GLOBAL AMNESIA

QUESTION

CJD

QUESTION

RETT SYNDROME

QUESTION

QUESTION

NEUROSYPHILIS SEE GYAEN NOTES

QUESTION

HYPOTHYROIDISM

DELIRIUM
Including Psychosis

DELIRIUM - DEF & DIAGNOSIS

Aka Acute confusional state refers to acute

brain syndrome/failure with impairment of
consciousness
Accompanied by change in cognition that is not
accounted for by pre-existing dementia

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

OTHER FEATURES NOT NEEDED FOR DX

Sleep-wake cycle disturbance
Disturbed psychomotor behaviour
Emotional disturbance
Delusions
Poor insight

CAUSES OF DELIRIUM

Multifactorial contributory factors:

Infections

Drug intoxication

Anti-cholinergics
Anxiolytics/hypnotics
Anticonvulsants
Opiates and opiate like drugs

Disorders of electrolyte/fluid balance

Chest (Pneumonia), Urine (UTI), Skin

(cellulitis)

Dehydration
Uraemia
Hypercalcaemia
Hypo/Hyper Na+ (cant be cause alone)

Alcohol or drug withdrawal

CAUSES OF DELIRIUM

Multifactorial contributory factors:

Organ failure

Endocrine

BM and thyroid (hypo & hyper)

Epileptic
Intracranial pathology

Cardiac, liver, respiratory

Head injury, space-occupying lesion, raised ICP

NOTE: ACUTE STROKE rarely causes delirium

Pain

CAUSES OF DELIRIUM

Multifactorial contributory factors:

Recreational Drugs

Alcohol
Marijuana
LSD
Amphetamines
Cocaine
Opiates
Inhalants

ASSESSMENT OF DELIRIUM

History & Ex
Finding contributory factors
Collateral Hx
Assess cognition
Vital signs and clues

Sats <95% - cardiopulmonary pathology

Temp infection
Any focal neurology
Dehydration or fluid overloaded

ASSESSMENT OF DELIRIUM

Investigation

Simple tests blood, urine

Baseline

Repeat clinical investigation

More advanced Ix
CT/MRI brain
EEG
CSF examination

DDX DELIRIUM

Anxiety if agitated (check conscious levels)

Primary mental illness (e.g. schizophrenia)

If there is hallucinations and delusions

TREATMENT OF DELIRIUM

Treating
The underlying cause
Competency in patients 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

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

FALLS
& Funny Turns

FALL OVERVIEW

Fall is an event that results in a person nonintentionally coming to rest at a lower level
(usually floor)
Common & Important

Resulting in:
Fear
Injury
Dependency
Instutionalisation
Duty

ASSESSMENT FOLLOWING FALL

Typical Hx
Tripped
Fracture or non-fracture injury
Found on floor
Secondary consequences of falling

DRUGS ASSOCIATED WITH FALLS

Polypharmacy (>4 drugs any type) INDEPENDENT

RISK FACTOR
Common drug causes:
BZDs & other hypnotics
Anti-depressants (TCA & SSRI)
Anti-psychotics
Opiates
Diuretics
Anti-HTN esp ACEI & alpha-blockers
Anti-arrhythmics
Anti-convulsants
Skeletal muscle relaxants
Hypoglycaemics

(long-acting oral drugs: glibenclamide)

Insulin

EXAMINING IN FALLS

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

FALLS IX

MX: REDUCING FALLS 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 FALLS

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

SYNCOPE & 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)

SYNCOPE & PRESYNCOPE

Overview:
Major cause of morbidity
Recurrent in 1/3
Risk increases with age and CVD
Cause of serious injuries (fractures) & hospital
admissions

SYNCOPE & PRESYNCOPE CAUSES

Categories
Peripheral factors
Vasovagal syncope
Carotid sinus syndrome
Pump problem

MI or ischaemia
Arrythmia
Tachy- or Brady- e.g. VT, SVT, AF, complete heart block etc.

Outflow obstruction

E.g. aortic stenosis

Pulmonary embolism

SYNCOPE &
PRESYNCOPE DDX

Seizure Disorder

SYNCOPE 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)

SYNCOPE 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)

SYNCOPE 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

SYNCOPE 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

SYNCOPE HISTORY

5. Recovery period
Observed by eye witness
Rapid recovery = cardiac cause
Prolonged drowsiness & confusion = seizure

SYNCOPE EX & IX

SYNCOPE MANAGEMENT

BALANCE

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)

BALANCE & DYSEQUILIBRIUM

Problems arising:
Peripheral nerves

Joint Receptors

Age-related changes decrease visual acuity

Disease e.g. cataracts, glaucoma, etc

Ears

Weak due to inactivity, disease, medication

Reduced muscle mass of ageing

Eyes

Degenerative joint disease (arthritis)

Postural muscles

Neuropathy

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

BALANCE & DYSEQUILIBRIUM

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

DIAGNOSIS OF DIZZINESS TYPE

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 TYPE DIZZINESS

Cerebral Ataxia
MS
Vascular
Tumour

Sensory Ataxia
Tabes dorsalis
Neuropathy
Drugs
Anticonvulsants
Hypnotics
Alcohol
Extra-pyramidal
Parkinsons Disease and others
Normal pressure hydrocephalus

IMBALANCE IX
MRI Brain scan
Check drug level
Nerve Conduction
Treponema pallidum ELISA

IMBALANCE MX
Lower drug intake
Levodopa if extrapyramidal
Steriods (MS)
Surgery

SPINNING: VERTIGO TYPE OF DIZZINESS

Causes:

Peripheral
Labyrinthitis
Menieres disease
Benign paroxysmal positional vertigo

Central
Basilar insufficiency
MS

VERTIGO IX
Pure tone audiogram
Caloric test
Positional tests

Hallpike manoeuvre

MRI brain
MRA extra-cranial vessels

VERTIGO MX

ANXIETY TYPE OF DIZZINESS

Causes:

Panic disorder with over-breathing

Fatigue & depression
Hysteria

Investigations:

Hyperventilate 1-2mins
Refer to psychiatrist = CBT
Therapeutic brain scan

Management:
Reassure
Psychiatrist referral

DROP ATTACKS

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)

PRE-SYNCOPE CAUSE:
ORTHOSTATIC (POSTURAL) HYPOTENSION

Orthostatic hypotension is caused primarily by

gravity-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

CAUSES OF ORTHOSTATIC HYPOTENSION

Drugs
Chronic HTN
Volume Depletion

Sepsis

Dehydration, acute haemorrhage

Vasodilatation

Autonomic failure

Pure, diabetic, Parkinsons

Prolonged bed rest

Adrenal insufficiency
Raised intrathoracic pressure

Bowel or bladder evacuation, cough

ORTHOSTATIC HYPOTENSION MX

Conservative
Minimise/avoid precipitant
Advise on posture & standing (extra pendent alarm)
Support stockings
Water or salt depletion sorted

Medical (if symptoms persists)

Fludrocortisone
Midodrine (alpha-agonist: CI= IHD)
Demopressin (intranasal)

CAROTID SINUS SYNDROME - OVERVIEW

Episodic, symptomatic bradycardia +/hypotension
Due to hypersensitive carotid baroreceptor reflex

Resulting in syncope or near-syncrope

Common in older patients esp >80yrs

CAROTID SINUS SYNDROME PATHOPHYSIOLOGY

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

CAROTID SINUS SYNDROME

ASSOCIATIONS & 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

SUBTYPES OF CSS

Three subtypes:
Cardioinhibitory

Vasodepressor

Sinus pause >3 secs

BP fall >50mmHg

Mixed

Both sinus pause & BP fall

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

Stop aggravating drugs

AV sequential pacing = Cardio-inhibitory Type CSS

Increase circulating volume = Vasodepressor Type CSS

With flucortisome or midodrine

FALLS 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

OSCE STYLE FROM VIRTUAL PATIENTS

OSCE STYLE FROM VIRTUAL PATIENTS

OSCE STYLE FROM VIRTUAL PATIENTS

OSCE STYLE FROM VIRTUAL PATIENTS

URINE DIPSTICK

ECG

BLOOD TEST

BLOOD TEST INTERPRETATION

CXR

CT HEAD

X-RAY

MX

ANATOMY

GARDENS CLASSIFICATION

GARDENS CLASSIFICATION

THR

FOLLOW UP

OSTEOPOROSIS & FRACTURES

OVERVIEW

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

Facts

Fractures in UK & Europe due to osteoporosis occurs

in >50yrs
1 in 2 women
1 in 5 women

PATHOPHYSIOLOGY

Trabecular bone affected:

Crush fratucres common

E.g. little old lady being little and having dowagers 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 FACTORS = PRIMARY

FHx history
Alcohol > 4 units daily
RA
BMI <22
Prolonged mobility
Untreated menopause

SECONDARY RISK FACTORS

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

CLASSIFICATION OF
OSTEOPOROSIS

TYPE 1 = POSTMENOPAUSAL

TYPE 2 = SENILE

IDIOPATHIC = <50YRS

MOST COMMON order Fractures in OA

MALE

FEMALE

1. HIP
FRACTURES
2. COLLES

1. VERTEBRAL
FRACTURE 20%
2. HIP FRACTURE
3. COLLES

IX - OVERVIEW

Imaging
X-ray just good for fracture
DEXA

Bloods
Ca, PO4, ALP = all normal
Do specific ones to rule out secondary causes

DEXA

NEW:

IX

IX

CASE HISTORY

MX - CONSERVATIVE

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

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

Raloxifene (SERM)

Prevents osteoporosis in postmenopausal women

Increases CVD and breast cancer risk

Less breast cancer risk

Calcitionin

Reduces calcium breakdown and increase absorption into bones

MX - MEDICAL

OTHERS

MX

Denosumab:
A monoclonal Ab
to RANK ligand
SC twice yearly
Reduce
reabsorption

Recombinant PTH
For those who still
suffer fractures
even if on treatment
Increases risk of
renal malignancy

MX

DDX

DDX

HOMEOSTASIS
Deranged Na+ and K+

VOLUME DEPLETION & DEHYDRATION

Causes:

Multifactorial
Blood loss
Diuretics
Gastrointestinal losses (diarrhoea, NG drainage)
Sequestration of fluid
Poor oral intake
Fever

VOLUME DEPLETION & DEHYDRATION

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

NA+ & H2O

HYPOVOLAEMIA

EUVOLAEMIA

HYPERVOLAEMIA

DRUGS CAUSING HYPO NA+

Diuretics
SSRI
Carbamezapine
NSAIDs

Combination of Diuretics and SSRI

Others
Opiates
Anti-depressants - MAOI & TCA
Oral Hypoglycaemics (sulphonylureas ide)
PPIs
ACE Inhibitors
Barbiturates

HYPO NA+ ASSESSMENT CX

Mild cases

Na+ 115-125mM

Subtle or absent S&S

Lethargy
Confusion
Altered personality

Na+ <115mM
Delirium
Coma
Fits
Death

HYPO NA+ ASSESSMENT CAUSES

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
Addisons disease
SIADH
Older people multiple causes
HF, diuretics and acute diarrhoea

HYPO NA+ IX
Clinical History
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

HYPONATRAEMIA MX
Treat underlying cause
Not to recover Na+ rapidly

B/c

Risks of central pontine myelinolysis

Leading to quadriparesis and cranial nerve abnormalities

Aim to get to 130mM within few days

By raising Na+ by <10mM for 24 hours
Full correction take weeks

SIADH

Definition

characterized by excessive release of antidiuretic hormone from

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

Conc salty urine

Na+ <125mM
Plasma osmolarity <260mOsm/L
Osmolarity>200mOsm/L & Na+>20mM

NORMAL VOLUME STATUS

NORMAL RENAL, THYROID, CARDIAC & ADRENAL
FUNCTION

SIADH - CAUSES

Surgical stress

Neoplasms

CNS Disease

Trauma, subdural haematoma, stroke & meningoencephalitis

Lung Disease

Bronchogenic (SMALL LUNG CANCER), pancreatic

Including TB, pneumonia, bronchietasis

Some Drugs causing low Na+

SIADH - IX - SHORT ACTH SIMULATION

TEST (SHORT SYNACTHEN TEST)

SIADH - TREATMENT
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

HYPERNATRAEMIA

Causes
Dehydration
Poor oral intake or too much water loss

Rare

Diarrhoea
Vomiting
Diuretics
Uncontrolled DM

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)

HYPER NA+ CX

Clinical features

Hypotension (supine &/or orthostatic)

Sunken features
Urine scanty and concentrated
Lethargy
Confusion
Coma
Fits

HYPER NA+ IX
Na+ = Raised
PCV = Raised
Urea & Creatinine = High
Hb and albumin = high

K+ low in Conns

HYPER NA+ MX
Encourage oral fluid
IV fluids
Fluid infusion

Not too rapid cause cerebral oedema

NOTE: mild hypernatraemia is clinically

important!

HYPERKALAEMIA

>6.5mmol/L = EMERGENCY!!!!!!!!!!!!!!!!!

Can lead to:

Myocardial hyperexcitability
Causing VF & cardiac arrest

Signs & Symptoms

Fast irregular pulse

Chest pain
Palpitations
Light Headedness
Weakness

HYPERKALAEMIA CAUSES
Oliguric renal failure
K+ sparing diuretics
Rhabdomyolysis
Metabolic acidosis
Excess K+ therapy
Addisons disease
Massive blood transfusion
Burns
Drugs e.g. ACEI, suxamethonium
Artefactual result

HYPERKALAEMIA

Ix

ECG features:
Tall tented T-waves
Small P-waves
A wide QRS complex (become sinusoidal)
VF

Note artefactual results:

Haemolysis
Contamination with postassium EDTA anticoagulation
Thrombocytopaenia
Delayed analysis

ECG

HYPERKALAEMIA MX NON-URGENT

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

HYPERKALAEMIA - URGENT

HYPOKALAEMIA

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

HYPOKALAEMIA

ECG signs:
Small or inverted T-waves
Prominent U-waves (after T waves)
Long P-R interval
Depressed ST segments

HYPOKALAEMIA
Causes:
Diuretics

Vomiting & Diarrhoea

Pyloric stenosis
Cushings syndrome/steroids/ACTH
Conns syndrome

Indicated by raised HCO3

[HTN, Hypokalaemic alkalosis not on diuretics]

Alkalosis
Purgative and liquorice abuse
Renal tubular failure

HYPOKALAEMIA

Hypokalaemic Periodic Paralysis

Intermittent weakness lasting upto 72 hours

Due to K+ shifting from extra-to intracellular fluid

HYPOKALAEMIA TREATMENT

Mild

>2.5mmol/L No symptoms
Give oral K+ supplements
Review K+ after 3 days

Severe

<2.5mmol/L +/- dangerous symptoms

Give IV K+ cautiously never give IV STAT!!!
DO NOT GIVE K+ if oliguric

CALCIUM & PHOSPHATE

PHYSIOLOGY & BLOODS

OVERVIEW OF NORMAL HOMEOSTASIS

PTH
Raises Ca
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

OVERVIEW OF NORMAL HOMEOSTASIS

Vitamin D3

Activated version causes

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
60% free active!

Corrected total Ca for albumin

Add 0.1mmol/L to Ca for every 4g/L that albumin is

below 40g/L

(subtract instead if above 40g/L)

HYPERCALCAEMIA BONES, STONES, GROANS

& PSYCHIC MOANS

S&S

Abdominal pain
Vomiting
Constipation
Polyuria
Polydipsia
Depression, Confusion
Weight loss, Anorexia
Tiredness, weakness
HTN
Pyrexia
Renal Stones, renal failure
Cardiac Arrest

HYPERCALCAEMIA - INVESTIGATIONS

Most common causes

Malignancy
Primary hyperparathyroidism

To differentiate

Malignancy
Low albumin
Low Cl Alkalosis
Low K+
Raised PO4
Raised ALP

Primary hyperparathyroidism

Raised PTH

TREATING ACUTE HYPERCALCAEMIA

Esp if >3.5mmol/L & symptomatic

1) Correct dehydration

IV 0.9% saline

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

HYPOCALCAEMIA

HYPOCALCAEMIA

QUESTION

HYPERPARATHYROIDISM

BONE BIOCHEMISTRY
Hypercalcaemia
Bone Disease - Osteoporosis

OVERVIEW

OSTEOPOROSIS SEE SLIDES LATER

Implies reduced bone mass
Types

Primary (age-related) or Secondary due to another

condition or drugs

Consequence depends on part of bone affected:

Trabecular bone crush fractures of vertebrae
Cortical bone long bone fracture Neck of femur

OSTEOPOROSIS OVERVIEW

Prevalence

F>M (esp >50)

Risk factors

For primary
Age
Parental history of hip fracture
SMOKING
Alcohol >4 units daily
RA
BMI<22 being thin
Prolonged immobility/ sedentary life
Untreated menopause/premature

OSTEOPOROSIS

Medications worsening osteoporosis

Long-term heparin therapy
PPI
Glitazone
Aromatase Inhibitors e.g. anatrozole

IF OSTEOPOROSIS IS GLUCOCORTICOID
INDUCED E.G. ASTHMA DRUGS

OSTEOPOROSIS PREVENTION
Alendronate is first line
Vitamin D & Calcium

Raloxifene - SERM