HCOE Revision Slides.pdf

8/19/2019 HCOE Revision Slides.pdf

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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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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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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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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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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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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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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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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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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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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



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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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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



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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

Documents

HCOE Revision Slides.pdf