Session 1

Question 1

Older Age Normal ageing LO Cognitive decline and Dementia LO Nutrition in the elderly LO

Answer 1

(In my opinion)

Question 2

1. What is the effect of Ageing and the Respiratory System? 2. These changes occur as a result of? 3. ? are common post-operative complications in the elderly 4. These complications are increased in? 5. What else leads to progressive increase in the number of episodes of arterial desaturation during sleep (with advancing age)

Answer 2

1. • Lung and chest wall compliance decrease with advancing age. - Total lung capacity (TLC), Forced Vital Capacity (FVC), Forced Expiratory Volume in 1 second (FEV1) and Vital Capacity are all reduced as people age. 2. reduction in elastic support of the airways and leads to increased collapsibility of alveoli and terminal conducting airways. 3. Atelectasis, pulmonary emboli and pneumonia 4. smokers, patients with chronic chest disease & those undergoing abdominal or thoracic surgery. 5. advancing age, loss of elastic tissue around the oropharynx can lead to collapse of the upper airway. Sleep or sedative states may result in partial or complete obstruction of the airway

Question 3

Ageing and the Pharmacokinetics 1. Elderly patients have an increased sensitivity to what type of drugs? 2. Why do elderly patients have a slower metabolism and elimination of drugs?

Answer 3

1. CNS depressant drugs 2. reduced hepatic and renal function

Question 4

1. What is the effect of age on the skin

Answer 4

1. • thin skin - fragile subcutaneous blood vessels = bruise easily 2. Achieving and securing venous access can be difficult

Question 5

What is the effect of Ageing and the Cardiovascular system, more specifically the vascularture?

Answer 5

Large and medium sized vessels become less elastic: -> less compliant -> raised systemic vascular resistance and hypertension -> left ventricular strain & left ventricular hypertrophy

Question 6

What is the effect of age on heart conduction?

Answer 6

• Cardiac conducting cells dec in no. making heart block, ectopic beats, arrhythmias & atrial fibrillation more prevalent. • Atrial contraction contributes approximately one third of the volume towards normal ventricular filling, patients with atrial fibrillation suffer a reduction in cardiac output of about 30%.

Question 7

1. What is the effect of age on CO 2. Results in?/ clinical significance?

Answer 7

1. CO falls by 3% per decade which is due to reduced stroke volume & ventricular contractility. 2. Increases the arm-brain circulation time for drugs & means intravenous anaesthesia is achieved more slowly & with reduced doses of anaesthetic agent.

Question 8

What is the effect of changes effect drug dosage?

Answer 8

Reduced CO -> delayed onset of IV anaesthesia Reduced total body water and increased adipose tissue -> altered volume of distribution of some drugs Plasma proteins are reduced -> decreased protein binding and increased free drug availability.

Question 9

Ageing and the Renal System 1. What is the effect of age on the renal system?

Answer 9

1. GFR is thought to decrease by 1% per year > 20 years due to a progressive loss of renal cortical glomeruli A reduction in renal perfusion secondary to reduced CO & atheromatous vascular disease leads to a decline in renal function.

Question 10

Ageing and the Renal System 1. In addition diabetes mellitus is increasingly common. How does this relate to the effect of age on the kidneys? 2. Prostatism in males can lead to?

Answer 10

1. Inc age -> inc diabetes -> Inc in use of nephrotoxic drugs such as non-steroidal anti-inflammatory drugs (NSAID’s) and angiotensin converting enzyme inhibitors (ACE inhibitors) 2. Inc age in males -> inc incidence of prostatism -> obstructive nephropathy and dehydration is common in the elderly especially during illness

Question 11

CNS 1. Cerebrovascular disease is common in the elderly secondary to 2. ? is reduced by 30% by the age of 80 years

Answer 11

1. diffuse atherosclerosis & hypertension. 2. Neuronal density

Question 12

1. What are the Endocrine and Metabolic Effects of Ageing?

Answer 12

1. The BMR falls by 1% per year after the age of 30. Fall in metabolic activity & reduced muscle mass may cause impaired thermoregulatory control.

Question 13

What is the meaning of Polypharmacy

Answer 13

Many patients take multiple medications on a regular basis and the effects of these medications on the individual’s physiology must be taken into account.

Question 14

Define dementia

Answer 14

Syndrome caused by a number of brain disorders which cause

• > memory loss
• > decline in some other aspect of cognition
• > difficulties with activities of daily living

Question 15

What are the different types of dementia?

Answer 15

Question 16

1. What is Alzheimer’s disease?
2. Risk factors

Answer 16

1. • progressive degeneration of the cerebral cortex
     - widespread cortical atrophy
     - Neurons affected develop surrounding amyloid plaques, neurofibrillary tangles, and produce less acetylcholine
2. Ageing.

Caucasian.

Family history. Small increased risk - 3.5-fold increase if a first-degree family member is affected.

It is more common in women. (67% is in women, and 55% in men, unlike other types of dementia.)

Apolipoprotein E4 variant - the largest known genetic risk factor in late-onset sporadic Alzheimer’s disease, but wide differences in prevalence of the genotype in populations studied.

Head injury.

Risk factors associated with vascular disease; particularly hypercholesterolaemia, hypertension and diabetes implicated.

3.

Question 17

Onset of Alzheimer’s disease is insidious, and it usually progresses slowly over 7-10 years.

Symptoms include:

Answer 17

Early:

memory loss i.e. Repeat statements and questions

Progresses:

Difficulties with language

Apraxia

Late:

Psychiatric symptoms - depression, hallucinations, delusions

Behavioural problems - disinhibition, aggression, agitation

Inhaling food or liquid into the lungs (aspiration)

Question 18

Investigations for Alzheimer’s

Answer 18

Diagnosis based on comprehensive assessment:

• Hx, Ex, cognitive and MSE
• Bloods
• Investigations

Investigations

Ensure no treatable cause has been missed, by arranging FBC, ESR or CRP, MSU, U&E, LFT, glucose, Ca2+, TFT, B12 and folate (red cell folate). Don’t always believe normal B12s: assays are known often to be inaccurate and methylmalonic acid or homocysteine levels may be more helpful[6]. If in doubt, one should treat.

VDRL/TPHA should not be performed routinely - only if risk factors are present.

Consider blood cultures, CXR and MRI scan, and psychometric testing as appropriate to confirm diagnosis.

Specialist assessment is required to determine the subtype of dementia. If this cannot be done on clinical grounds, perfusion hexamethylpropyleneamine oxime (HMPAO) single-photon emission computed tomography (SPECT) may be used to distinguish between Alzheimer’s disease, vascular dementia and frontotemporal dementia. This is not useful in the presence of Down’s syndrome.

CSF examination may occasionally be helpful if Creutzfeldt-Jakob disease or other forms of rapidly progressive dementia are suspected[7].

Genetic clinical genotype analysis should only be requested where an inherited cause is suspected.

Involve impairment of at least two of the following domains:

Ability to acquire and remember new information

Judgement, ability to reason or handle complex tasks

Visuospatial ability

Language functions

Personality and behaviour

Question 19

What are the treatable causes of dementia?

Answer 19

Potentially treatable dementias (fewer than 5%):

Substance abuse

Hypothyroidism

Space-occupying intracranial lesions

Normal pressure hydrocephalus

Syphilis

Vitamin B12 deficiency

Folate deficiency

Pellagra

Question 20

What does management of Alzheimer’s include?

Answer 20

1. Written information about:

The symptoms and signs of dementia

Course and prognosis

Treatments

Local care and support services

Support groups

Sources of financial and legal advice, and advocacy

Medico-legal issues, including driving

Local information sources, including libraries and voluntary organisations

2. Non-pharmacological:

Music therapy

Art therapy

3. Care plan
4. Factors which may exacerbate violent or aggressive behaviour, or increase the risk of harm to self or others include:

Overcrowding

Lack of privacy

Boredom or lack of activity

5.

Question 21

1. treatment of Alzheimer’s -> pharmacological

Answer 21

AChE inhibitor treatment (donepezil, galantamine or rivastigmine) should be considered in patients with mild or moderate Alzheimer’s disease.

These drugs have cholinergic side-effects and should be started at a low dose, and then be titrated according to response.

Question 22

1. Causes?
2. Pathology

Answer 22

1. Genetic, lifestyle and environmental factors
2. Plaques. These clumps of a protein called beta-amyloid may damage and destroy brain cells in several ways, including interfering with cell-to-cell communication. Although the ultimate cause of brain-cell death in Alzheimer’s isn’t known, the collection of beta-amyloid on the outside of brain cells is a prime suspect.

Tangles. Brain cells depend on an internal support and transport system to carry nutrients and other essential materials throughout their long extensions. This system requires the normal structure and functioning of a protein called tau.

In Alzheimer’s, threads of tau protein twist into abnormal tangles inside brain cells, leading to failure of the transport system. This failure is also strongly implicated in the decline and death of brain cells.

Question 23

Management: palliative and end-of-life care

Answer 23

• Physical, psychological, social and spiritual support
• Oral nutrition encouraged
• Percutaneous endoscopic gastrostomy (PEG) -> transient dysphagia
  (not recommended in patients with severe dementia, as there is no evidence of increased survival or reduced complications. Decisions to withhold nutritional support should be taken within a legal and ethical framework)
• Fever may be managed with antipyretics and mechanical cooling.
• Palliative antibiotics should be given after an individual assessment of the patient.
• Resuscitation is unlikely to succeed in patients with severe dementia.

Question 24

Lewy body dementia

1. Symptoms
2. Pathogenesis

Answer 24

Visual hallucinations: Hallucinations may be one of the first symptoms, and they often recur. They may include seeing shapes, animals or people that aren’t there. Sound (auditory), smell (olfactory) or touch (tactile) hallucinations are possible.

Movement disorders. Signs of Parkinson’s disease (parkinsonian symptoms), such as slowed movement, rigid muscles, tremor or a shuffling walk may occur

Poor regulation of body functions (autonomic nervous system). Blood pressure, pulse, sweating and the digestive process are regulated by a part of the nervous system that is often affected by Lewy body dementia. This can result in dizziness, falls and bowel issues such as constipation.

Cognitive problems. You may experience thinking (cognitive) problems similar to those of Alzheimer’s disease, such as confusion, poor attention, visual-spatial problems and memory loss.

Sleep difficulties. You may have rapid eye movement (REM) sleep behavior disorder, which can cause you to physically act out your dreams while you’re asleep.
Fluctuating attention. Episodes of drowsiness, long periods of staring into space, long naps during the day or disorganized speech are possible.

Depression. You may experience depression sometime during the course of your illness.

Apathy. You may have loss of motivation.

Question 25

Lewy body dementia

1. Risk factors
2. Medication

Answer 25

1. Being older than 60
   Being male
   Having a family member with Lewy body dementia or Parkinson’s disease
2. NICE and SIGN guidelines advise that cholinesterase inhibitors - eg rivastigmine - at daily doses of 6 mg and above, can be helpful in treating cognitive decline in people with DLB. However the most recent Cochrane review suggests the evidence of benefit remains unclear.

Question 26

1. What is Vascular dementia (VaD)?
2. Aetiology
3. Risk factors for VaD include:
4. Prognosis
5. Prevention

Answer 26

1. • group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease (multiple infarcts, single strategic infarct or small vessel disease.)
2. • Stroke-related VaD. This incorporates multi-infarct dementia, the result of a series of small strokes, which in themselves may not be recognised, and single-infarct dementia, which occurs after a larger stroke.

Subcortical VaD (small-vessel disease or Binswanger’s disease).[2]

Mixed dementia. Changes of both VaD and Alzheimer’s disease are found together in the brain. The distinction between VaD and Alzheimer’s dementia is becoming increasingly blurred because vascular risk factors play a role in both diseases and both types of dementia may co-exist in the same patient. Similar patterns of biochemical abnormalities are also seen on proton magnetic resonance spectroscopy.[3]However, where they are seen mostly in white matter in VaD, in Alzheimer’s dementia they predominate in cortical grey matter.

3. History of stroke or transient ischaemic attack (TIA).

Atrial fibrillation.

Hypertension.

Diabetes mellitus.

Hyperlipidaemia.

Smoking.

Obesity.

Coronary heart disease.

Family history of stroke or cardiovascular disease

4. Worse than that of Alzheimer’s disease, carrying an average life expectancy of three to five years

5.
Maintaining a healthy blood pressure.
Keeping cholesterol in check.
Prevent or control diabetes.
Optimal glycaemic control
Smoking cessation

Question 27

Frontotemporal dementia

1. PATHOPHYSIOLOGY
2. SYMPTOMS

Answer 27

1.• Lobar distribution – unlike diffuse nature of Alzheimer’s

• Clumps of abnormal proteins within brain cells
• Pick bodies
• Loss of neurones
• Spongy vacuolisation of frontal and temporal lobes

2.Different symptoms depending on subtype.

• Behavioural variant FTD: Loss of inhibition, Inappropriate social behaviour And loss of motivation but without depression
• Semantic: loss of vocabulary, loss of recognition of faces/objects.
• Progressive non-fluent aphasia: slow, difficult speech, loss of literacy skills.

Question 28

Frontotemporal dementia

1. COURSE
2. TREATMENT

Answer 28

1. • Slow progression with worsening symptoms

• 3 separate syndromes converge and overlap as disease progresses
• Gradual decline in social cognitive and neurological abilities
• 8-10 years survival from diagnosis

2. • No treatment to stop progression

• Management to support and alleviate symptoms
• Support referral e.g. help with organising stable routine, speech and language therapy, social support.
• Pharmacological – stop any drugs that may exacerbate confusion & memory problems, SSRI’s (selective serotonin reuptake inhibitors) may help behavioural symptoms

Question 29

Frontotemporal dementia

1. PREVENTION

Answer 29

1. • Genetic testing where strong family history

• Genetic counselling beforehand

​

Question 30

Some subtypes of frontotemporal dementia are marked by the impairment or loss of speech and language difficulties.
Two types of primary progressive aphasia are considered frontotemporal dementia. Primary progressive aphasia is characterized by an increasing difficulty in using and understanding written and spoken language. For example, people may have trouble finding the right word to use in speech or naming objects.
Semantic dementia is one type of primary progressive aphasia. It’s also known as semantic variant primary progressive aphasia. Individuals with semantic dementia have prominent difficulty naming (anomia) and may replace a specific word with a more general word such as “it” for pen. They may also lose knowledge of word meaning.Progressive agrammatic (nonfluent) aphasia is another type of primary progressive aphasia characterized by nonfluent and hesitant speech. Speech may sound telegraphic with misuse of pronouns and errors in sentence construction.

Question 31

What is the problem with having malnourised elderly patients?

Answer 31

• longer hospital admission
• respond less well to treatment
• 3x more likely to develop complications after surgery
• higher mortality rates

Question 32

How do we screen for malnutrition?

Answer 32

Malnutrition Universal Screening Tool (MUST)