Passmed wrong answers

Question 1

What is acute confusional state and what are the risk factors?

Answer 1

Acute confusional state is also known as delirium or acute organic brain syndrome. It affects up to 30% of elderly patients admitted to hospital.
It is characterised using the Confusion Assessment Method as an acute onset of a change in mental state from the patient’s baseline with inattention, in addition to either disorganised thinking or altered consciousness. Sleep-wake cycle is often reversed.

Predisposing factors include:
- age > 65 years
- background of dementia
- significant injury e.g. hip fracture
- frailty or multimorbidity
- polypharmacy

Question 2

What can precipitate delirium?

Answer 2

The precipitating events are often multifactorial and may include:
- infection: particularly urinary tract infections
- metabolic: e.g. hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration
- change of environment
- any significant cardiovascular, respiratory, neurological or endocrine condition
- severe pain
- alcohol withdrawal
- constipation
- medications eg opioids
- Hypoxia

Question 3

What are the features of delirium?

Answer 3

Features - a wide variety of presentations
- memory disturbances (loss of short term > long term)
- may be very agitated or withdrawn
- disorientation
- mood change
- visual hallucinations
- disturbed sleep cycle
- poor attention

Question 4

How is delirium managed?

Answer 4

1. treatment of the underlying cause
2. modification of the environment
3. haloperidol or olanzapine as the first-line sedative
   - management can be challenging in patients with Parkinson’s disease, as antipsychotics can often worsen Parkinsonian symptoms
   careful reduction of the Parkinson medication may be helpful
4. if symptoms require urgent treatment then the atypical antipsychotics quetiapine and clozapine are preferred

Question 5

What is the distinctive feature of vascular dementia?

Answer 5

Vascular dementia can present in a stepwise manner, with sudden progression of symptoms corresponding to new vascular events between stable periods. The past medical history of vascular risk factors are also supportive.

Question 6

What is vascular dementia?

Answer 6

Vascular dementia (VD) is the second most common form of dementia after Alzheimer disease. It is not a single disease but a group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease. Vascular dementia has been increasingly recognised as the most severe form of the spectrum of deficits encompassed by the term vascular cognitive impairment (VCI). Early detection and an accurate diagnosis are important in the prevention of vascular dementia.

Question 7

What are the 3 main subtypes of vascular dementia?

Answer 7

1. Stroke-related VD – multi-infarct or single-infarct dementia
2. Subcortical VD – caused by small vessel disease
3. Mixed dementia – the presence of both VD and Alzheimer’s disease

Question 8

What are the risk factors for vascular dementia?

Answer 8

Risk factors
- History of stroke or transient ischaemic attack (TIA)
- Atrial fibrillation
- Hypertension
- Diabetes mellitus
- Hyperlipidaemia
- Smoking
- Obesity
- Coronary heart disease
- A family history of stroke or cardiovascular

Rarely, VD can be inherited as in the case of CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy).

Question 9

What are the features of vascular dementia?

Answer 9

Patients with VD typically presents with
Several months or several years of a history of a sudden or stepwise deterioration of cognitive function.

Symptoms and the speed of progression vary but may include:
- Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
- The difficulty with attention and concentration
- Seizures
- Memory disturbance
- Gait disturbance
- Speech disturbance
- Emotional disturbance

Question 10

How is vascular dementia diagnosed?

Answer 10

Diagnosis is made based on:
1. A comprehensive history and physical examination
2, Formal screen for cognitive impairment
3. Medical review to exclude medication cause of cognitive decline
4. MRI scan – may show infarcts and extensive white matter changes

NINDS-AIREN criteria for probable vascular dementia:
1. Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event
- established using clinical examination and neuropsychological testing
2. Cerebrovascular disease
- defined by neurological signs and/or brain imaging
3. A relationship between the above two disorders inferred by:
- the onset of dementia within three months following a recognised stroke
- an abrupt deterioration in cognitive functions
- fluctuating, stepwise progression of cognitive deficits

Question 11

How is vascular dementia managed?

Answer 11

1. General management
   - Treatment is mainly symptomatic with the aim to address individual problems and provide support to the patient and carers
   - Important to detect and address cardiovascular risk factors – for slowing down the progression
2. Non-pharmacological management
   - Tailored to the individual
   - Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
   - Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication
3. Pharmacological management
   - There is no specific pharmacological treatment approved for cognitive symptoms
   - Only consider AChE inhibitors or memantine for people with vascular dementia if they have suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia or dementia with Lewy bodies.
   - There is no evidence that aspirin is effective in treating patients with a diagnosis of vascular dementia.

Question 12

Which medications are associated with an increased mortality in dementia patients?

Answer 12

Antipsychotics are associated with a significant increase in mortality in dementia patients and should only be used with caution for patients at risk of harming themselves or others, or when the agitation, hallucinations, or delusions are causing them severe distress as in this case.

Question 13

How is Alzheimer’s disease managed?

Answer 13

1. Non-pharmacological management
   - a range of activities to promote wellbeing that are tailored to the person’s preference
   - group cognitive stimulation therapy for patients with mild and moderate dementia
   - other options to consider include group reminiscence therapy and cognitive rehabilitation
2. Pharmacological management
   - the three acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) as options for managing mild to moderate Alzheimer’s disease
   - memantine (an NMDA receptor antagonist) is in simple terms the ‘second-line’ treatment for Alzheimer’s, NICE recommend it is used in the following situation reserved for patients with:
   *moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
   *as an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
   *monotherapy in severe Alzheimer’s
3. Managing non-cognitive symptoms
   - NICE does not recommend antidepressants for mild to moderate depression in patients with dementia
   - antipsychotics should only be used for patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress

Question 14

When is donepezil use for alzheimer’s disease contraindicated?

Answer 14

contraindicated in patients with bradycardia
adverse effects include insomnia

Question 15

What are the 3 types of delirium?

Answer 15

There are three subtypes of delirium -
1. hyperactive,
2. hypoactive, and
3. mixed.

People are well acquainted with the hyperactive form, but the hypoactive subtype is very common as well. Symptoms include being withdrawn, lethargic, and slow to respond.

Question 16

What are the types of frontotemporal dementia?

Answer 16

Frontotemporal lobar degeneration (FTLD) is the third most common type of cortical dementia after Alzheimer’s and Lewy body dementia.

There are three recognised types of FTLD
1. Frontotemporal dementia (Pick’s disease)
2. Progressive non fluent aphasia (chronic progressive aphasia, CPA)
3. Semantic dementia

Question 17

What are the common features of the 3 types of frontotemporal lobar dementia?

Answer 17

• Onset before 65
• Insidious onset
• Relatively preserved memory and visuospatial skills
• Personality change and social conduct problems

Question 18

What are the features of Pick’s disease (frontotemporal dementia)? What changes in the brain are seen?

Answer 18

• May also be called behavioural-variant frontotemporal dementia*
  This is the most common type of frontotemporal lobar dementia and is characterised by personality change and impaired social conduct. Other common features include hyperorality, disinhibition, increased appetite, loss of sympathy/empathy, perseveration/ compulsive behaviours, executive dysfunction with relative sparing of memory and visuospatial functions.

Focal gyral atrophy with a knife-blade appearance is characteristic of Pick’s disease.

Macroscopic changes seen in Pick’s disease include:-
Atrophy of the frontal and temporal lobes

Microscopic changes include:-
- Pick bodies - spherical aggregations of tau protein (silver-staining)
- Gliosis
- Neurofibrillary tangles
- Senile plaques

Question 19

Is frontotemporal dementia treated similarly to Alzheimer’s disease?

Answer 19

No

NICE do not recommend that AChE inhibitors or memantine are used in people with frontotemporal dementia

Question 20

What is the main feature of chronic progressive aphasia (CPA)?

Answer 20

This is a subtype of frontotemporal dementia so the common features are seen.

Here the chief factor is non fluent speech. They make short utterances that are agrammatic. Comprehension is relatively preserved.

Question 21

What is the main feature of semantic dementia?

Answer 21

This is a subtype of frontotemporal dementia so the common features are seen.

Here the patient has a fluent progressive aphasia. The speech is fluent but empty and conveys little meaning. Unlike in Alzheimer’s memory is better for recent rather than remote events.

Question 22

What risk does lorazepam increase in geriatric patients?

Answer 22

Risk of falls

Question 23

What is Lewy body dementia and what is the characteristic pathology?

Answer 23

Lewy body dementia is an increasingly recognised cause of dementia, accounting for up to 20% of cases. The characteristic pathological feature is alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.

The relationship between Parkinson’s disease and Lewy body dementia is complicated, particularly as dementia is often seen in Parkinson’s disease. Also, up to 40% of patients with Alzheimer’s have Lewy bodies.

Question 24

What are the features of Lewy body dementia?

Answer 24

1. progressive cognitive impairment
   - typically occurs before parkinsonism, but usually both features occur within a year of each other. This is in contrast to Parkinson’s disease, where the motor symptoms typically present at least one year before cognitive symptoms
   - cognition may be fluctuating, in contrast to other forms of dementia
   - in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
2. parkinsonism
3. visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
4. REM-sleep behaviour

Question 25

How is lewy body dementia diagnosed?

Answer 25

• usually clinical
• single-photon emission computed tomography (SPECT) is increasingly used. It is currently commercially known as a DaTscan. Dopaminergic iodine-123-radiolabelled 2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123-I FP-CIT) is used as the radioisotope. The sensitivity of SPECT in diagnosing Lewy body dementia is around 90% with a specificity of 100%

Question 26

How is Lewy body dementia managed?

Answer 26

• both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s.
• neuroleptics (antipsychotics) should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism.

Question 27

How can frailty be formally assessed?

Answer 27

1. Evaluation of gait speed
2. Self-reported health status
3. PRISMA-7 questionnaire

Question 28

What is the definition of frailty?

Answer 28

A state of impaired homeostasis leading to increased vulnerability to minor stressor events.

Question 29

What does the PRISMA-7 questionnaire entail?

Answer 29

The PRISMA-7 questionnaire is composed of seven questions that enquire about age, sex, health problems, help at home, mobility and social support. If the respondent answers ‘yes’ on 3 or more questions, this indicates an increased risk of frailty and the need for further clinical review.

Question 30

What is the definition of multimorbidity?

Answer 30

The presence of two or more long-term health conditions, including: Defined physical or mental health conditions, learning disabilities, symptom complexes such as chronic pain, sensory impairments and alcohol or substance misuse

Question 31

What are the most common comorbid conditions?

Answer 31

1. Hypertension is the most prevalent disorder that exists comorbidly with other disorders such as pain, diabetes and hearing loss
2. Depression and anxiety are the most common mental health disorders that exist comorbidly with other conditions such as pain, hypertension and irritable bowel syndrome
3. Other conditions that are found in multimorbidity include chronic pain, prostate disorders, thyroid disorders and coronary artery disease

Question 32

What are the risk factors for multimorbidity?

Answer 32

• Increasing age
• Female sex
• Low socioeconomic status
• Tobacco and alcohol usage
• Lack of physical activity
• Poor nutrition and obesity

Question 33

What are the complications of multimorbidity?

Answer 33

• Decreased quality of life and life expectancy
• Increased treatment burden: Difficulties in understanding and self-managing condition as well as adherence to lifestyle changes
• Mental health issues: Those with cognitive impairment are particularly vulnerable
• Polypharmacy: Adverse drug events increase in prevalence as the number of chronic conditions increases
• Negative impact on carers welfare

Question 34

How should multimorbidity be assessed?

Answer 34

1. Identify those who may benefit from the recognition of multimorbidity, opportunistically in routine care or through healthcare records
2. Patients may require a multimorbidity approach if they:
   *Have difficulties with daily activities,
   *are frail,
   *are prescribed over 10 medications, or
   *frequently seek emergency care services
3. Establish the extent of disease burden: Discuss mental health issues, wellbeing and the interaction between their health and quality of life
4. Investigate how their treatment burden affects their daily activities
5. Ask about social circumstances and assess their health literacy
6. Assess the adequacy of pain management particularly in chronic pain conditions
7. Frailty should be specifically assessed through the evaluation of gait speed, self-reported health status, or the PRISMA-7 questionnaire: The PRISMA-7 involves questions considering the age, sex, health problems, assistance required and walking aid use of the patient

Question 35

What are the key features for managing multimorbidity?

Answer 35

1. Reducing treatment burden and optimising care is the goal in managing comorbidity
   - Maximise the benefits of existing treatments
   - Offer alternative follow-up arrangements if they are struggling to meet them
   - Reduce the number of high risk medications being prescribed and consider the use of non-pharmacological treatments
   - Consider a ‘bisphosphonate holiday’ in those taking bisphosphonates for longer than three years as there is no consistent evidence of continued benefits after this point. Discuss stopping bisphosphonates after 3 years and include patient choice, fracture risk and life expectancy in the discussion.
   - Consider the use of screening tools such as STOPP/ START in older people to recognise medicine safety concerns: STOPP identifies medications where the risk outweighs the therapeutic benefits in certain conditions and START suggests medications that may provide additional benefits ie proton pump inhibitors for gastroprotection in patients on medications increasing bleeding risk
   - Especially consider stopping the use of medications such as NSAIDS, warfarin and aspirin in patients with peptic ulcer disease, and pay particular attention to the prescription of reno-toxic or renally cleared drugs in reduced renal function
   - Ask patients about the benefits and harms of their individual treatments, considering the overall prognostic benefit
2. Promote self-management through education and engagement strategies
   - Support carers and families of patients
   - Use the action plan to follow up with the patient at agreed points: NHS England recommends a yearly review of all medications for people aged over 65, however, medications should be reviewed periodically to ensure that patients are being informed, given adequate laboratory tests and that treatments are optimised

Question 36

What are the risk factors for Alzheimer’s?

Answer 36

• increasing age
• family history of Alzheimer’s disease
  5% of cases are inherited as an autosomal dominant trait
• mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form
• apoprotein E allele E4 - encodes a cholesterol transport protein
• Caucasian ethnicity
• Down’s syndrome

Question 37

What are the pathological changes in Alzheimer’s disease?

Answer 37

Pathological changes
1. macroscopic:
widespread cerebral atrophy, particularly involving the cortex and hippocampus

2. microscopic:
   cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
   hyperphosphorylation of the tau protein has been linked to AD
3. biochemical
   there is a deficit of acetylcholine from damage to an ascending forebrain projection

*Neurofibrillary tangles
paired helical filaments are partly made from a protein called tau
tau is a protein that interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules
in AD tau proteins are excessively phosphorylated, impairing its function

Question 38

What tool can help with prescribing new medications in patients with multiple morbidities?

Answer 38

START (screening tool to alert doctors to the right treatment) tool. It is used in patients with multiple morbidities, especially elderly patients, to decide whether the introduction of a new medication will be beneficial. It is used in patients undergoing polypharmacy to assess the benefit of starting a new medication.

Question 39

Which questionnaire can be used to confirm frailty?

Answer 39

PRISMA-7 is a validated questionnaire that can be used to confirm frailty in an individual. Frailty is defined as a state of impaired homeostasis leading to increased vulnerability to minor stressor events. If individuated early, it can be managed and lead to great improvements to patient care in the long term.

Question 40

Which parts of the brain are affected in Alzheimer’s disease?

Answer 40

Cortex and hippocampus