Flashcards in Geriatrics - Prescribing in older people Deck (67):
What is the definition of inappropriate prescribing?
Inappropriate prescribing is defined as:
- prescribing drugs which are contraindicated
- prescribing drugs with an inappropriate dose or duration
- prescribing drugs which are likely to adversely affect prognosis
- failure to use a drug which could improve a patients outcome
Why is inappropriate prescribing more common in older patients?
1) Older patients have a higher prevalence of chronic disease.
2) Higher levels of polypharmacy (defined as 4 drugs or more) increases the risk of drug-drug and drug-disease interactions
3) Age related changes in physiology, such as altered renal and hepatic function
What happens to pharmacodynamics as we age?
Pharmacodynamics looks at the physiological effect drugs have on the body. Changes as we age lead to altered (increased or decreased) sensitivity to certain classes of drugs.
- Beta blockers
- Beta agonists
For example, older patients are less sensitive to propranolol because although the drug binds normally to the receptor, changes to the GPCR second messenger system affect the cells response to the drug.
What is meant by pharmacokinetics?
Pharmacokinetics is what the body does to the drug. It includes:
With ageing, metabolism and excretion of many drugs decrease, requiring dose adjustment of some drugs. This is especially important for drugs, with a narrow therapeutic index.
Do changes in drug absorption with age produce any clinically important effects?
No. Age related changes in the GIT are not clinically significant as they do not affect the absorption of most drugs.
How is the distribution of drugs affected by age?
With ageing, total body fat increases, and therefore increases the volume of distribution for fat soluble drugs.
Total body water however, decreases. This decreases the apparent volume of distribution of drugs that are water soluble.
Serum albumin also decreases and this INCREASES the affects of albumin bound drugs as the level of unbound drug increases as a consequence.
How does hepatic metabolism change with age?
The majority of drugs are metabolised by the hepatic route. Reduced liver volume and enzyme activity means that hepatic metabolism of many drugs decreases.
To prevent toxic accumulation doses must be reduced, or dosing intervals increased.
How is renal elimination affected by age?
Reduction in GFR with age, is important for drugs that are renally excreted. Changes in the GFR decrease the excretion of these drugs.
Digoxin is an example of a renally excreted drug with a narrow therapeutic index that often requires a dose reduction as we get older to prevent toxicity.
What is the STOPP START criteria?
This consists of criteria for potentially inappropriate drugs called STOPP (Screening Tool of Older Persons Prescriptions) and criteria for potentially indicated drugs called START (Screening Tool to Alert to Right Treatment).
Give some examples of drugs affecting the cardiovascular system that should be stopped in the elderly as part of the STOPP START guidance
Loop diuretic as first line monotherapy for hypertension
CCBs with chronic constipation
Use of aspirin + warfarin without stomach protection
Use of diltiazam or verapamil with NYHA Class III or IV heart failure
Give some examples of CNS drugs that should be stopped under the STOPP START guidance
TCAs with dementia
TCAs with glaucoma
TCAs with cardiac conductive abnormalities
Long term neuroleptics as long term hypnotics
Anticholinergics to treat extrapyramidal side effects of neuroleptic medication
Examples of GIT drugs that may need stopping in accordance with the STOPP START criteria
Diphenoxylate, loperamide or codeine phosphate to treat diarrhoea of unknown cause
Prochlorperazine or metoclopramide with Parkinsonism
PPI for peptic ulcer disease at therapeutic dose for >8 weeks
Respiratory drugs that may need reviewing as per STOPP START guidance
Theophylline as monotherapy for COPD
Systemic corticosteroids instead of inhaled corticosteroids for maintenance therapy in mild-moderate COPD
Nebulised ipratropium with glaucoma
What musculoskeletal drugs would you consider stopping in an elderly patient under the STOPP START guidance?
NSAID with a history of peptic ulcer disease or GI bleeding
NSAID with moderate-severe hypertension
NSAID with heart failure
Warfarin and NSAID together
Drugs affecting the urogenital system that you may considering stopping in an elderly patient?
Bladder antimuscarinic drugs and dementia
Bladder antimuscarinic drugs and glaucoma
Alpha blockers in males with frequent incontinence
Endocrine drugs that may need reviewing in elderly patients
Glibenclamide or chlorpropamide with type 2 diabetes
Beta blockers in those with type 2 diabetes and frequent hypoglycaemic episodes - i.e. > 1 per month
Oestrogens without progesterone in patients with intact uterus
Name some drugs that are associated with increased falls risk in elderly patients
BZDs (sedative, may cause imbalance)
Neuroleptic drugs (may cause gait dyspraxia, Parkinsonism)
First generation antihistamines (sedative, may impair sensation)
What cardiovascular drugs would you consider starting in an elderly patient?
Warfarin in the presence of chronic AF
Aspirin in AF, where warfarin is contraindicated
Aspirin or clopidogrel with a documented history of atherosclerosis is patients with sinus rhythm
ACEi in chronic heart failure
What CNS drugs would you consider initiating in elderly patients according to the START criteria?
L-DOPA in idiopathic Parkinson's disease with definite functional impairment and disability
Antidepressant in moderate to severe depressive symptoms lasting at least 3 months
What gastrointestinal drugs should be started in elderly patients as per the START criteria?
Proton pump inhibitor with severe gastro-oesophageal reflux disease or peptic stricture requiring dilatation.
Fibre supplement for chronic, symptomatic diverticular disease with constipation.
Respiratory medications that should be started as per the START criteria
Regular inhaled beta 2 agonist or anticholinergic agent for mild to moderate COPD.
Regular inhaled corticosteroid for moderate-severe asthma of COPD, where predicted FEV1 is <50%.
Home oxygen with documented chronic type 1 respiratory failure (pO2 <8kPa) or type 2 respiratory failure.
What musculoskeletal medication should be given to elderly patients as part of the START criteria?
DMARDs with active moderate-severe rheumatoid disease lasting >12 weeks.
Bisphosphonates in patients taking maintenance oral corticosteroid therapy.
Calcium and vitamin D supplementation in patients with osteoporosis (radiological evidence or previous fragility fracture).
What anti-emetic is a good alternative to metoclopramide in patients with Parkinson's disease?
Ondansetron, which is a 5-HT3 receptor antagonist, would be the preferred option.
What is the definition of dementia?
Dementia is a term for a syndrome characterised by acquired global impairment of higher mental functions WITHOUT impairment of consciousness.
The key mental functions that are impaired are:
- Cognition: memory impairment, speech and language problems, difficult carrying out complex actions (apraxia) such as dressing or somatosensory integration (e.g. differentiating between a toilet and wastebin)
- Neuropsychiatric features: character or behavioural changes
Diagnosis always requires a history of acquired progressive impairment.
What is delirium? What is the criteria for delirium?
Delirium is a term for a characteristic acquired syndrome of acute onset.
The ICD-10 criteria for delirium is:
- impaired consciousness or attention
- global cognitive impairment (incoherence, forgetfulness, disorientation)
- psychomotor changes
- disturbed sleep/wake cycle
It is often referred to as an acute confusional state. Its rapid onset, fluctuating course and transience help distinguish it from dementia. Although this is not always clear, so a Confusion Assessment Method (CAM) can be used to aid the diagnosis.
What are the risk factors for delirium?
What can precipitate delirium?
1) Medicines - esp. anticholinergics, BZDs, anti-parkinson agents
2) Infection - esp. RTIs and UTIs
3) Metabolic problems - e.g. hypothermia, dehydration and AKI
4) Substance misuse - especially acute alcohol withdrawel
5) Direct brain insult - e.g. post seizure
What are the core features of depression?
Reduced enjoyment (anhedonia)
Somatic (biological) symptoms may also be present:
- diurnal variation in mood
- reduced/ increased appetite
- waking early/ hypersomnia
How common is depression in the elderly population?
Depression is the most common mood disorder in the elderly. Significant depression (sometimes with strong suicidal ideation, and delusions of guilt or hopelessness) is found in:
- 10-15% of community patients
- 20% of older hospital patients
- 30-40% of care home residents
What is the recommended treatment for depression?
The recommended treatment is watchful waiting in mild and short lived cases, and anti-depressants or CBT in moderate and long lived cases. This is usually effective, but recurrence is common. The long term suicide risk or attempted suicide risk for depression is 10% and this appears the same for young and old.
What is mania or hypomania?
Mania or hypomania are conditions characterised by elevated mood, increased energy and self important ideas. Episodes characteristically occur in bipolar effective disorder, when depression or just low mood may be seen at other times. Lifetime prevalence of bipolar is 1%, however new cases during old age are rare.
What are the pathological features of Alzheimer's disease (AD)?
AD is the most common cause of dementia, accounting for at least half of cases. Neurotoxicity is caused by extracellular beta amyloid plaques and intracellular neurofibrillary tangles caused by tau protein. Neuroimaging reveals to space occupying lesions and may show generalised cortical atrophy and (highly suggestive) thinning of the temporal lobe and hippocampi.
What are the important clinical features of Alzheimer's disease?
Neuropsychological assessments will typically show diffuse deficits in short term memory, impairment of language, and as the condition progresses, impairment of judgement, visuospatial ability and in sustaining attention.
Onset of the condition is typically insidious and delays to diagnosis are therefore common.
Prognosis is between 5-10 years from diagnosis.
On average, a family history doubles the risk of someone developing AD over their lifetime.
Which patients are most at risk of AD?
There is no reliable biomarker for predicting which patients are likely to develop AD. At risk groups include those with mild cognitive impairment, which refers to patients with a cognitive deficit (usually amnesic type) significantly greater than the expected given age and education but no clear evidence of dementia and preserved function. Patients with MCI have a 10-15% risk of developing AD (although many remain stable and revert to normal cognitive ageing).
Because AD is so common, even atypical presentations such as those below the age of 65 are likely to be due to AD. NEVER exclude it from your differential.
How common is vascular dementia?
Pure vascular dementia accounts for approximately 17% of dementias. Mixed dementia (mixture of AD and vascular dementia accounts for a further 10%). Vascular dementia is caused by cerebrovascular disease. At post mortem, multiple infarctions and/or extensive small vessel disease will be found.
How can vascular dementia be distinguished from AD?
In practice distinguishing VD from AD is not easy. The classic description of VD is of abrupt onset with acute stroke, or so called, "step wise" progression, with plataeus of stable function followed by sudden deterioration.
The features that most reliably distinguish VD from AD are:
- abrupt onset
- history of stroke
- CT/MRI evidence of infarction and/or extensive periventricular white matter lesions
Be aware that a degree of small vessel disease is common on neuroimaging in older people. There is a poor correlation between radiological changes and severity of clinical symptoms.
How common is dementia with Lewy bodies?
DLB is now established as the third most common cause of dementia, accounting for 4% of cases. Unlike vascular dementia, DLB can be more easily distinguished from AD.
What are the key features of DLB?
- Dementia, in which attention and visuo-spatial deficits may well be prominent
- two of these make DLB more likely, one possible
What drugs are DLB patients very sensitive to?
Symptoms of DLB become acutely worse with neuroleptic medication. Other features to be aware of:
- visual hallucinations are well formed and persistent
- parkinsonism is spontaneous (rather than drug induced)
- fluctuating cognition is striking and rapid
How can DLB be distinguished from Parkinson's disease dementia (PDD)?
Distinguishing DLB from Parkinson's Disease Dementia (PDD) can be difficult. Typically, if there is a year or more delay between onset of parkinsonism and onset of dementia, then PDD is diagnosed; under 1 year, DLB is diagnosed. The DaTscan is the dopamine transporter test currently available to assist diagnosis; it can only be requested by specialists.
Which medication has been shown to give clinical improvement in Parkinsons disease dementia?
Pre clinical evidence suggests that PDD is associated with a deficit in cholinergic transmission. Rivastigmine is a cholinesterase inhibitor for which clinical efficacy has been demonstrated in clinical trials for patients with mild to moderate dementia.
What is fronto-temporal dementia?
The term FTD actually refers to a group of conditions which cause predominantly frontal lobe and temporal lobe degeneration. About 2% of all cases of dementia are due to FTD, though the prevalence increases in working age where it is the second commonest cause of dementia after Alzheimer's. Some cases are due to motor neurone disease, but the most common type is Pick's disease. Pick's disease often starts in the 6th decade, is more likely among females, and has a strong family history. Time to death is typically 6-8 years.
What are the clinical features of fronto-temporal dementia?
Early loss of social awareness and insight.
Excessive exploration of objects or the environment (spatial abilities are preserved).
Insidious onset, slow progression.
Emotional change including impulsivity, elation, anxiety, or emotional unconcern.
Rigid, inflexible cognitive style.
Speech deficits, for example poor verbal output, echolalia, concrete responses and perseveration.
How should you investigate FTD?
When you investigate someone with suspected FTD, a history of early onset (45-65 years) and a family history are suggestive. Structural imaging (CT or MRI) will typically show frontal and/or anterior temporal lobe tissue loss, and the EEG is normal. Neuropsychological testing will usually show impairment on frontal lobe tests, even if language and attention is preserved. Current trials suggest anti-dementia medicines are not effective.
What questions in the history are important in suspected cases of dementia?
Get a collateral history.
When you take a history, focus on whether the patient shows acquired and progressive impairment of:
1) ADLs - washing, cooking, managing finances, dressing
2) Cognition - memory impairment, speech difficulty, problems carrying out complex actions and understanding sensory information
3) Neuropsychiatric features - changes in character or behaviour
Think about the following:
Does the person repeat themselves over and over?
Does the person get mixed up over days and dates?
Does the person forget to take their tablets?
Does the person struggle with bills and money?
Can the person wash, dress, cook?
Does the person experience problems finding the right words?
What is the IQCODE?
The IQCODE is administered to an informant outlining changes in everyday cognitive function independent of pre-morbid ability, including functional tasks like recall of dates, conversations, whereabouts of objects, handling finances, and using gadgets. It takes 10 minutes, and increases accuracy of diagnoses versus cognitive assessment alone.
If you suspect a patient has dementia what screening tools are available?
What is the AMTS?
This is a screening tool to test for dementia. The AMTS is a 10-item scale that you can use in the hospital setting and primary care. It will take you 3-4 minutes to conduct, and will assess orientation, registration, recall and concentration. Scores of 6 or below screen effectively for dementia.
What is the clock drawing test?
Numerous versions of this test exist. It requires that you ask a patient to draw a clock face with numbers and hands (indicating a dictated time). This assessment is quick to conduct, requires no training and is easy to score. It also shows fairly good sensitivity and specificity as a screening test. It will assess only one part of cognitive dysfunction seen in dementia, and conditions such as stroke will directly affect it.
What is the MMSE?
You can easily administer this examination in around 10 minutes, with minimal training. The MMSE will assess cognitive function in the areas of orientation, memory, attention and calculation, language and visual construction. Scores of 23/24 (from 30) indicates significant cognitive impairment. The MMSE is a screening tool, not a diagnostic test.
What is a MoCA?
Montreal Cognitive Assessment. It requires minimal training to carry out, and would take you around 10 minutes to conduct. It assesses attention and concentration, executive function, memory, language, conceptual thinking, calculation and orientation. Scores of 25/30 or lower are considered to suggest significant cognitive impairment. It performs as well as the MMSE, and as it assesses executive function, it is particularly useful for patients with vascular impairment.
What detailed cognitive assessments can be undertaken for suspected dementia?
Addenbrookes cognitive assessment revised (ACE-R)
Cambridge assessment of memory and cognition (CAMCOG)
These are longer to undertake but give more detailed diagnostic specificity.
When should imaging be used in the diagnosis of dementia?
Every patient with suspected dementia should have structural imaging, either a CT or MRI scan of the brain. The purpose is to rule out structural brain lesions such as tumours, infarction, haematomas, or normal pressure hydrocephalus.
Increasingly, they are used to improve precision of diagnoses of Alzheimer's dementia. In particular, confirmed thinning of medial temporal lobes and hippocampi increase accuracy of Alzheimer's dementia diagnosis. There is little to choose between CT and MRI; MRI is more expensive, but detects smaller lesions (especially small vessel disease). A CT brain scan is still more readily available, but involves ionizing radiation.
What functional imaging can be undertaken for suspected cases of dementia?
SPECT scanning can help distinguish between Alzheimer's, vascular and fronto-temporal dementias. It is recommended when fronto-temporal dementia is a differential diagnosis.
DaTscanTM (Ioflupane I 123 injection) imaging can help distinguish Parkinsonian syndromes from Alzheimer's.
PET imaging is rarely available outside research centres. EEG is usually unhelpful, being often normal in earlier stages of Alzheimer's.
What investigations are recommended by NICE in suspected cases of dementia?
Always perform the following:
Liver Function Tests
Thyroid Function Tests
Vitamin B-12 / folate concentrations
These should be directed by history and examination:
Human Immunodeficiency Virus (HIV) and syphillis
What 4 medications are available for dementia in the UK?
These are the "anti-dementia" medications and include the cholinesterase inhibitors:
And the partial NMDA antagonist:
Mild to moderate AD = cholinesterase inhibitors
Moderate to severe AD/ contraindications to cholinesterase inhibitors = Memantine
Mild to moderate PDD = Rivastigmine
What agents are used to treat vascular dementia, FTD and DLB?
At the moment there is inadequate evidence to support the use of any of the anti-dementia medications for the treatment of VD. Evidence is not strong enough to support a licence for use in vascular dementia. However many patients in clinical practice have both Alzheimer’s disease and cerebrovascular pathology, so clinicians will commonly treat patients with mixed Alzheimer’s and vascular pathology.
There is evidence to offer patients with Lewy body dementia a trial of a cholinesterase inhibitor. NICE guidance does not preclude this.
There is no evidence to support the prescription of cholinesterase inhibitors in fronto-temporal dementia. Of all the options fronto-temporal dementia is least likely to co-exist with Alzheimer's disease. In clinical practice cholinesterase inhibitors are almost never prescribed for patients with fronto-temporal dementia.
What commonly prescribed medicines can adversely effect cognition?
1) Antimuscarinic agents - these include medicines that have pharmacological action dependent on antimuscarinic effects (e.g. oxybutynin for bladder instability) or those that have antimuscarinic adverse effects (e.g. tricyclic antidepressants for depression or pain as well as many antipsychotics). These have all been shown to affect cognition, worsening cognitive performance in the short- and long-term.
2) Hypnotics and anxiolytics - sedatives such as benzodiazepines undoubtedly affect cognition in dementia, and may be associated with postural instability. Those with a longer half-life, or active metabolites, such as diazepam, are more likely to accumulate and have a greater adverse effect on cognition, compared to those with a shorter half-life, such as lorazepam which has no active metabolites.
What are the adverse effects of the cholinesterase inhibitors?
They include nausea, vomiting, diarrhoea, muscle cramps, insomnia, bradycardia, syncope and fatigue. Their occurrence can be reduced by initiating treatment at a low dose, taking the medicine with meals, and increasing the dose slowly.
Patients at increased risk for developing ulcers (e.g. those with a history of ulcer disease or those receiving concurrent non-steroidal anti-inflammatory drugs (NSAIDs)), should be monitored for symptoms. Owing to their cholinomimetic action, cholinesterase inhibitors should be prescribed with care to patients with a history of asthma or obstructive pulmonary disease.
Acetylcholinesterase inhibitors may have vagotonic effects on heart rate (e.g. bradycardia) because of their pharmacological action. The potential for this action may be particularly important in patients with 'sick sinus syndrome' or other supraventricular cardiac conduction conditions, such as sinoatrial or atrioventricular block. Memantine may be an option for these patients.
What is BPSD?
Behavioural and Psychological Symptoms of Dementia.
Up to 90% of patients with dementia will experience some behavioural and psychological symptoms. The aetiology of this is multifactorial. The most common symptoms are:
Agitation, resulting in aggression
What is the maximum dose of denopazil licensed for the treatment of AD?
What drugs should be avoided when treating BPSD?
Long acting anxyiolytics (e.g. diazepam) - have the potential to accumulate and increase risk of adverse effects such as confusion; incr. falls risk
Conventional antipsychotics (e.g. haloperidol) - extrapyramidal side effects, increase confusion and anticholinergic effects.
How should BPSD be managed?
Discuss symptoms and possible treatments with family and carers.
Consider non pharmacological interventions first, unless the individual is in great distress or at risk to themselves or others.
Unfortunately, at present no single non-pharmacological intervention has an evidence base that would justify its use as a direct alternative to pharmacological management, However, consider that:
- Antipsychotics are all associated with an increased risk of mortality and morbidity (particularly with neuroleptic sensitivity in dementia with Lewy bodies).
- Improvements in BPSD are often seen over a four to six week period without the need for any pharmacological intervention in patients with dementia.
When can antipsychotics be used for BPSD?
Some antipsychotics may be appropriate for BPSD in the following situations:
1) Symptoms are severe, causing significant distress or placing the patient or others at risk.
2) Non-pharmacological interventions have been tried, and have failed or are inappropriate.
3) They may also be helpful in combination with non-pharmacological intervention.
Conventional (typical) antipsychotics such as haloperidol have traditionally been used to treat BPSD. However, they are associated with sedation, extrapyramidal side-effects (EPSE) (i.e. movement disorders) and increased confusion, making them largely unsuitable, other than in the very short-term (i.e. in a delirious patient). They also have some anticholinergic properties that may further compromise cognition.
Atypical antipsychotics have less potential to cause sedation and EPSE. However, they are not without risk, and the potential for harm such as stroke must be carefully evaluated.
What is the only antipsychotic licensed for use in BPSD?
However be aware that:
The licensed dose for this indication is much lower than for other indications (initially 250 micrograms twice a day, up to a maximum of 1 mg twice a day).
It is licensed for no more than six weeks of treatment in patients experiencing 'persistent' aggression in Alzheimer's dementia.
Some evidence supports greater efficacy for risperidone in treatment of aggressive (but not non-aggressive) agitation.
What is the NICE guidance regarding antipsychotics for BPSD?
Do not use antipsychotics for mild-to-moderate BPSD in:
- Lewy body dementia, because of the risk of severe adverse reactions.
- Alzheimer's disease, vascular dementia or mixed dementias, because of the increased risk of cerebrovascular adverse events and death.
Antipsychotics can be used for severe BPSD provided the duration of treatment is short, there is a therapeutic target, the cerebrovascular risk has been discussed, the patient is reviewed regularly, and treatment is initiated at the lowest dose and up titrated.