Geris + palliative Flashcards
1
Q
Q: What is another name for acute confusional state?
A
A: Delirium or acute organic brain syndrome.
2
Q
Q: Name three predisposing factors for acute confusional state.
A
A: Age > 65 years, background of dementia, significant injury (e.g. hip fracture), frailty or multimorbidity, polypharmacy.
3
Q
Q: List three precipitating events for acute confusional state.
A
A: Infection (e.g. urinary tract infections), metabolic issues (e.g. hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration), change of environment, any significant cardiovascular, respiratory, neurological, or endocrine condition, severe pain, alcohol withdrawal, constipation.
4
Q
Q: What type of memory disturbance is more prominent in acute confusional state?
A
A: Loss of short-term memory is greater than long-term memory.
5
Q
Q: What are some features of acute confusional state?
A
A: Memory disturbances, agitation or withdrawal, disorientation, mood change, visual hallucinations, disturbed sleep cycle, poor attention.
6
Q
Q: What is the first-line sedative recommended by the 2006 Royal College of Physicians guidelines for managing acute confusional state?
A
A: Haloperidol 0.5 mg.
7
Q
Q: According to the 2010 NICE delirium guidelines, what medications can be used to manage acute confusional state?
A
A: Haloperidol or olanzapine.
8
Q
Q: Why can management of acute confusional state be challenging in patients with Parkinson’s disease?
A
A: Antipsychotics can often worsen Parkinsonian symptoms.
9
Q
Q: What medications are preferred for urgent treatment of symptoms in Parkinson’s patients with acute confusional state?
A
A: The atypical antipsychotics quetiapine and clozapine.
10
Q
Q: Besides treating the underlying cause, what is another management strategy for acute confusional state?
A
A: Modification of the environment.
11
Q
Q: What type of disease is Alzheimer’s and what percentage of dementia cases in the UK does it account for?
A
A: Alzheimer’s disease is a progressive degenerative disease of the brain, accounting for the majority of dementia cases in the UK.
12
Q
Q: What non-pharmacological management does NICE recommend for Alzheimer’s disease?
A
A: Offering ‘a range of activities to promote wellbeing that are tailored to the person’s preference’ and group cognitive stimulation therapy for patients with mild and moderate dementia.
13
Q
Q: Name two other non-pharmacological therapies that may be considered for Alzheimer’s disease according to NICE.
A
A: Group reminiscence therapy and cognitive rehabilitation.
14
Q
Q: Which three acetylcholinesterase inhibitors are recommended by NICE for managing mild to moderate Alzheimer’s disease?
A
A: Donepezil, galantamine, and rivastigmine.
15
Q
Q: What is memantine and in what situations is it recommended by NICE?
A
A: Memantine is an NMDA receptor antagonist recommended for patients with moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors, as an add-on drug for moderate or severe Alzheimer’s, or as monotherapy for severe Alzheimer’s.
16
Q
Q: What is NICE’s stance on the use of antidepressants for depression in patients with Alzheimer’s disease?
A
A: NICE does not recommend antidepressants for mild to moderate depression in patients with dementia.
17
Q
Q: Under what circumstances does NICE recommend the use of antipsychotics in Alzheimer’s patients?
A
A: Antipsychotics should only be used for patients at risk of harming themselves or others, or when agitation, hallucinations, or delusions are causing severe distress.
18
Q
Q: What is a relative contraindication for the use of donepezil?
A
A: Donepezil is relatively contraindicated in patients with bradycardia.
19
Q
Q: What is an adverse effect of donepezil?
A
A: Insomnia.
20
Q
Q: What type of disease is Alzheimer’s, and what percentage of dementia cases in the UK does it account for?
A
A: Alzheimer’s disease is a progressive degenerative disease of the brain, accounting for the majority of dementia cases in the UK.
21
Q
Q: List three risk factors for Alzheimer’s disease.
A
A: Increasing age, family history of Alzheimer’s disease, and Caucasian ethnicity.
22
Q
Q: What percentage of Alzheimer’s cases are inherited as an autosomal dominant trait, and what genes are involved?
A
A: 5% of cases are inherited as an autosomal dominant trait. The involved genes include amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14), and presenilin 2 (chromosome 1).
23
Q
Q: Which apoprotein allele is associated with Alzheimer’s disease, and what does it encode?
A
A: Apoprotein E allele E4 is associated with Alzheimer’s disease, and it encodes a cholesterol transport protein.
24
Q
Q: Why is Down’s syndrome a risk factor for Alzheimer’s disease?
A
A: Individuals with Down’s syndrome have an extra copy of chromosome 21, which contains the gene for amyloid precursor protein, leading to an increased risk of developing Alzheimer’s disease.
25
Q: Describe the macroscopic pathological changes seen in Alzheimer's disease.
A: Widespread cerebral atrophy, particularly involving the cortex and hippocampus.
26
Q: What are the microscopic pathological changes seen in Alzheimer's disease?
A: Cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein.
27
Q: What biochemical deficit is seen in Alzheimer's disease?
A: There is a deficit of acetylcholine due to damage to an ascending forebrain projection.
28
Q: What are neurofibrillary tangles, and what protein are they partly made from?
A: Neurofibrillary tangles are paired helical filaments partly made from a protein called tau.
29
Q: What is the function of tau protein in a healthy brain, and how is it impaired in Alzheimer's disease?
A: Tau protein interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules. In Alzheimer's disease, tau proteins are excessively phosphorylated, impairing its function.
30
Q: What is a key characteristic of the onset of delirium compared to dementia?
A: Delirium has an acute onset.
31
Q: How does the impairment of consciousness differ between delirium and dementia?
A: Impairment of consciousness is present in delirium but not typically in dementia.
32
Q: Describe the fluctuation of symptoms in delirium.
A: Symptoms of delirium fluctuate, often being worse at night with periods of normality.
33
Q: What type of abnormal perception is more indicative of delirium than dementia?
A: Illusions and hallucinations are more indicative of delirium.
34
Q: What emotional states are commonly associated with delirium?
A: Agitation and fear.
35
Q: Are delusions more common in delirium or dementia?
A: Delusions are more common in delirium.
36
Q: What are the most common causes of dementia in the UK?
A: Alzheimer's disease, followed by vascular and Lewy body dementia.
37
Q: Name two assessment tools recommended by NICE for diagnosing dementia in a non-specialist setting.
A: 10-point cognitive screener (10-CS) and the 6-Item cognitive impairment test (6CIT).
38
Q: Which assessment tools are not recommended by NICE for diagnosing dementia in a non-specialist setting?
A: Abbreviated mental test score (AMTS), General practitioner assessment of cognition (GPCOG), and mini-mental state examination (MMSE).
39
Q: What MMSE score suggests dementia?
A: A score of 24 or less out of 30.
40
Q: What tests does NICE recommend in primary care to exclude reversible causes of dementia?
A: FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12, and folate levels.
41
Q: To whom are patients commonly referred for dementia evaluation?
A: Old-age psychiatrists, sometimes working in 'memory clinics'.
42
Q: What is the purpose of neuroimaging in secondary care for dementia patients?
A: To exclude other reversible conditions (e.g., subdural haematoma, normal pressure hydrocephalus) and to provide information on aetiology to guide prognosis and management.
43
Q: According to the 2011 NICE guidelines, what is considered essential in the investigation of dementia?
A: Structural imaging.
44
Q: What are the most common causes of dementia?
A: Alzheimer's disease, cerebrovascular disease (multi-infarct dementia, 10-20%), and Lewy body dementia (10-20%).
45
Q: Name three rarer causes of dementia that account for approximately 5% of cases.
A: Huntington's disease, Creutzfeldt-Jakob disease (CJD), and Pick's disease (atrophy of frontal and temporal lobes).
46
Q: What percentage of AIDS patients are affected by dementia due to HIV?
A: 50% of AIDS patients.
47
Q: List three important differentials of dementia that are potentially treatable.
A: Hypothyroidism, Addison's disease, and B12/folate/thiamine deficiency.
48
Q: Name three more potentially treatable causes of dementia.
A: Syphilis, brain tumour, and normal pressure hydrocephalus.
49
Q: What condition caused by head injury is an important differential for dementia?
A: Subdural haematoma.
50
Q: Which mental health condition is an important differential for dementia?
A: Depression.
51
Q: Name two types of chronic drug use that can be important differentials for dementia.
A: Alcohol and barbiturates.
52
Q: What systems are involved in normal gait?
A: The neurological system (basal ganglia and cortical basal ganglia loop), the musculoskeletal system, and effective processing of senses such as sight, sound, and sensation (fine touch and proprioception).
53
Q: Name three medical conditions that can lead to gait abnormalities and increase the risk of falls in the elderly.
A: Diabetes, rheumatoid arthritis, and Parkinson's disease.
54
Q: List five risk factors for falling in the elderly.
A: Lower limb muscle weakness, vision problems, polypharmacy (4+ medications), incontinence, and depression.
55
Q: What is the significance of having four or more risk factors for falling?
A: Individuals with four or more risk factors have up to a 78% chance of falling.
56
Q: What should be established from the history when assessing a patient who has fallen?
A: Where and when the patient fell, any witnesses, associated features before/during/after the fall, why the patient thinks they fell, past falls, systems review, past medical history, and social history.
57
Q: Why is it important to review a patient's medication when assessing falls risk?
A: Patients on more than four drugs are more likely to fall, so suspect or unnecessary medications should be stopped or swapped.
58
Q: Name two types of medications that can cause postural hypotension and are associated with falls.
A: Nitrates and diuretics.
59
Q: What bedside tests are important when investigating falls?
A: Basic observations, blood pressure, blood glucose, urine dip, and ECG.
60
Q: What blood tests should be considered when investigating falls?
A: Full Blood Count, Urea and Electrolytes, Liver function tests, and bone profile.
61
Q: What imaging might be required when investigating falls in the elderly?
A: X-ray of chest/injured limbs, CT head, and cardiac echo.
62
Q: What functional tests are recommended for patients with a history of falls?
A: The 'Turn 180° test' or the 'Timed up and Go test'.
63
Q: Who should be offered a multidisciplinary assessment after a fall?
A: Patients over 65 with more than two falls in the last 12 months, a fall that requires medical treatment, or poor performance/failure to complete the 'Turn 180° test' or the 'Timed up and Go test'.
64
Q: What should be done for individuals who fall but do not meet the criteria for a multidisciplinary assessment?
A: They should be reviewed annually and given written information on falls.
65
Q: What are the three recognised types of frontotemporal lobar degeneration (FTLD)?
A: Frontotemporal dementia (Pick's disease), Progressive non-fluent aphasia (chronic progressive aphasia, CPA), and Semantic dementia.
66
Q: What are common features of frontotemporal lobar dementias?
A: Onset before 65, insidious onset, relatively preserved memory and visuospatial skills, personality change, and social conduct problems.
67
Q: What is the most common type of frontotemporal lobar degeneration?
A: Pick's disease.
68
Q: What are some common features of Pick's disease?
A: Personality change, impaired social conduct, hyperorality, disinhibition, increased appetite, and perseveration behaviors.
69
Q: What is the characteristic macroscopic change seen in Pick's disease?
A: Focal gyral atrophy with a knife-blade appearance and atrophy of the frontal and temporal lobes.
70
Q: Name three microscopic changes seen in Pick's disease.
A: Pick bodies (spherical aggregations of tau protein, silver-staining), gliosis, neurofibrillary tangles, and senile plaques.
71
Q: What does NICE recommend regarding the use of AChE inhibitors or memantine in people with frontotemporal dementia?
A: NICE do not recommend that AChE inhibitors or memantine are used in people with frontotemporal dementia.
72
Q: What is the chief feature of progressive non-fluent aphasia (CPA)?
A: Non-fluent speech with short, agrammatic utterances and relatively preserved comprehension.
73
Q: What is the main characteristic of semantic dementia?
A: Fluent progressive aphasia where speech is fluent but empty and conveys little meaning.
74
Q: How does memory in semantic dementia differ from that in Alzheimer's disease?
A: In semantic dementia, memory is better for recent rather than remote events, unlike in Alzheimer's disease.
75
Q: What is the characteristic pathological feature of Lewy body dementia?
A: Alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic, and neocortical areas.
76
Q: What percentage of dementia cases is accounted for by Lewy body dementia?
A: Up to 20% of dementia cases.
77
Q: How does Lewy body dementia typically present in relation to Parkinsonism?
A: Cognitive impairment usually occurs before parkinsonism, and both features typically occur within a year of each other.
78
Q: What are the early impairments seen in Lewy body dementia in contrast to Alzheimer's disease?
A: Early impairments in attention and executive function rather than just memory loss.
79
Q: What type of hallucinations are commonly seen in Lewy body dementia?
A: Visual hallucinations, although delusions and non-visual hallucinations may also be present.
80
Q: What diagnostic tool is increasingly used for Lewy body dementia?
A: Single-photon emission computed tomography (SPECT), commercially known as a DaTscan.
81
Q: What is the sensitivity and specificity of SPECT in diagnosing Lewy body dementia?
A: The sensitivity is around 90%, and the specificity is 100%.
82
Q: What treatments are used for Lewy body dementia?
A: Acetylcholinesterase inhibitors (e.g., donepezil, rivastigmine) and memantine, as they are in Alzheimer's.
83
Q: Why should neuroleptics be avoided in Lewy body dementia?
A: Patients are extremely sensitive to neuroleptics and may develop irreversible parkinsonism.
84
Q: What clinical history might suggest Lewy body dementia in relation to antipsychotic use?
A: A history of a patient who has deteriorated following the introduction of an antipsychotic agent.
85
Q: What is multimorbidity?
A: The presence of two or more long-term health conditions, including physical or mental health conditions, learning disabilities, symptom complexes like chronic pain, sensory impairments, and substance misuse.
86
Q: What is the estimated prevalence of multimorbidity in older adults?
A: Multimorbidity is common in older adults, with an estimated prevalence of 27.2% in a cohort of 403,985 adults.
87
Q: Which gender has a higher prevalence of multimorbidity?
A: Females have a higher prevalence of multimorbidity than males.
88
Q: What is the most common physical comorbid condition in multimorbidity?
A: Hypertension is the most prevalent physical comorbid condition, often associated with pain, diabetes, and hearing loss.
89
Q: What are the most common mental health comorbidities seen with multimorbidity?
A: Depression and anxiety are the most common mental health conditions that coexist with physical disorders like pain, hypertension, and irritable bowel syndrome.
90
Q: What are some risk factors for developing multimorbidity?
A: Increasing age, female sex, low socioeconomic status, tobacco and alcohol usage, lack of physical activity, poor nutrition, and obesity.
91
Q: What are some complications of multimorbidity?
A: Decreased quality of life and life expectancy, increased treatment burden, mental health issues, polypharmacy, and negative impact on carer welfare.
92
Q: What should be assessed when evaluating a patient with multimorbidity?
A: Disease burden, treatment burden, mental health issues, social circumstances, health literacy, pain management, frailty, and functional status.
93
Q: What screening tools can be used to assess frailty in multimorbidity?
A: The PRISMA-7 questionnaire and gait speed evaluation are used to assess frailty.
94
Q: What is the goal in managing multimorbidity?
A: The goal is to reduce treatment burden and optimise care by maximising existing treatments, reducing high-risk medications, and promoting self-management.
95
Q: What is the STOPP/START screening tool?
A: STOPP identifies medications with risks outweighing benefits, while START suggests beneficial medications, such as proton pump inhibitors for gastroprotection in patients on medications that increase bleeding risk.
96
Q: What should be considered in the management of patients with multimorbidity?
A: Consider medication reviews, alternative follow-up arrangements, stopping unnecessary medications (e.g., NSAIDs, warfarin), and develop an individualised management plan with patient education and family support.
97
Q: How often should medications be reviewed for people over 65?
A: NHS England recommends a yearly review of medications for people aged over 65, but periodic reviews should be done to ensure treatment optimisation.
98
Q: What are pressure ulcers?
A: Pressure ulcers are localized injuries to the skin and/or underlying tissue, typically over bony prominences, caused by prolonged pressure, often due to immobility, paralysis, or advancing age.
99
Q: What are the main risk factors for developing pressure ulcers?
A: Malnutrition, incontinence (urinary and faecal), lack of mobility, and pain (which reduces mobility) are the main risk factors.
100
Q: What is the Waterlow score?
A: The Waterlow score is a widely used tool to assess the risk of pressure ulcers. It includes factors such as body mass index, nutritional status, skin type, mobility, and continence.
101
Q: What are the stages of pressure ulcers according to the European Pressure Ulcer Advisory Panel classification system?
Grade 1: Non-blanchable erythema of intact skin.
Grade 2: Partial thickness skin loss involving the epidermis or dermis.
Grade 3: Full thickness skin loss involving subcutaneous tissue, possibly extending to the fascia.
Grade 4: Extensive tissue destruction or necrosis, involving muscle, bone, or supporting structures.
102
Q: What is the typical appearance of a Grade 1 pressure ulcer?
A: Non-blanchable erythema of intact skin, with possible indicators such as discolouration, warmth, oedema, induration, or hardness, particularly in individuals with darker skin.
103
Q: How is a Grade 2 pressure ulcer characterized?
A: It is a superficial ulcer with partial thickness skin loss involving the epidermis or dermis, often appearing as an abrasion or blister.
104
Q: How is a Grade 3 pressure ulcer characterized?
A: Full thickness skin loss with damage to or necrosis of subcutaneous tissue, which may extend down to, but not through, the underlying fascia.
105
Q: How is a Grade 4 pressure ulcer characterized?
A: Extensive destruction or tissue necrosis, possibly involving muscle, bone, or supporting structures with or without full thickness skin loss.
106
Q: What is the management approach for pressure ulcers?
Maintain a moist wound environment (e.g., hydrocolloid dressings, hydrogels).
Avoid using soap on the wound.
Routine wound swabs are not recommended unless clinically necessary.
Antibiotics should be prescribed based on clinical evidence of infection.
Consider referral to a tissue viability nurse and surgical debridement for selected cases.
107
Q: Why should wound swabs not be done routinely in pressure ulcer management?
A: Most pressure ulcers are colonized with bacteria, and routine swabs are unlikely to provide useful information unless there is evidence of surrounding infection or cellulitis.
108
Q: What is vascular dementia?
A: Vascular dementia (VD) is the second most common form of dementia, caused by cognitive impairment due to ischaemia or haemorrhage resulting from cerebrovascular disease. It includes conditions like multi-infarct dementia, subcortical dementia, and mixed dementia (with Alzheimer's).
109
Q: What percentage of dementia cases in the UK are vascular dementia?
A: Vascular dementia accounts for about 17% of dementia cases in the UK.
110
Q: What are the main subtypes of vascular dementia?
Stroke-related VD (multi-infarct or single-infarct dementia)
Subcortical VD (due to small vessel disease)
Mixed dementia (VD combined with Alzheimer's disease)
111
Q: What are the common risk factors for vascular dementia?
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
Rarely, inherited conditions like CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)
112
Q: How do patients with vascular dementia typically present?
Stepwise or sudden deterioration in cognitive function over months or years
Symptoms include focal neurological deficits (visual, sensory, motor), attention and concentration difficulties, memory issues, gait and speech disturbances, and emotional disturbances.
113
Q: What is the diagnostic approach for vascular dementia?
Comprehensive history and physical examination
Cognitive impairment screening
Medical review to exclude medication causes of cognitive decline
MRI scan to identify infarcts and white matter changes
NINDS-AIREN criteria for probable vascular dementia, which includes cognitive decline, cerebrovascular disease, and evidence of a relationship between the two (e.g., dementia onset within three months of a stroke, stepwise progression of symptoms)
114
Q: What is the role of imaging in diagnosing vascular dementia?
A: MRI scans are used to detect infarcts and white matter changes characteristic of cerebrovascular disease, which helps in diagnosing vascular dementia.
115
Q: What are the general management strategies for vascular dementia?
Symptomatic treatment tailored to the individual's needs
Address cardiovascular risk factors (hypertension, diabetes, etc.) to slow progression
Provide support for patients and carers
116
Q: What non-pharmacological treatments are recommended for vascular dementia?
Cognitive stimulation programmes
Multisensory stimulation
Music and art therapy
Animal-assisted therapy
Managing challenging behaviours with clear communication and environmental adjustments
117
Q: What is the pharmacological management for vascular dementia?
There is no specific pharmacological treatment for cognitive symptoms of vascular dementia.
AChE inhibitors or memantine may be used if there is comorbid Alzheimer's disease, Parkinson's disease dementia, or dementia with Lewy bodies.
Aspirin and statins have not been proven effective for treating vascular dementia.
118
Q: What underlying causes of confusion should be considered in palliative care?
A: Underlying causes of confusion in palliative care may include hypercalcaemia, infection, urinary retention, and medication. These should be identified and treated appropriately.
119
Q: What is the first-choice medication for agitation and confusion in palliative care?
A: The first-choice medication for agitation and confusion in palliative care is haloperidol.
120
Q: What are other options for managing agitation and confusion in palliative care if haloperidol is ineffective?
A: If haloperidol is ineffective, other options include:
Chlorpromazine
Levomepromazine
121
Q: What medication is best for treating agitation or restlessness in the terminal phase of illness?
A: In the terminal phase of illness, midazolam is considered the best treatment for agitation or restlessness.
122
Q: What is the first-line medication for intractable hiccups in palliative care?
A: Chlorpromazine is licensed for the treatment of intractable hiccups in palliative care.
123
Q: What other medications are used for managing hiccups in palliative care if chlorpromazine is ineffective?
Haloperidol
Gabapentin
124
Q: What medication is used for hiccups in palliative care when hepatic lesions are present?
A: Dexamethasone is used for hiccups in palliative care, particularly if there are hepatic lesions.
125
Q: What is the most common cause of nausea and vomiting in palliative care?
A: The most common causes are reduced gastric motility and chemical disturbances (e.g. due to opioids or chemotherapy).
126
Q: What are the six broad syndromes of nausea and vomiting in palliative care?
The six syndromes are:
Reduced gastric motility
Chemically mediated
Visceral/serosal
Raised intra-cranial pressure
Vestibular
Cortical (anxiety, pain, or anticipatory nausea)
127
Q: What is the first-line medication for nausea and vomiting caused by reduced gastric motility?
A: Metoclopramide and domperidone are first-line treatments for reduced gastric motility.
128
Q: Which medications are used for chemically mediated nausea and vomiting, such as those caused by opioids?
A: Key treatments include ondansetron, haloperidol, and levomepromazine.
129
Q: What are the first-line treatments for visceral/serosal causes of nausea and vomiting (e.g. constipation or oral candidiasis)?
A: Cyclizine and levomepromazine are first-line treatments. Hyoscine (anti-cholinergic) may also be useful.
130
Q: What is the recommended first-line treatment for nausea and vomiting due to raised intra-cranial pressure?
A: Cyclizine is first-line, and dexamethasone can also be used. Radiotherapy may be considered for cranial tumours.
131
Q: What is the first-line treatment for vestibular nausea and vomiting?
A: Cyclizine is the first-line treatment for vestibular causes of nausea and vomiting.
132
Q: How should anticipatory nausea be treated in palliative care?
A: Lorazepam, a short-acting benzodiazepine, can be used for anticipatory nausea.
133
Q: When should parenteral administration of anti-emetics be considered?
A: Parenteral anti-emetics are preferred if the patient is vomiting, has malabsorption, or suffers from severe gastric stasis and cannot take oral medications.
134
Q: Which medications are used to treat cortical nausea and vomiting, particularly due to anxiety or anticipatory nausea?
A: Cyclizine, ondansetron, and metoclopramide can be trialed. Short-acting benzodiazepines like lorazepam are particularly useful for anticipatory nausea.
135
Q: What is the first-line opioid treatment for patients with advanced and progressive disease according to NICE guidelines?
A: Oral modified-release (MR) morphine is recommended as first-line treatment, with oral immediate-release morphine for breakthrough pain.
136
Q: What is the starting dose of oral modified-release morphine for patients with no comorbidities?
A: Start with 20-30mg of MR morphine daily and use 5mg oral morphine for breakthrough pain (e.g. 15mg MR morphine twice a day and 5mg oral morphine solution as needed).
137
Q: What should be prescribed for all patients initiating strong opioids?
A: Laxatives should be prescribed for all patients starting strong opioids to prevent constipation.
138
Q: What is the breakthrough dose of morphine according to SIGN guidelines?
A: The breakthrough dose of morphine is one-sixth of the daily dose of morphine.
139
Q: What is the recommended approach for increasing the opioid dose?
A: The next dose should be increased by 30-50% when increasing the opioid dose.
140
Q: What are the preferred opioids in patients with chronic kidney disease?
A: Oxycodone is preferred in palliative patients with mild-moderate renal impairment, while alfentanil, buprenorphine, and fentanyl are preferred in severe renal impairment.
141
Q: What treatments can be used for metastatic bone pain in addition to strong opioids?
A: In addition to strong opioids, bisphosphonates, radiotherapy, and denosumab may be used to treat metastatic bone pain.
142
Q: What side effect of opioids is usually transient, and which is persistent?
A: Nausea and drowsiness are usually transient, while constipation is usually persistent.
143
Q: What is the conversion factor for oral morphine to oral oxycodone?
A: Oral oxycodone is typically 1.5-2 times stronger than oral morphine.
144
Q: What is the conversion factor for oral morphine to subcutaneous morphine?
A: For subcutaneous morphine, divide oral morphine dose by 2.
145
Q: What is the equivalent oral morphine dose for a 12 microgram fentanyl patch?
A: A 12 microgram fentanyl patch is approximately equivalent to 30mg oral morphine daily.
146
Q: What should be considered when prescribing opioids in patients with cancer pain?
A: In addition to opioids, bisphosphonates and radiotherapy may be used for bone pain, and patients should be referred to an oncologist for further treatment options like radiotherapy.
147
Q: What opioid causes less sedation and vomiting than morphine but more constipation?
A: Oxycodone generally causes less sedation, vomiting, and pruritis than morphine but can cause more constipation.
148
Q: Why are secretions more troubling for family members than for the patient in the last days of life?
A: Secretions are common in the last days of life, but patients are often not troubled by them, while family members may find them distressing.
149
Q: What conservative measures should be taken for managing secretions in palliative care?
Avoid fluid overload by stopping IV or subcutaneous fluids.
Educate the family that the patient is likely not troubled by the secretions.
150
Q: What is the first-line medical treatment for managing secretions in palliative care?
A: Hyoscine hydrobromide or hyoscine butylbromide is used first-line for managing secretions.
151
Q: Which is considered less sedative, hyoscine hydrobromide or hyoscine butylbromide?
A: Hyoscine butylbromide may be less sedative than hyoscine hydrobromide.
152
Q: What other medication can be used for managing secretions in palliative care if necessary?
A: Glycopyrronium bromide can also be used to manage secretions in palliative care.
153
Q: When should a syringe driver be considered in palliative care?
A: A syringe driver should be considered when a patient is unable to take oral medication due to nausea, dysphagia, intestinal obstruction, weakness, or coma.
154
Q: What are the two main types of syringe drivers used in the UK?
Graseby MS16A (blue): Delivery rate is given in mm per hour.
Graseby MS26 (green): Delivery rate is given in mm per 24 hours.
155
Q: What is the preferred solution for most drugs in syringe drivers?
A: Most drugs are compatible with water for injection. However, some drugs require sodium chloride 0.9%, including granisetron, ketamine, ketorolac, octreotide, and ondansetron.
156
Q: Which drugs are commonly used in syringe drivers for nausea and vomiting?
Cyclizine
Levomepromazine
Haloperidol
Metoclopramide
157
Q: What drugs are commonly used in syringe drivers for respiratory secretions or bowel colic?
Hyoscine hydrobromide
Hyoscine butylbromide
Glycopyrronium bromide
158
Q: Which drugs are commonly used in syringe drivers for agitation/restlessness?
Midazolam
Haloperidol
Levomepromazine
159
Q: What is the preferred opioid for pain management via syringe driver?
A: Diamorphine is the preferred opioid for pain management in syringe drivers.
160
Q: What are some mixing and compatibility issues with drugs in syringe drivers?
Diamorphine is compatible with most other drugs used, including dexamethasone, haloperidol, hyoscine butylbromide, and midazolam.
Cyclizine may precipitate with diamorphine at higher doses.
Cyclizine is incompatible with several drugs including clonidine, dexamethasone, ketamine, and metoclopramide.
