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FINALS > Care of the elderly/palliative > Flashcards

Care of the elderly/palliative Flashcards

1
Q

COTE ASSESSMENT
What is frailty?
Is it inevitable?

A
  • State of increased vulnerability resulting from ageing-associated decline in reserve + function across multiple physiological systems resulting in compromised ability to cope with everyday or acute stressors
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2
Q

COTE ASSESSMENT

What are the geriatric giants?

A

4 I’s –

  • Instability (falls)
  • Immobility
  • Intellectual impairment (confusion)
  • Incontinence
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3
Q

COTE ASSESSMENT

What are the geriatric 5Ms?

A
  • Mind = dementia, delirium, depression
  • Mobility = impaired gait + balance, falls
  • Medications = polypharmacy, medication burden, adverse effects
  • Multi-complexity = multi-morbidity, biopsychosocial
  • Matters most = individual health outcomes + preferences
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4
Q

COTE ASSESSMENT

What is acopia?

A
  • Social admission = unable to cope with ADLs
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5
Q

COTE ASSESSMENT
What is a comprehensive geriatric assessment?
What is the process?

A
  • Development of a coordinated, integrated plan for treatment + long-term support
  • Assessment > problem list > personalised care plan > intervention > regular planned review > assessment etc.
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6
Q

COTE ASSESSMENT

What is rehabilitation?

A
  • Process of restoring a patient to maximum function
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7
Q

COTE ASSESSMENT
What is pharmacodynamics?
How does this change for the elderly?

A
  • What the DRUG does to the BODY

- Elderly prone to ADRs such as postural hypotension, confusion, bowel issues

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8
Q

COTE ASSESSMENT
What is pharmacokinetics?
How does this change for the elderly?
Example?

A
  • What the BODY does to the DRUG
  • Changes in absorption, distribution, metabolism + excretion of drugs
  • Decreased excretion = prone to toxicity from lower doses
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9
Q

COTE ASSESSMENT

What are some potential problems with polypharmacy?

A
  • Drug interactions, increased SEs + pill burden

- Can affect compliance + lead to decreased pt satisfaction

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10
Q

MEDICO-LEGAL ASPECTS

What is the purpose of the Mental Capacity Act, 2005?

A
  • Empower + protect people >16y who lack capacity to make their own decisions about their care + treatment since 1/10/07
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11
Q

MEDICO-LEGAL ASPECTS

What is the two-step test in MCA?

A
  • Does the person have an impairment of their mind or brain? E.g. dementia, severe LD, brain injury, coma
  • Is this impairment significant enough to deem them unable of making a particular decision?
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12
Q

MEDICO-LEGAL ASPECTS

What are the 4 aspects of assessing capacity?

A
  • Does the pt UNDERSTAND the information?
  • Can the pt RETAIN that information?
  • Can the pt use the information to WEIGH UP the pros + cons?
  • Can the pt COMMUNICATE their decision back (ensure different methods explored)
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13
Q

MEDICO-LEGAL ASPECTS

What are the 5 principles underpinning the MCA?

A
  • Assume capacity until proven otherwise
  • Maximise decision-making capacity (all practical support to help them make decision given)
  • Apparent unwise decision ≠ incapacity
  • All decisions on behalf of patient in best interests
  • Least restrictive option should be chosen
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14
Q

MEDICO-LEGAL ASPECTS

What are some important considerations about a person’s capacity status?

A
  • Can fluctuate with time (temporary cognitive impairment like delirium)
  • Decision specific so may have capacity for some decisions, do not just completely write off
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15
Q

MEDICO-LEGAL ASPECTS

What is the role of an independent mental capacity advocate (IMCA)?

A
  • Support + represent people who lack capacity and do not have anyone else to represent them in a major decision
  • Cannot make a decision on pt’s behalf but contributes
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16
Q

MEDICO-LEGAL ASPECTS

What are some important considerations when making best interest decisions?

A
  • Encourage participation
  • Find out the person’s views (past + present wishes, beliefs, values)
  • Avoid discrimination
  • Could they regain capacity? Can it wait?
  • Identify all relevant circumstances
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17
Q

MEDICO-LEGAL ASPECTS

Who would you consult when making best interest decisions?

A
  • Carers, relatives, close friends, appointed attorneys
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18
Q

MEDICO-LEGAL ASPECTS

What is a deprivation of liberty safeguard, DoLS (new name Liberty Protection Safeguards)?

A
  • Necessary to deprive a patient or resident of their liberty as they lack capacity to consent to treatment or care to keep them safe from harm
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19
Q

MEDICO-LEGAL ASPECTS

What are some conditions of DOLS?

A
  • Must be in care home or hospital
  • Act in best interests
  • Suffering from a mental disorder
  • Restrictions would deprive their liberty
  • Least restrictive
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20
Q

MEDICO-LEGAL ASPECTS
How should a DoLS be attained?
What are the limitations of an urgent DoLS?

A
  • Officially verified by local DoLS team apart from an urgent DoLS which can be executed without prior formal authorisation
  • Up to 7d
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21
Q

MEDICO-LEGAL ASPECTS

What is an advanced directive?

A
  • Written statement made by patient WITH capacity regarding their future wishes for treatment which comes into effect when they subsequently lack capacity
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22
Q

MEDICO-LEGAL ASPECTS

What are the 2 aspects of advanced directives?

A
  • Advanced refusal of treatments = legally binding

- Advanced request for treatment = less legal binding as cannot request treatment

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23
Q

MEDICO-LEGAL ASPECTS
What is a Lasting Power of Attorney?
What are the two types?
What makes it valid?

A
  • Legal contract drawn up by a patient WITH capacity who nominates another person to make decision on their behalf when they lose capacity
  • Financial and property or health and welfare
  • Must be registered with Office of the Public Guardian
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24
Q

MEDICO-LEGAL ASPECTS

What is an alternative to an LPA?

A
  • Court Appointed Deputy by the court of protection appoints once person lacks capacity
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25
Q

DELIRIUM

What is delirium?

A
  • Acute confusional state, fluctuates in severity, usually reversible
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26
Q

DELIRIUM

What is the aetiology of delirium?

A

PINCH ME –

  • Pain
  • Infection (UTI, pneumonia)
  • Nutrition (thiamine, B12 + folate deficiency)
  • Constipation (faecal impaction)
  • Hydration (dehydrated)
  • Metabolic/medication
  • Environment/electrolytes (changes in environment, hyper/hypo Ca2+, Na+, K+)
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27
Q

DELIRIUM

What are some metabolic/medication causes of delirium?

A
  • Hyper/hypo thyroid + glycaemia

- Opioids, anticholinergics, Parkinson’s meds, steroids, BDZs

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28
Q

DELIRIUM

Who are high risk patients that require screening on admission?

A
  • > 65y
  • Background of dementia
  • Significant injury = hip fracture
  • Frailty or multi-morbidity
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29
Q

DELIRIUM

What are the core features of delirium?

A
  • Impaired consciousness
  • Cognitive disturbance
  • Acute/fluctuating course (worse at night = sundowning)
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30
Q

DELIRIUM

What are the two sub-types of delirium and how do they present?

A
  • Hyperactive = agitation, hallucinations, delusions, restless
  • Hypoactive (less recognisable) = withdrawn, lethargic, quiet
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31
Q

DELIRIUM

What is a suitable screening tool for delirium?

A
  • Abbreviated mental test (AMT)
  • Montreal Cognitive Assessment (MOCA) <26
  • Mini mental state examination
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32
Q

DELIRIUM
What investigations would you do in delirium?
What else would you consider?

A
  • “Confusion/delirium screen”
  • FBC, CRP, B12 + folate, U&Es, Ca2+, ?phosphate, TFTs, LFTs, glucose, INR + clotting, blood + urine cultures
  • Imaging = CXR + CT head
  • Referral to memory clinic or old age psychiatrist if ?dementia syndrome
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33
Q

DELIRIUM
How does delirium differ from dementia for…

i) deterioration?
ii) course?
iii) consciousness?
iv) thought content?
v) hallucinations?

A

i) Rapid (hours-days) + reversible vs. slow (months-years) + not reversible
ii) Acute + fluctuating vs. insidious + progressive
iii) Clouded vs. alert
iv) Vivid, complex + muddled vs impoverished
v) V common, visual vs. in 1/3rd, auditory/visual

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34
Q

DELIRIUM

What is the conservative management of delirium?

A
  • Logistics = side room, same staff members, talk/listen
  • Orientate = big clocks, calendars, family visits + personal belongings
  • Treat sensory impairments (glasses, hearing aids)
  • Prevent several ward changes
  • Sleep hygiene (promote sleeping at night)
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35
Q

DELIRIUM

In hyperactive delirium, how do you manage de-escalation?

A
  • Non-pharmacological de-escalation = talking to de-fuse
  • PO 0.5mg haloperidol or lorazepam (LBD/Parkinson’s)
  • IM/IV haloperidol or lorazepam
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36
Q

ALZHEIMER’S DISEASE

What is the pathophysiology of Alzheimer’s disease?

A
  • Accumulation of beta-amyloid peptide plaques which result in degeneration of cerebral cortex with cortical atrophy + loss of acetylcholine.
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37
Q

ALZHEIMER’S DISEASE
What are the causes of Alzheimer’s disease?
What are some risk factors?

A
  • Unknown but most common type of dementia

- FHx, increasing age, Down’s syndrome

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38
Q

ALZHEIMER’S DISEASE
What genes have been implicated to…

i) familial early-onset Alzheimer’s?
ii) late onset Alzheimer’s?

A

i) APP gene, presenilin 1 + 2 (autosomal dominant)

ii) Apolipoprotein E (ApoE)

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39
Q

ALZHEIMER’S DISEASE

What is the clinical presentation of Alzheimer’s

A

4As of Alzheimer’s –

  • Amnesia (recent memories lost first)
  • Apraxia (inability to carry out skilled tasks = button clothes, use cutlery)
  • Agnosia (recognition problems)
  • Aphasia (word finding problems)
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40
Q

ALZHEIMER’S DISEASE
On CT/MRI head in Alzheimer’s disease, what are the…

i) macroscopic pathological changes?
ii) microscopic or histological pathological changes?

A

i) Diffuse cerebral atrophy (small brain, esp. cortext + hippocampus), increased sulcal widening, enlarged ventricles
ii) Neuronal loss, neurofibrillary tangles (aggregation of tau proteins), beta-amyloid plaques

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41
Q

ALZHEIMER’S DISEASE

What is the management of Alzheimer’s?

A
  • Cognitive stimulation therapy, group reminiscence therapy
  • AChEi (donepezil, rivastigmine) for mild–mod
  • NMDA antagonist (memantine) for mod–severe
  • ?Antipsychotics if risk of harm or significant agitation or delusions
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42
Q

VASCULAR DEMENTIA
What is vascular dementia?
What are the risk factors?

A
  • Dementia 2º to ischaemia to brain 2º to vascular damage, 2nd commonest type
  • AF, stroke/TIA, CVD = HTN, DM, hypercholesterolaemia, smoking
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43
Q

VASCULAR DEMENTIA

What is the clinical presentation of vascular dementia?

A
  • Stepwise deterioration with short periods of stability then suddenly decline
  • Focal neurology
  • Memory/gait/speech/emotional disturbance
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44
Q

VASCULAR DEMENTIA

What investigation would you do in vascular dementia and what would it show?

A
  • CT head = infarcts, significant small vessel disease
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45
Q

VASCULAR DEMENTIA

What is the management of vascular dementia?

A
  • Vascular risk factor Mx = lifestyle, optimise co-morbidities
  • ONLY consider AChEi or memantine if suspected co-morbid Alzheimer’s, Parkinson’s dementia or LBD
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46
Q

LEWY-BODY DEMENTIA
What is the pathophysiology of Lewy-Body dementia?
What condition is LBD associated to and how can you differentiate?

A
  • Presence of Lewy bodies (alpha-synuclein inclusions) in the basal ganglia (substantia nigra) + cerebral cortex
  • Dementia > movement signs = LBD
  • Movement sign > dementia = Parkinson’s dementia
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47
Q

LEWY-BODY DEMENTIA

What is the clinical presentation of Lewy-Body dementia?

A
  • Progressive cognitive impairment with fluctuating cognition
  • Vivid visual hallucinations
  • Parkinsonism
  • REM sleep behaviour disorder
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48
Q

LEWY-BODY DEMENTIA

What is the management of Lewy-Body dementia?

A
  • SPECT/DaTscan being used more
  • Both AChEi + memantine being used as in Alzheimer’s
  • SENSITIVE to antipsychotics, can lead to irreversible Parkinsonism
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49
Q

FT DEMENTIA
What is frontotemporal lobe dementia?
What is is a specific cause?

A
  • Dementia syndrome 2º to atrophy of frontal + temporal lobes
  • Pick’s disease = Pick’s bodies (silver-staining tau protein) found on post-mortem
50
Q

FT DEMENTIA

What are some associations with frontotemporal lobe dementia?

A
  • Younger age of onset
  • Often FHx
  • Associated with MND
51
Q

FT DEMENTIA

What is the clinical presentation of frontotemporal lobe dementia?

A
  • Frontal lobe = personality change + disinhibition

- Temporal lobe = speech disturbances = expressive dysphasia, non-fluent)

52
Q

CJD

What is Creutzfeldt-Jacob Disease (CJD)?

A
  • Prion infection which infects the brain causing spongiform encephalopathy
53
Q

CJD

What is the aetiology of CJD?

A
  • Sporadic (may have FHx or idiopathic)

- Variant (vCJD) aka Mad Cow’s disease from eating contaminated beef

54
Q

CJD

What is the clinical presentation of CJD?

A
  • Rapidly fatal dementia
  • Myoclonic jerks
  • Mood + personality changes
55
Q

HYDROCEPHALUS
What is normal pressure hydrocephalus?
What is the clinical presentation

A
  • Accumulation of CSF that causes ventricles in brain to become enlarged
  • ‘Wet, wacky, wobbly’ = urinary incontinence, dementia (can be controlled or reversed with treatment), ataxia
56
Q

HYDROCEPHALUS

What is the investigation and management of normal pressure hydrocephalus?

A
  • CT/MRI head showing enlarged ventricles

- Ventriculoperitoneal shunt to drain excess fluid

57
Q

PSEUDODEMENTIA
What is pseudodementia?
How does it present?

A
  • Cognitive impairment secondary to mental illness (often depression)
  • “Don’t know” answers (no confabulation), short duration, short- and long-term memory loss depression Sx, recent loss of loved one
58
Q

FALLS

What are some neurological causes of falls?

A
  • Stroke
  • PD/HD
  • Visual impairment
  • Peripheral neuropathy
59
Q

FALLS

What are some cardiovascular causes of falls?

A
  • Syncope
  • Postural hypotension
  • MI
  • Arrhythmias
60
Q

FALLS

What are some iatrogenic causes of falls?

A
  • BDZs

- Anti-hypertensives (ACEi, CCB, beta-blockers, diuretics)

61
Q

FALLS

What are some power causes of falls?

A
  • Muscle weakness
  • Loss of balance
  • Pain (OA)
62
Q

FALLS
What are some environmental causes of falls?
Any other causes?

A
  • Loose rugs, pets, unstable footwear, poor lighting

- Delirium, hypoglycaemia, alcohol

63
Q

FALLS
What clinical scale can be used to assess frailty?
What investigations would you do in a fall?

A
  • Rockwood clinical frailty scale
  • FBC, U&E, glucose, LFTs, bone profile (calcium, phosphate, PTH, vitamin D)
  • 24h ECG, echo if ?cardiac, XR limbs, CXR, CT head
  • Tilt table if unexplained syncope, normal ECG + no structural heart disease
64
Q

FALLS

What are some complications of a long-lie following a fall?

A
  • Pressure ulcers
  • Dehydration
  • Rhabdomyolysis
  • Hypothermia
65
Q

FALLS

What is rhabdomyolysis?

A
  • Skeletal muscle breakdown leading to release of intracellular contents
66
Q

FALLS

What can cause rhabdomyolysis?

A
  • Crush injuries
  • Prolonged immobilisation (long lie)
  • Prolonged seizures
  • Burns
  • Compartment syndrome
  • Statins
67
Q

FALLS

What are the features of rhabdomyolysis?

A
  • AKI (acute tubular necrosis)
  • Elevated CK, potassium + phosphate
  • Myoglobinuria = Coca-Cola urine
  • Low calcium
68
Q

FALLS

What is the management of rhabdomyolysis?

A
  • IV fluids to maintain good urine output

- Rarely urinary alkalinization or dialysis

69
Q

FALLS

What is the general management of falls prevention?

A
  • Medication review
  • Provide good footwear + walking aid access
  • Call bell close to hand
  • Physio + OT
  • Correct sensory impairments incl. good lighting
  • Alarms = pullcord or pendant alarms
70
Q

POSTURAL HYPOTENSION

What is the pathophysiology of postural hypotension?

A
  • When standing, gravity causes blood to pool in legs + abdo which decreases BP as less blood circulating back to heart
  • Normally, baroreceptors near heart + carotid arteries sense this lower BP + increase the BP but in postural hypotension, something interrupts this mechanism
71
Q

POSTURAL HYPOTENSION

What are some causes of postural hypotension?

A
  • Iatrogenic = diuretics, ACEi, beta blockers, nitrates, L-dopa, anticholinergics
  • Autonomic dysfunction = DM, Parkinson’s disease
  • Endo = Addison’s disease
  • Hypovolaemia
72
Q

POSTURAL HYPOTENSION
What is the clinical presentation of postural hypotension?
How is it diagnosed?

A
  • Dizziness, syncope + falls after standing

- Lying/standing BP = drop ≥20mmHg in SBP or ≥10mmHg in DBP

73
Q

POSTURAL HYPOTENSION

What is the conservative management of postural hypotension?

A
  • Drinks lots of water
  • Medication review
  • Compression stockings
  • Advice = rise from sitting slowly, elevate head of bed
74
Q

POSTURAL HYPOTENSION

What is the pharmacological management of postural hypotension?

A
  • Fludrocortisone = mineralocorticoid = Na/water retention > SE oedema
  • Midodrine = alpha-adrenergic agonist (when cause is autonomic dysfunction)
75
Q

PRESSURE ULCERS
What is an ulcer?
What is a pressure ulcer?
Where would you commonly find them?

A
  • Areas of skin necrosis due to pressure-induced ischaemia

- Sacrum, heels, greater trochanters, shoulders

76
Q

PRESSURE ULCERS

What are the main risk factors for developing pressure ulcers and how these are screened for?

A

Waterlow score –

  • PVD (poor healing/reduced tissue perfusion)
  • Immobility (#, pain)
  • Dehydration + malnourishment
  • Obesity
  • Incontinence
77
Q

PRESSURE ULCERS

What are the different grades for pressure ulcers?

A
  • I = non-blanching erythema with intact skin
  • II = broken skin or blistering (epidermis ± dermis only)
  • III = full-thickness skin loss involving damage/necrosis of subcutaneous tissue
  • IV = extensive loss, destruction/necrosis of muscle, bone, joint or tendon
78
Q

PRESSURE ULCERS

What are some investigations for pressure ulcers?

A
  • FBC (WCC), cultures
  • CRP/ESR
  • Swabs for MC&S if infected
  • XR for bone involvement (?osteomyelitis)
79
Q

PRESSURE ULCERS

How can pressure ulcers be prevented?

A
  • Mobilise
  • Repositioning (6º or 4º if high risk)
  • Pressure mattress
  • Barrier creams
  • Regular skin assessments
80
Q

PRESSURE ULCERS

What is the management of pressure ulcers?

A
  • Pain relief
  • Moist environment promotes healing = hydrocolloid dressings + hydrogels
  • Refer to tissue viability nurse
  • May need surgical debridement
81
Q

MALNUTRITION

What is the NICE definition of malnutrition?

A
  • BMI <18.5 or
  • Unintentional weight loss >10% in past 3–6m or
  • BMI <20 and unintentional weight loss >5% in past 3–6m
82
Q

MALNUTRITION

What are the three main causes of malnutrition and what can lead to them?

A
  • Inadequate nutritional intake = reduced appetite, dysphagia, pain, dementia
  • Increased nutrient requirements = sepsis, cancer
  • Malabsorption = IBD, coeliac disease, drains
83
Q

MALNUTRITION
What investigations would you do in someone with malnutrition?
What tool should you use on those at risk?

A
  • U+Es, LFTs + ECG prior to commencing feedings, albumin (low)
  • Malnutrition Universal Screening Tool (MUST) on admission
84
Q

MALNUTRITION
What are the components of MUST?
What do the scores mean?

A
  • BMI = 18.5-20 (1), <18.5 (2)
  • Hx of weight loss = 5-10% (1) ≥10% (2)
  • Acutely unwell or likely to have no intake >5d (2)
  • 1 = medium risk (observe, if inadequate set goals to improve intake)
  • ≥2 = high risk (refer to dietician, set goals to improve intake)
85
Q

MALNUTRITION

What are some consequences of malnutrition?

A
  • Impaired immunity + recovery
  • Loss of muscle mass
  • Risk of refeeding syndrome
  • Deficiency syndromes
86
Q

MALNUTRITION
What is the overall principle for the management of malnutrition?
What is trialled after that?
If you are unable to sufficiently supplement their diet orally, what do might you need to consider?

A
  • Food first = food fortification (add full-fat cream to mashed potato)
  • Oral nutritional supplements (ONS) e.g., Fortisip
  • Enteral/Parenteral feeding
87
Q

MALNUTRITION
What are the 4 main types of enteral feeding?
What are the drawbacks?

A
  • Nasogastric tube, nasojejunal tube, percutaneous endoscopic gastrostomy/jejunostomy
  • Diarrhoea, aspiration, refeeding syndrome, appearance
88
Q

MALNUTRITION
What is an NG tube?
How long is it used for?
How do you confirm its placement?

A
  • Tube feeds into stomach, inserted on ward
  • Short-term <30d
  • Gold standard = pH aspirate ≤5.5 if not CXR
89
Q

MALNUTRITION
What is an NJ tube?
How long is it used for?

A
  • Tube feeds into stomach, radiological guidance

- Short-term <60d

90
Q

MALNUTRITION
What are the indications for PEG?
What are the indications for PEJ?

A
  • Long-term replacement, dysphagia, CF

- Long-term replacement, delayed gastric emptying, upper GI surgery

91
Q

MALNUTRITION
What is parenteral feeding?
What method is used?

A
  • Feeding when gut is inaccessible or unable to absorb sufficient nutrients
  • IV access via peripherally inserted central catheter (PICC) or central line
92
Q

MALNUTRITION
What are the indications for parenteral feeding?
What are the drawbacks?

A
  • Short bowel syndrome, bowel obstruction or bowel rest

- Thrombosis, sepsis, metabolic acidosis, refeeding syndrome

93
Q

OSTEOPOROSIS

What is osteoporosis?

A
  • Characterised by decreased bone mineral density due to micro-architectural deterioration of bone tissue leading to risk of fragility fractures
94
Q

OSTEOPOROSIS

What are the risk factors for osteoporosis?

A

SHATTERED

  • Steroids
  • Hyper/hypothyroid
  • Alcohol/smoking
  • Thin (low BMI)
  • Testosterone low (F)
  • Early menopause
  • Renal/liver failure
  • Relatives (FHx)
  • Erosive bone disease (RA)
  • Dietary Ca2+ low
95
Q

OSTEOPOROSIS

What is the clinical presentation of osteoporosis?

A
  • Fragility fractures
  • Vertebral = acute back pain, height loss, kyphosis, but often incidental finding
  • Distal radius = Colles’ #
  • Neck of femur
96
Q

OSTEOPOROSIS
What initial investigations should you do in osteoporosis?
What risk score can you use and what does it tell you?

A
  • FBC, U&E, LFTs, TFTs, CRP, bone profile (calcium, phosphate, PTH) = normal as not mineral issue
  • XR spine first-line for # (wedging of vertebrae, old # = sclerotic)
  • FRAX = 10-year probability of fragility # for patients 40–90y
97
Q

OSTEOPOROSIS

What are the various parts of the FRAX tool?

A
  • Personal = age, sex, kg, height (cm)
  • PMHx = RA, previous #, 2º osteoporosis
  • DHx = glucocorticoids
  • FHx = parental hip #
  • Social Hx = smoking, alcohol ≥3 units/day
  • Other = femoral neck BMD
98
Q

OSTEOPOROSIS

What is the management of FRAX scores?

A
  • Low risk = reassure + lifestyle advice
  • Intermediate risk = dual-energy x-ray absorptiometry (DEXA) scan gold standard for bone mineral density
  • High risk = bone protection
99
Q

OSTEOPOROSIS
What are the two scores you get from a DEXA scan?
What do the results mean?

A
  • T-score = based on bone mass of young reference population
  • Z-score = adjusted for their demographics (age, gender, ethnicity)
  • T-score ≤ -2.5 = osteoporosis
  • –2.5 < T-score ≤ –1 = osteopenia (low bone mass)
  • –1 < T-score ≤ 1 = healthy
100
Q

OSTEOPOROSIS

What is the general lifestyle management for osteoporosis?

A
  • Quit smoking
  • Reduce alcohol
  • Weight bearing exercises
101
Q

OSTEOPOROSIS

How do you manage fragility fractures in osteoporosis?

A
  • ≥75y = start PO bisphosphonate without DEXA scan

- <75y = DEXA scan then calculate FRAX

102
Q

OSTEOPOROSIS

How do you manage corticosteroid-induced osteoporosis?

A
  • ≥65y = previous fragility # = bone protection

- <65y = DEXA scan, if T-score 0-–1.5 repeat in 1–3y, if < –1.5 = bone protection

103
Q

OSTEOPOROSIS
What bone protection is offered in osteoporosis?
What is the first line management?

A
  • All offered vitamin D + calcium supplementation unless clinician confident they have adequate intake
  • Bisphosphonate such as PO alendronate 70mg weekly
104
Q

OSTEOPOROSIS
What is the mechanism of action of bisphosphonates?
What important patient information should you give?
What are some potential adverse effects?

A
  • Inhibit osteoclasts by reducing recruitment + promoting apoptosis
  • Take on empty stomach, plenty of water, stay upright for 30m
  • Oesophageal reactions (oesophagitis, ulcers), osteonecrosis of jaw, risk of atypical stress # of proximal femoral shaft, hypocalcaemia
105
Q

OSTEOPOROSIS

What are the other management options for bone protection in osteoporosis?

A
  • 2nd line = risedronate
  • 3rd line = strontium ranelate or raloxifene (SERMs)
  • Last line = denosumab (monoclonal Ab to RANK-ligand)
  • ?Teriparatide (recombinant PTH which increases osteoblast activity)
106
Q

PRESCRIBING IN PALLIATIVE CARE

What are the main symptoms experienced in end of life?

A
  • Pain
  • Nausea and vomiting
  • Secretions
  • Agitation and confusion
  • Breathlessness
107
Q

PRESCRIBING IN PALLIATIVE CARE
How do you go about starting morphine?
What else should you consider prescribing?
How much should you increase doses by?

A
  • Morphine MR 30mg (15mg BD) with 5mg IR for breakthrough pain
  • Co-prescribe laxatives + anti-emetics if nausea persists
  • 30–50%
108
Q

PRESCRIBING IN PALLIATIVE CARE
What opioids would you use in renal impairment?
How do you calculate breakthrough pain dose?

A
  • Oxycodone if mild-mod, buprenorphine + fentanyl if severe

- 1/6th–1/10th daily opioid dose

109
Q

PRESCRIBING IN PALLIATIVE CARE

What are some side effects of opioids?

A
  • Transient = nausea, drowsiness

- Persistent = constipation

110
Q

PRESCRIBING IN PALLIATIVE CARE
What are some common opioid conversions?

i) PO codeine > PO morphine?
ii) PO morphine > SC morphine?
iii) PO morphine > SC diamorphine?
iv) PO morphine > PO oxycodone

A

i) ÷ 10
ii) ÷ 2
iii) ÷ 3
iv) ÷ 1.5

111
Q

PRESCRIBING IN PALLIATIVE CARE

What are the 6 main causes of nausea and vomiting in palliative care?

A
  • Reduced gastric motility
  • Chemically mediated
  • Visceral
  • Raised ICP
  • Vestibular
  • Cortical
112
Q

PRESCRIBING IN PALLIATIVE CARE
What causes reduced gastric motility N+V?
What is the management?
What important caution is there?

A
  • Opioid and serotonin + dopamine receptors related
  • First line = metoclopramide or domperidone (pro-kinetics)
  • Metoclopramide C/I if complete bowel obstruction, GI perforation or immediately following gastric surgery
113
Q

PRESCRIBING IN PALLIATIVE CARE
What causes chemically mediated N+V?
What is the management?

A
  • Secondary to hypercalcaemia, opioids or chemo

- First line = ondansetron (5-HT3 receptor antagonist), haloperidol or levomepromazine

114
Q

PRESCRIBING IN PALLIATIVE CARE
What causes visceral mediated N+V?
What is the management?

A
  • Constipation, PO candidiasis

- First line = cyclizine (H1 receptor antagonist) or levomepromazine

115
Q

PRESCRIBING IN PALLIATIVE CARE
What causes raised ICP N+V?
What is the management?

A
  • Secondary to cerebral mets

- First line = cyclizine or dexamethasone

116
Q

PRESCRIBING IN PALLIATIVE CARE
What causes vestibular N+V?
What is the management?

A
  • Activation of acetylcholine + histamine receptors
  • First line = cyclizine
  • Refractory = metoclopramide or prochlorperazine
117
Q

PRESCRIBING IN PALLIATIVE CARE
What causes cortical N+V?
What is the management?

A
  • Anxiety, pain, and/or anticipatory nausea, related to GABA + histamine
  • Anticipatory = BDZ like lorazepam, or ondansetron
118
Q

PRESCRIBING IN PALLIATIVE CARE

What is the management of secretions?

A
  • Conservative = avoid fluid overload, educate family that unlikely troublesome
  • First line = hyoscine butyl/hydrobromide
  • Glycopyrronium bromide may be used
119
Q

PRESCRIBING IN PALLIATIVE CARE

What is the management of agitation and confusion?

A
  • First line = haloperidol

- Other = chlorpromazine (also hiccups), levomepromazine

120
Q

PRESCRIBING IN PALLIATIVE CARE

What is the management of breathlessness

A
  • Therapeutic oxygen
  • Morphine
  • Midazolam if anxiety related

FINALS (20 decks)

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