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GERIATRICS Flashcards

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1
Q

DELIRIUM
What is delirium?

A
  • Transient, acute syndrome characterised by disturbance of consciousness, perception, sleep-wake cycle, emotion + cognition
  • Acute confusional state, fluctuates in severity, usually reversible
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2
Q

DELIRIUM
what are the causes of delirium?

A

PINCH ME –
- Pain
- Infection (UTI, pneumonia, septicaemia)
- 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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3
Q

DELIRIUM
What are some metabolic/medication causes of delirium?

A
  • Hyper/hypo thyroid + glycaemia
  • Hypercortisolaemia
  • Substance misuse
  • Withdrawal (incl. delirium tremens)
  • Opioids, anticholinergics, Parkinson’s meds, steroids, BDZs, interactions
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4
Q

DELIRIUM
What are some other causes of delirium?

A
  • Urinary retention, vascular events (CVA, MI)
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5
Q

DELIRIUM
Who are high risk patients that require screening on admission?

A
  • > 65y, men, previous delirium
  • Pre-existing cognitive deficit (dementia, PD, stroke)
  • Sensory impairment (hearing/visual)
  • Significant illness (hip #, cancer)
  • Poor nutrition
  • Hx of alcohol excess
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6
Q

DELIRIUM
What are the 2 sub-types of delirium?
Which is more dangerous?

A
  • Hyperactive = agitated/aggressive, hallucinations, delusions, wandering + restless
  • Hypoactive = withdrawn, quiet, lethargic, lacks concentration, slow
  • Hypoactive as less likely to be recognised
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7
Q

DELIRIUM
What is the ICD-10 diagnostic criteria for delirium?

A
  • Impaired consciousness + inattention (poor conc, memory deficit, “clouding of consciousness”)
  • Perceptual OR cognitive disturbance (agitation, hallucinations > Lilliputian)
  • Acute onset + fluctuating course (often worse at night = sundowning)
  • Evidence it may be related to a physical cause
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8
Q

DELIRIUM
What are some other/non-specific features of delirium?

A
  • Disinhibition
  • Falls
  • Loss of appetite
  • Labile mood
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9
Q

DELIRIUM
What is a suitable screening tool for delirium?

A

4AT (≥4 = likely) –
- Alertness
- AMT4 (age, DOB, hospital name, year)
- Attention (list months backwards)
- Acute change or fluctuating course

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10
Q

DELIRIUM
What other cognitive tools can be used in the assessment of delirium/dementia?

A
  • GP-COG (GP assessment of cognition)
  • 6-CIT (6-item cognitive impairment test)
  • AMT (abbreviated mental test)
  • MOCA (Montreal Cognitive Assessment, <26/30)
  • MMSE
  • ACE-III
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11
Q

DELIRIUM
What general investigations would you do/enquiry about in a patient with delirium?

A
  • Full physical exam
  • Vitals (?sepsis), ECG
  • Check if passed stools
  • Check nutritional + hydration status
  • Confusion screen
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12
Q

DELIRIUM
What is a confusion screen?

A
  • FBC, B12 + folate, U+Es, Ca2+, ?phosphate, TFTs, LFTs, glucose, INR + clotting, blood + urine cultures, ?CRP/ESR
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13
Q

DELIRIUM
What other investigations or referral could you consider other than bloods?

A
  • CXR or CT head if indicated
  • Referral to memory clinic or old age psychiatrist
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14
Q

DELIRIUM
What is the mainstay of delirium management?

A
  • Identify + treat cause with sufficient nutrition, hydration + mobilisation
  • Maximise orientation + make environment safe + comforting
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15
Q

DELIRIUM
How should a patient be managed in the first instance?

A

Conservative de-escalation
- Talk to pt + listen to them
- Quiet bay or side room
- Big clocks, calendars, same staff members for orientation
- Family visits + personal belongings (pictures)
- Tx sensory impairments (glasses, hearing aids)
- Prevent ward changes
- Sleep hygiene (promote night sleep, not daytime)

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16
Q

DELIRIUM
Sometimes conservative de-escalation is inadequate and medications may be required. What are some options?

A
  • Short-term antipsychotics – haloperidol 0.5mg or olanzapine
  • Short-acting BDZ like lorazepam 0.5mg (caution may exacerbate confusion + over sedate)
  • Long-acting BDZ if withdrawing (chlordiazepoxide, diazepam)
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17
Q

DEMENTIA
What is dementia?

A
  • Syndrome of acquired, chronic, global impairment of higher brain function in an alert patient, which interferes with ability to cope with daily living
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18
Q

DEMENTIA
What time frame is used?

A
  • Deterioration present for ≥6m for diagnosis
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19
Q

DEMENTIA
What are the 2 types of dementia and where is affected?

A
  • Cortical dementias affect the cerebral cortex
  • Subcortical dementia affect the basal ganglia + thalamus
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20
Q

DEMENTIA
Give some examples of cortical dementia

A
  • AD, lewy-body, frontotemporal
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21
Q

DEMENTIA
How does cortical dementia present?
Give some examples.

A
  • Memory impairment, dysphasia, visuospatial impairment (apraxia), problem solving + reasoning deficit
  • AD, lewy-body, frontotemporal
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22
Q

DEMENTIA
How does subcortical dementia present?
Give some examples

A
  • Psychomotor slowing, impaired memory retrieval, depression/apathy, executive dysfunction, personality change, language preserved
  • PD, Huntington’s, alcohol-related + AIDS
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23
Q

DEMENTIA
How does delirium differ from dementia for…

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

A

i) Rapid (hours-days) + usually 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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24
Q

DEMENTIA
What are some diagnostic features of dementia?

A
  • Multiple cognitive deficits (memory, orientation, language, reasoning)
  • Resulting impairment in ADLs (washing, dressing)
  • Clear consciousness
  • Other common Sx include behavioural + psychological Sx of dementia (BPSD), sleep issues (insomnia, daytime drowsiness, nocturnal restlessness)
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25
DEMENTIA What are behavioural + psychological symptoms of dementia (BPSD)? What causes them?
- Heterogenous group of non-cognitive symptoms + behaviours seen in dementia - Same causes as delirium
26
DEMENTIA How does behavioural + psychological symptoms of dementia (BPSD) present?
- Anxiety/depression, agitation, psychosis (may think nurses out to get them), disinhibition
27
DEMENTIA What is the management of behavioural + psychological symptoms of dementia (BPSD)?
- Exclude/Tx underlying cause, similar Mx to delirium (supportive environment, meds last line), educate family/carer about Sx + causes
28
DEMENTIA What are some general investigations for dementia?
- Full Hx + collateral with full physical exam + MSE - Check for reversible causes with confusion screen ± CXR ± CT head
29
DEMENTIA What might a MMSE score indicate in dementia?
MMSE (/30) – - 21–26 = mild, 14–20 = mod, 10–14 mod-severe, <10 = severe cognitive impairment
30
DEMENTIA What might an Addenbrooke's cognitive examination III (ACE-III) score indicate in dementia?
ACE-III (/100) – - <82 likely dementia + need abnormal scores in ≥2 domains (attention/orientation, memory, language, visuospatial, fluency)
31
DEMENTIA What type of imaging may be used in dementia?
- SPECT to differentiate between Alzheimer's + frontotemporal - DaTscan shows 'comma' in normal but 2 dots in Lewy body + Parkinson's dementia at the basal ganglia
32
DEMENTIA What biological treatment can be used in dementia?
- Bio = risperidone for agitation (apart in Lewy-Body)
33
DEMENTIA What psychological treatment can be used in dementia?
- Psycho = CBT for depression, counselling, reminiscence therapy + reality orientation, keep stimulated with puzzles, word searches, activities
34
DEMENTIA What social treatment can be used in dementia?
- OT assessment to remain independent (pendent, labels on cupboards, key safe, carers, handrails) - Physio assessment - Encourage family visits + photos - Animal/pet therapy, music, arts + crafts - Care plans + advanced directives before worsens - Services – Dementia UK, Alzheimer's society, Age UK, admiral nurses
35
ALZHEIMER'S DISEASE What is the pathophysiology of Alzheimer's disease?
- Accumulation of beta-amyloid peptide plaques which result in degeneration of cerebral cortex with cortical atrophy + loss of acetylcholine.
36
ALZHEIMER'S DISEASE What is the onset of Alzheimer's disease like and why?
- Insidious onset dementia due to generalised deterioration of the brain
37
ALZHEIMER'S DISEASE What neurotransmitters are affected?
- ACh, noradrenaline, serotonin, somatostatin
38
ALZHEIMER'S DISEASE What are the causes of Alzheimer's disease?
- Unknown but most common type of dementia
39
ALZHEIMER'S DISEASE What is the epidemiology?
- >65y, if <65 then early onset + associated with more rapid decline + FHx
40
ALZHEIMER'S DISEASE What condition has increased rates of Alzheimer's?
- Down's syndrome (most develop by 50)
41
ALZHEIMER'S DISEASE What genes have been implicated to... i) familial early-onset Alzheimer's? ii) late onset Alzheimer's?
i) APP gene, presenilin 1 + 2 (autosomal dominant) ii) Apolipoprotein E (ApoE)
42
ALZHEIMER'S DISEASE What are some risk factors for Alzheimer's?
- CVD = HTN, DM, hypercholesterolaemia, smoking - FHx
43
ALZHEIMER'S DISEASE What is the clinical presentation of Alzheimer's
4As of Alzheimer's – - Amnesia (recent memories poor, disorientation about time) - Apraxia (unable to button clothes, use cutlery) - Agnosia (unable to recognise body parts, objects, people) - Aphasia (later feature, mixed receptive/expressive) Insidious + progressive course of short-term memory loss Sx in early disease
44
ALZHEIMER'S DISEASE On CT/MRI head in Alzheimer's disease, what are the macroscopic pathological changes?
Diffuse cerebral atrophy (shrunken brain), increased sulcal widening, enlarged ventricles
45
ALZHEIMER'S DISEASE On CT/MRI head in Alzheimer's disease, what are the microscopic or histological pathological changes?
Neuronal loss, neurofibrillary tangles, beta-amyloid plaques
46
ALZHEIMER'S DISEASE What is the management of Alzheimer's?
- No cure, does not improve life expectancy but thought to slow rate of decline + allow functioning at higher level - AChEi (donepezil, rivastigmine) for mild–mod - NMDA antagonist (memantine) for mod–severe
47
VASCULAR DEMENTIA What causes vascular dementia?
- Any type of vascular disease affecting blood vessels of brain
48
VASCULAR DEMENTIA What are the risk factors?
- CVA/TIA = 9x increased risk of dementia - CV = HTN, DM, hypercholesterolaemia, smoking - Hx of peripheral vascular disease, IHD
49
VASCULAR DEMENTIA What is the clinical presentation of vascular dementia?
- Stepwise deterioration with short periods of stability then suddenly decline - Patchier cognitive impairment than Alzheimer's - Focal neuro signs if caused by stroke
50
VASCULAR DEMENTIA What would a CT head show in vascular dementia?
- ≥1 areas of cortical infarction (white on CT), may show micro-infarcts
51
VASCULAR DEMENTIA What is the management of vascular dementia?
Not reversible but prevent further decline – - Lifestyle (lose weight, healthy diet, stop smoking + alcohol) - Atorvastatin 80mg if high cholesterol - Optimise co-morbidities (HTN, DM) - Aspirin or clopidogrel (75mg OD)
52
LEWY-BODY DEMENTIA What is the pathophysiology of Lewy-Body dementia?
- Presence of Lewy bodies (protein deposits) in the basal ganglia + cerebral cortex, typically presents between 50–80y
53
LEWY-BODY DEMENTIA What might it be confused with?
- Delirium due to fluctuating consciousness + hallucinations
54
LEWY-BODY DEMENTIA What condition is Lewy-Body dementia closely associated to?
- Parkinson's disease (25% of PD patients will develop)
55
LEWY-BODY DEMENTIA How can you differentiate between lewy-body dementia and parkinsons disease?
- Dementia before movement signs = Lewy-body dementia - Movement before dementia signs = Parkinson's dementia
56
LEWY-BODY DEMENTIA What is the clinical presentation of Lewy-Body dementia?
- Fluctuating onset, progression, cognition + consciousness - Vivid visual hallucinations (small children, animals) - Parkinsonism (tremor, stooped + shuffling gait, hypomimia) - Frequent falls - REM sleep behaviour disorder (sleep walking, aggression) commonly precedes other Sx - Rapid decline more so than other types
57
LEWY-BODY DEMENTIA What is the management of Lewy-Body dementia?
- Conservative management - AChEi used in mild–mod (rivastigmine 1st line), memantine last resort - SENSITIVE to antipsychotics, can make worse + lead to neuroleptic malignant syndrome
58
FT DEMENTIA What are 2 common features in frontotemporal (FT) dementia?
- Early personality changes + relative intellectual sparing.
59
FT DEMENTIA What are some pathological features of frontotemporal dementia?
- Microscopic = ubiquitin + tau deposits
60
FT DEMENTIA What causes FT dementia?
- Unknown, younger mean age of onset - Can be due to neurosyphilis (typically causes frontal lobe Sx such as aggression + personality change), associated with MND
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FT DEMENTIA What are the i) frontal lobe symptoms ii) temporal lobe symptoms iii) generic features of FT dementia?
i) Euphoria, disinhibition, personality changes + emotional blunting ii) Speech disturbances (progressive non-fluent aphasia, may end up mute), expressive dysphasia iii) Insidious onset with poor insight, amnesia not as severe as Alzheimer's
62
FT DEMENTIA What are the temporal lobe symptoms of FT dementia?
Speech disturbances (progressive non-fluent aphasia, may end up mute), expressive dysphasia
63
FT DEMENTIA What are the frontal lobe symptoms of FT dementia?
i) Euphoria, disinhibition, personality changes + emotional blunting
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FT DEMENTIA What is the management of FT dementia?
- No specific treatment - SSRIs may help behavioural symptoms
65
MILD COG IMPAIRMENT What is mild cognitive impairment?
- Cognitive impairment without functional impairment (ADLs minimally affected)
66
MILD COG IMPAIRMENT How does it present?
- Reduced fluency + some short-term memory difficulties
67
MILD COG IMPAIRMENT How does it progress?
- 1/3rd improve, 1/3rd stable, 1/3rd progress to dementia
68
FALLS What is a fall?
- Event that results in unintentionally coming to rest at a lower level, usually the floor
69
FALLS What are some neurological causes of falls?
- Stroke - PD or other movement disorders (Huntington's) - Visual impairment - Peripheral neuropathy or myopathy
70
FALLS What are some cardiovascular causes of falls?
- Vasovagal or situational syncope - Postural hypotension - MI, arrhythmias - Dehydration or shock
71
FALLS What are some iatrogenic causes of falls?
- BDZs (sedative so impairs coordination) - Polypharmacy (combination of drugs + interactions) - Anti-hypertensives (ACEi, CCB, beta-blockers, diuretics) - Anti-depressants + anti-psychotics
72
FALLS What are some power causes of falls?
- Inactivity > muscle weakness - Dizziness/loss of balance or proprioception (vertigo) - Pain/MS > osteoarthritis
73
FALLS What are some environmental causes of falls?
- Loose rugs - Pets - Furniture - Unstable footwear - Poor lighting
74
FALLS What are some other causes of falls?
- Infection or sepsis - Delirium - Incontinence - Hypoglycaemia - Alcohol (intoxication, neuropathy, Korsakoff's or Wernicke's)
75
FALLS What parts of the history are important when assessing falls?
- Collateral Hx - Circumstances (timing, physical environment) - Sx before + after fall - Previous falls, #, syncope or near misses - PMH for co-morbidities - Functional performance (assess ADLs)
76
FALLS What clinical examinations would you perform?
- CVS (LSBP, HR + rhythm, murmurs esp. AS) - MSK (assess footwear, joints for deformity + stiffness) - Neuro (identify stroke, peripheral neuropathy, ?Parkinson's)
77
FALLS What clinical scale can be used to assess frailty?
- Rockwood clinical frailty scale (from very fit, vulnerable, moderately frail to terminally ill)
78
FALLS What investigations would you do for someone presenting with a fall?
- FBC, B12 + folate, U+Es, Ca2+, phosphate, glucose, TFTs, vitamin D - 24h ECG, ECHO if ?cardiac cause - Head-up tilt table testing if unexplained syncope with normal ECG + no structural heart disease
79
FALLS What are some complications of a long-lie following a fall?
- Pressure ulcers - Dehydration - Rhabdomyolysis - Hypothermia
80
FALLS What is rhabdomyolysis?
- Skeletal muscle breakdown due to traumatic, chemical or metabolic injury
81
FALLS What can cause rhabdomyolysis?
- Crush injuries - Prolonged immobilisation following a fall - Prolonged seizures - Hyperthermia - Neuroleptic malignant syndrome
82
FALLS How may rhabdomyolysis present?
- Urine may be dark ('Coca-Cola urine) + urinalysis +ve to Hb but without RBCs
83
FALLS What markers are elevated in rhabdomyolysis? Is that an issue?
- K+, phosphate, myoglobin + creatinine kinase - Myoglobin is nephrotoxic as causes acute tubular necrosis
84
FALLS What is the management of rhabdomyolysis?
- Measure U+Es, creatinine, CK levels + monitor urine output - Supportive with IV fluids, correct electrolytes, ?temporary dialysis
85
FALLS How can falls be prevented in a hospital setting?
- Treat infection, dehydration + delirium actively - Stop incriminating drugs or avoid staring them - Provide good quality footwear + access to walking aid - Keep a call bell close to hand - Good lighting
86
FALLS How can fall frequency be reduced?
- Drug review to reduce meds that can increase risk - Strength + balance training with physio (Tai Chi) - Walking aids - Environmental assessment + mods by OT - Ensure vision optimised with glasses
87
FALLS How can adverse consequences from falls be reduced?
- Osteoporosis detection + treatment - Alarms such as pullcord or pendant alarms to summon help - Supervision via visits from carers, family, neighbours
88
POSTURAL HYPOTENSION What is the pathophysiology of postural hypotension?
- 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 + send signals to brain to signal heart to beat faster, pump more blood, cause vasoconstriction + stabilise BP - In postural hypotension, something interrupts this mechanism
89
POSTURAL HYPOTENSION What are some iatrogenic causes of postural hypotension?
Diuretics, anti-hypertensives, antidepressants, polypharmacy
90
POSTURAL HYPOTENSION What are some cardiac causes of postural hypotension?
Aortic stenosis, arrhythmias, MI, cardiomyopathy, anaemia, CHF
91
POSTURAL HYPOTENSION What are some endocrine causes of postural hypotension?
DM, hypoadrenalism, hypothyroidism
92
POSTURAL HYPOTENSION What are some neuro causes of postural hypotension?
PD + PD+ syndromes
93
POSTURAL HYPOTENSION What are some other causes of postural hypotension? How common is it?
- Blood loss, dehydration + shock - Occurs in 30% of patients >70y
94
POSTURAL HYPOTENSION How may postural hypotension present?
- Postural light-headedness, dizziness, blurred vision - Weakness, fatigue, palpitations + headache may be present
95
POSTURAL HYPOTENSION What are these patients at risk of?
Risk of falls + syncope, CV disease or stroke
96
POSTURAL HYPOTENSION What investigations would you do to diagnose postural hypotension?
Lying + standing blood pressure - Abnormal drop in BP of ≥20/10mmHg within 3 minutes of standing (<20/10 is physiological) Investigate medical causes (FBC, U+Es, B12 + folate, TFTs, LFTs, CRP/ESR, ECG)
97
POSTURAL HYPOTENSION What is the conservative management of postural hypotension?
- Drinks lots of water - Avoid alcohol - Compression garments (stockings) - Stand slowly, elevating head of the person's bed
98
POSTURAL HYPOTENSION What is the pharmacological management of postural hypotension?
- Med review + stop causative agent - Fludrocortisone (raises BP by raised Na+ levels + affecting blood volume) but can cause uncomfortable oedema - Midodrine (when cause if autonomic dysfunction) but can cause retention, itchy scalp + paraesthesia
99
PRESSURE ULCERS What is an ulcer?
- Open sore caused by a break in the skin or mucous membrane which fails to heal
100
PRESSURE ULCERS What is a pressure ulcer?
Areas of skin necrosis due to pressure-induced ischaemia
101
PRESSURE ULCERS Where would you commonly find a pressure ulcer?
Sacrum, heels, greater trochanters, shoulders
102
PRESSURE ULCERS How rapidly can a new pressure ulcer develop?
- 2h of tissue ischaemia sufficient for subsequent development of ulcer + there's a considerable lag between ischaemic insult + resting ulcer
103
PRESSURE ULCERS When do they typically occur?
Just prior to or at time of admission
104
PRESSURE ULCERS How rapidly can an existing pressure ulcer develop?
Grade I can progress to deep ulcers over days-weeks without further insult
105
PRESSURE ULCERS What are 4 contributing factors to pressure ulcer development?
- Pressure - Shear - Friction - Moisture
106
PRESSURE ULCERS Explain how pressure causes pressure ulcers.
Capillary pressures >35mmHg compress capillaries + cause ischaemia
107
PRESSURE ULCERS Explain how shear causes pressure ulcers.
Skin pulled away from fixed axial skeleton so blood vessels can be kinked or torn (may occur during lifts or transfers)
108
PRESSURE ULCERS Explain how friction causes pressure ulcers.
Rubbing skin decreases integrity
109
PRESSURE ULCERS Explain how moisture causes pressure ulcers.
Sweat, urine + faeces cause maceration + decrease integrity
110
PRESSURE ULCERS What score is used to screen for risk of pressure ulcer development?
Waterlow score
111
PRESSURE ULCERS What are some risk factors for pressure ulcers?
- Peripheral vascular disease (poor healing, reduced tissue perfusion) - Immobility (#, pain) - Dehydration + malnourishment - Obesity - Incontinence
112
PRESSURE ULCERS What are the different grades for pressure ulcers?
- 0 = skin hyperaemia - 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 - Unstageable = depth unknown, base of ulcer covered by debris
113
PRESSURE ULCERS What are some investigations for pressure ulcers?
- FBC (WCC), cultures - CRP/ESR - Swabs for MC&S if infected - XR for bone involvement (?osteomyelitis)
114
PRESSURE ULCERS How can pressure ulcers be prevented?
- Keep pt as mobile as possible - Repositioning (6h or 4h in high risk) - Pressure redistributing mattress + chair and friction reduction (heel support, cushions) - Barrier creams as moist environment promotes healing - Regular skin assessment
115
PRESSURE ULCERS What is involved in a skin assessment?
- Check for areas of pain + discomfort, skin integrity at pressure areas - Colour changes - Variations in heat, firmness + moisture (incontinence, oedema, dry/inflamed skin)
116
PRESSURE ULCERS What is the management of pressure ulcers?
- Pain relief - Refer to tissue viability nurse - Empirical Abx then matched with sensitivities if signs of infection - Wound dressing (gels to soften, hydrogels often seaweed based for cavities) - Debridement with scalpel, maggots or topical streptokinase for grade 3/4
117
MALNUTRITION What is malnutrition?
- State in which a deficiency of energy, protein ± other nutrients causes measurable adverse effects on the body's form, composition, function + clinical outcome
118
MALNUTRITION What patients are at risk of malnutrition?
- Eaten little/nothing for >5d (or likely to do so) - Poor absorptive capacity - High nutrient losses - Increased nutritional needs from causes such as catabolism
119
MALNUTRITION What are the 3 broad categories of causes of malnutrition?
- Inadequate nutritional intake - Increased nutrient requirements - Inability to utilise ingested nutrients (malabsorption) (Or a combination)
120
MALNUTRITION What can cause inadequate nutrient intake?
Reduced appetite, pain, dysphagia, starvation, unfamiliar foods, mood
121
MALNUTRITION What can cause increased nutrient requirements?
Infection/wound healing, cancer, sepsis, surgery, trauma, liver disease
122
MALNUTRITION What can cause malabsorption?
- Poor gut absorption (IBD, coeliac), - increased losses from drains + wounds, - D+V, - pancreatic insufficiency
123
MALNUTRITION How is malnutrition defined?
- BMI <18.5kg/m^2 - Unintentional weight loss >10% in last 3–6m - BMI <20kg/m^2 AND unintentional weight loss >5% in last 3–6m
124
MALNUTRITION What investigations would you do in someone with malnutrition?
- U+Es, LFTs + ECG prior to commencing feedings - Serum albumin often marker of nutrition (can be inaccurate)
125
MALNUTRITION What tool should you use on those at risk of malnutrition?
Malnutrition Universal Screening Tool (MUST) on admission
126
MALNUTRITION What are the components of MUST?
- 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)
127
MALNUTRITION What do the MUST scores mean?
- 1 = medium risk (observe, if inadequate set goals to improve intake) - ≥2 = high risk (refer to dietician, set goals to improve intake)
128
MALNUTRITION What are some consequences of malnutrition?
- Impaired immunity, wound healing + recovery from illness - More hospital admissions, prolonged stays + refeeding syndrome - Loss of muscle mass (falls, more chest infections, decreased mobility) - Micronutrient deficiencies (selenium, zinc, Fe anaemia, vitamin D = osteomalacia)
129
MALNUTRITION What is the impact of the consequences from malnutrition?
- Lead to poorer prognosis - Reduced QOL - Greater healthcare needs
130
MALNUTRITION What is the overall principle for the management of malnutrition?
- Food first – if the gut works, use it - Snacks, nourishing drinks, food fortification (add full-fat cream to mashed potato)
131
MALNUTRITION What is the second line management of malnutrition? What are they? Who overviews this care and what is their role?
- Oral nutritional supplements (ONS) - Liquid/powder/semi-solid with macro + micronutrients (milkshake, semi-solid, soup) - Registered dietician Ax to take into account nutritional requirements, taste + texture preferences, suitability (vegan, halal), volume consideration (fluid restriction), cost into account > tailored prescription
132
MALNUTRITION What is the second line management of malnutrition?
- Oral nutritional supplements (ONS) - Liquid/powder/semi-solid with macro + micronutrients (milkshake, semi-solid, soup)
133
MALNUTRITION What is the role of a dietician?
- Only qualified HCP that assesses, Dx + Tx nutritional + dietary issues - Advice on therapeutic diets, appropriate feeding methods, identifies + advises on managing refeeding syndrome
134
MALNUTRITION If ONS fails, what two options for feeding are there and what is the difference?
- Enteral feeding = direct feeding into gut via tube in the stomach, duodenum or jejunum - Parenteral feeding = IV access (often peripheral inserted central catheter, PICC line or central line) where gut feeding is inaccesible or unable to absorb sufficient nutrients
135
MALNUTRITION What are the 4 different types of enteral feeding?
- Nasogastric tube = feeds into the stomach, can be inserted at ward level, short-term use (<30d) - Nasojejunal tube = feeds into jejunum, radiologically guided, short-term (<60d) - Percutaneous endoscopic gastrostomy (PEG) = long-term enteral nutrition - Post-pyloric/percutaneous endoscopic jejunostomy = long-term enteral nutrition
136
MALNUTRITION How do you confirm NG tube position on insertion?
- Check pH aspirate to (<5.5), - XR confirmation second line
137
MALNUTRITION How do you confirm NJ tube position on insertion?
Can't check using pH requires XR
138
MALNUTRITION What are the indications for PEG?
- Dysphagia (stroke, head + neck surgery, neuro conditions) - Cystic fibrosis (high nutritional requirements) - Oral nutrition intake inadequate + likely long-term
139
MALNUTRITION What are the indications for PEJ/surgical JEJ?
- Delayed gastric emptying - Upper GI/pancreatic surgery - High risk of aspiration or severe acute pancreatitis
140
MALNUTRITION What are the advantages of enteral feeding?
- Preserves gut mucosa + integrity (NG/NJ), - improves nutritional status, - inexpensive compared to parenteral nutrition
141
MALNUTRITION What are the disadvantages of enteral feeding?
- Tolerance (nausea, satiety, bowels both constipation + diarrhoea), - tube can be uncomfortable to place, - reduced QOL - appearance issues
142
MALNUTRITION What are the indications for parenteral feeding?
- Inadequate absorption (short bowel syndrome) - GI fistula - Bowel obstruction - Prolonged bowel rest - Severe malnutrition - Significant weight loss ± hypoproteinaemia when enteral therapy not possible
143
MALNUTRITION What are the advantages of parenteral feeding?
- Easily tolerated
144
MALNUTRITION What are the disadvantages of parenteral feeding?
- Risk of line infection, - expensive - invasive procedure
145
OSTEOPOROSIS What is osteoporosis?
- Systemic skeletal disease characterised by low bone mass + micro-architectural deterioration of bone tissue with consequent increase in bone fragility + susceptibility to fracture
146
OSTEOPOROSIS What are 2 factors that are important in determining likelihood of an osteoporotic fracture?
- Propensity to fall leading to trauma - Bone strength
147
OSTEOPOROSIS What makes up bone strength?
- Bone mineral density - Bone size - Bone micro-architecture - Bone mineralisation
148
OSTEOPOROSIS What happens to the bone micro-architecture in osteoporosis?
- Trabecular thickness decreases, especially in the horizontal plane, meaning fewer connections between trabecular + so overall decrease in trabecular strength
149
OSTEOPOROSIS What is the pathophysiology of osteoporosis?
- Imbalance between modelling + resorption - Inadequate formation of new bone during remodelling occurs - Excessive bone resorption (PTH can trigger this as RANK-ligand binds to RANK activating osteoclasts)
150
OSTEOPOROSIS What are 2 important components in calcium homeostasis?
- Vitamin D - Parathyroid hormone (PTH)
151
OSTEOPOROSIS What is the role of vitamin D?
- Increased Ca2+ absorption in gut + released from bone
152
OSTEOPOROSIS What is the role of PTH?
- Released from chief cells of parathyroid gland in response to low serum Ca2+ detected by Ca2+ sensor cells - Increased osteoclast activity, increased intestinal Ca2+ absorption, vitamin D activation + renal tubule reabsorption of Ca2+
153
OSTEOPOROSIS What are 2 important factors in osteoporosis development/primary causes?
- Increasing age - Post-menopause as oestrogen is protective
154
OSTEOPOROSIS What are the secondary causes/risk factors for osteoporosis?
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
155
OSTEOPOROSIS What is the clinical presentation of osteoporosis?
- Develops asymptomatic where # often first sign at common sites - Distal radius = Colles' # (fall on outstretched arms) - Proximal femur (neck of femur) - Vertebrae leading to shorter + stooped posture (lumbar, thoracic > kyphosis aka widow's stoop) - Hip
156
OSTEOPOROSIS What investigations would you do in someone suspected of osteoporosis?
- FBC, U+Es, TFTs, LFTs, biochemistry (Ca2+, phosphate, ALP + PTH all normal) - XR will show # (spinal = vertebral crush #) - Dual-energy x-ray absorptiometry (DEXA) scan gold standard to look at bone mineral density
157
OSTEOPOROSIS What does a DEXA scan look at? What 2 scores are generated?
- Lumbar spine + hip as commonly affected areas - T-score = standard deviation comparing how much higher/lower the patient's bone density is to bone density of healthy 30y/o - Z-score compares bone condition to others of their demographics
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OSTEOPOROSIS What DEXA T-scores are significant?
≤ -2.5 = osteoporosis (+ current fragility # = severe) -2.5 < T-score ≤ -1 = osteopenia (low bone mass) -1 < T-score < 1 = healthy
159
OSTEOPOROSIS What risk score can be calculated?
- FRAX
160
OSTEOPOROSIS What does the FRAX score tell you?
- 10-year probability of fragility # (hip, major osteoporotic) for patients aged 40–90
161
OSTEOPOROSIS What factors are assessed in the FRAX score?
- Personal = age, sex, weight, height - PMH = RA, previous #, secondary osteoporosis (renal/liver disease, coeliac, thyroid issues) - DH = glucocorticoids, lithium - FHx = parental hip # - Social = smoking, alcohol (≥3 drinks/day) - Other = femoral neck BMD
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OSTEOPOROSIS What is the management of the various FRAX score outcomes?
- Low risk = reassure, lifestyle, follow up in 5y - Intermediate = offer DEXA scan + Rx if appropriate - High risk = Rx
163
OSTEOPOROSIS What is the overall management of fragility fractures?
- Any patient should have calcium + vitamin D supplementation as well as bisphosphonate regardless of biochemistry as usually normal anyway
164
OSTEOPOROSIS What is the lifestyle advice for osteoporosis management?
- Quit smoking + alcohol - Weight-bearing exercise may increase BMD (walk) - Calcium + vitamin D rich diet + supplements (AdCal-D3) - Balance exercises to reduce risk of falls (tai chi)
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OSTEOPOROSIS What pharmacological management is there for osteoporosis?
- Bisphosphonates first line (alendronate) - Denosumab (s/c 6/12) human monoclonal antibody to RANK-ligand to increase BMD - HRT in early post-menopausal women - Teriparatide (recombinant human parathyroid peptide)
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OSTEOPOROSIS What are the benefits of HRT?
- Reduces # risk, - stops bone loss - prevents menopausal symptoms
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OSTEOPOROSIS What are the risks of HRT?
- Increased risk of breast cancer, stroke, CV disease + VTE
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OSTEOPOROSIS What is an alternative to HRT?
- Selective oestrogen-receptor modulators (SERMs) like raloxifene - Less breast cancer risk as stimulates oestrogen receptors just on bone
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OSTEOPOROSIS How do bisphosphonates, denosumab, HRT + SERMs compare to teriparatide?
- First lot are anti-resorptive meds which inhibits osteoclast activity + bone turnover - Teriparatide is anabolic which increases osteoblast activity + bone formation
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OSTEOPOROSIS Give some examples of bisphosphonate regimes
- PO 70mg alendronate once weekly - PO 35mg risedronate once weekly - IV 5mg zoledronate once yearly
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OSTEOPOROSIS What is the mechanism of action of bisphosphonates?
- Analogues of pyrophosphate, a molecule which decreases demineralisation in bone - Inhibit osteoclasts by reducing recruitment + promoting apoptosis
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OSTEOPOROSIS What are some important instructions to patients taking bisphosphonates?
- Take on empty stomach with plenty of water - Stay upright (sitting/standing for 30m)
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OSTEOPOROSIS What are some adverse effects of bisphosphonates?
- Reflux + oesophagitis - Osteonecrosis of jaw - Atypical stress # (proximal femoral shaft)
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OSTEOPOROSIS When should bisphosphonates be reviewed?
- After 5y on PO or 3y on IV
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OSTEOPOROSIS What is the process of reviewing bisphosphonates?
- Reassess prescription, - update FRAX score + DEXA scan
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OSTEOPOROSIS When should bisphosphonates be stopped?
- Consider holiday (18m-3y) if BMD improved + no fragility fractures
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OSTEOPOROSIS What factors would make you have to continue bisphosphonate treatment?
- On steroids - >75y - Previous hip/vertebral # or further # on Rx - High risk FRAX - DEXA T score -2.5 or less after Rx
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PHARMACOLOGY What is the mechanism of action of acetylcholinesterase inhibitors?
- Increase ACh as ACh is depleted in Alzheimer's to slow disease progression + aid cognitive issues
179
PHARMACOLOGY Give some examples of acetylcholinesterase inhibitors
Donepezil, rivastigmine
180
PHARMACOLOGY What are the side effects of acetylcholinesterase inhibitors?
- D+V, - nausea, - abdo pain (work systemically so GI upset) - bradycardia
181
PHARMACOLOGY What is the mechanism of action of N-methyl D receptor antagonists (NMDA)?
- Protects brain cells from excess glutamate (excitatory neurotransmitter) released from cells affected by Alzheimer's to prevent further damage, good for agitation + BPSD
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PHARMACOLOGY Give an example of NMDA?
- Memantine
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PHARMACOLOGY What are some side effects of NMDA?
- Confusion, - hallucinations, - agitation, - paranoid delusions
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PHARMACOLOGY When should NMDA be avoided?
Do not give in renal failure (low GFR) as nephrotoxic
185
INCONTINENCE What is incontinence?
- Involuntary leakage of urine/faeces at a time which is not socially acceptable
186
INCONTINENCE What are some causes of incontinence?
- MS - Stroke - Parkinson's - Spinal trauma - Cauda equina/cord compression - Brian tumour - Normal pressure hydrocephalus
187
INCONTINENCE What investigations would you do for incontinence?
- Urine MC&S for infections - MRI spine of ?cord compression - MRI head if ?MS or Parkinson's - Treat underlying cause if find one
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INCONTINENCE What is the management of incontinence?
- Pads, intermittent self-catheterisation or indwelling catheter - Permanent catheter if spinal cord damage/paralysis, surgery option if severe
189
URINARY RETENTION What is urinary retention?
- Inability to empty the bladder due to obstruction or decreased detrusor power
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URINARY RETENTION What are some causes of urinary retention?
- BPH (#1 cause in men) - Urethral strictures - Anticholinergics - Alcohol - Constipation - Infection - Cancer
191
URINARY RETENTION How does acute urinary retention present?
- Inability to pass urine, elderly may become agitated - Bladder tender on abdo exam - Contains around 600ml urine
192
URINARY RETENTION How does chronic urinary retention present?
- More insidious onset, often painless - Bladder capacity may be >1.5L - Can present with overflow incontinence, acute-on-chronic retention, lower abdo mass, UTI or renal failure
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URINARY RETENTION What might you find on clinical examination in urinary retention?
- Abdo = palpate + percuss bladder to assess extent of retention + if tender - PR = ?enlarged prostate, check tone for ?cauda equina
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URINARY RETENTION What other investigations would you do in urinary retention?
- FBC, U+E, CRP/ESR, LFTs, TFTs, PSA - Urine MC&S for infections - CT if concerned about cancer
195
URINARY RETENTION What is the conservative management of urinary retention?
(Tips to aid voiding) - Analgesia - Walk around - Stand to void - Sound of running water - Hot bath
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URINARY RETENTION What other management is there for urinary retention?
- Catheterise acutely with ?intermittent self-catheterisation at home needed - Alpha-blocker tamsulosin to relax muscles in bladder neck making easier to urinate (+ effect on prostate for BPH)
197
END OF LIFE CARE What is palliative care?
- Holistic management of a pt in whom death is likely to be soon + where curative treatment no longer possible
198
END OF LIFE CARE What are the aims of palliative care?
Help pt + relatives come to terms with death whilst optimising the quality of time left
199
END OF LIFE CARE What does palliative care involve?
MDT approach – physical Sx relief, social, psychological, spiritual + family support
200
END OF LIFE CARE What care should be given to an end of life patient?
- Basic care ALWAYS (warmth, comfort, shelter, freedom from pain, cleanliness, PO nutrition + hydration) - Artificial nutrition + hydration is considered treatment so may be withheld - Simplify meds, s/c if possible - Communication v important
201
END OF LIFE CARE How does a patient at the end of their life present?
- Sleepy, agitated, drifting in/out consciousness, confusion - Change in breathing pattern or dyspnoea - Decreased need for food + fluids - Loss of bladder or bowel control - Cold/bluish extremities, mottled skin - Death rattle
202
END OF LIFE CARE What is the death rattle? Is this dangerous?
- Reduced ability to clear saliva + mucous from back of throat + hypersecretion leading to noisy airway - No, not painful or uncomfortable
203
END OF LIFE CARE How is the death rattle managed?
- Hyoscine butylbromide if distressing
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END OF LIFE CARE What issues presenting at the end of life can be managed pharmacologically?
- Pain - Dyspnoea - Agitation + anxiety - Nausea - Constipation
205
END OF LIFE CARE In terms of managing end of life care, what should be given for regular medication?
Syringe driver
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END OF LIFE CARE In terms of managing end of life care, what should be given for pain + dyspnoea?
Morphine or oxycodone
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END OF LIFE CARE In terms of managing end of life care, what should be given for agitation, anxiety, or dyspnoea?
Midazolam
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END OF LIFE CARE In terms of managing end of life care, what should be given for nausea or agitation?
Haloperidol (other anti-emetics can be used like ondansetron)
209
END OF LIFE CARE In terms of managing end of life care, what should be given for constipation?
Start with stimulant laxative (senna) as opiates decrease peristalsis or stool softener if not on opiates, if not suppositories, enemas, PR evacuation
210
BPPV what is benign paroxysmal positional vertigo (BPPV)?
Benign paroxysmal positional vertigo (BPPV) is a peripheral vestibular disorder that manifests as sudden, short-lived episodes of vertigo elicited by specific head movements
211
BPPV what is the pathophysiology?
- calcium deposits (canaliths) floating in the semicircular canals which activates the vesticulo-ocular reflex
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BPPV what are the causes?
50-70% = primary (idiopathic) secondary - head trauma - labyrinthitis - vestibular neuronitis - Meniere's disease - migraines
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BPPV what are the investigations?
- clinical exam - full cranial nerve exam + otoscope - Dix-hallpike manoeuvre = diagnostic - head turned 45 degrees then lie back and flex neck 30 degrees - positive = nystagmus triggered by movement
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BPPV what is the management?
- patient education and reassurance - repositioning manoeuvres - 3 position particular repositioning manoeuvre (PRM) - if manoeuvres are ineffective surgery may be helpful
215
HEART FAILURE what is it?
Inability of the heart to deliver blood and thus oxygen at a rate that is commensurate with the requirements of the body
216
HEART FAILURE what are the different categories of heart failure?
1. Systolic failure = ability of heart to pump blood around the body is impaired 2. Diastolic failure = inability of ventricles to relax and fill fully 3. Acute failure = New onset acute or decompensation of chronic. 4. Chronic heart failure = Develops/progresses slowly and arterial pressure is well maintained until late
217
HEART FAILURE what are the risk factors for heart failure?
1. >65 y/o 2. African descent 3. Men 4. Obesity 5. Previous MI
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HEART FAILURE Why are men more commonly effected by heart failure than women?
Women have 'protective hormones' meaning they are less at risk of developing HF
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HEART FAILURE what is the pathophysiology?
When the heart fails, compensatory mechanisms attempt to maintain CO As HF progresses, these mechanism are exhausted and become pathophysiological
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HEART FAILURE What are the compensatory mechanisms in heart failure?
1. Sympathetic system 2. RAAS 3. Natriuretic peptides 4. Ventricular dilation 5. Ventricular hypertrophy
221
HEART FAILURE Explain how the sympathetic system is compensatory in heart failure and give one disadvantage of sympathetic activation
Improves ventricular function by increasing HR and contractility = CO maintained BUT it also causes arteriolar constriction which increases afterload and so myocardial work
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HEART FAILURE Explain how the RAAS system is compensatory in heart failure and give one disadvantage of RAAS activation
Reduced CO leads to reduced renal perfusion, this activates RAAS --> increased fluid retention so increased preload BUT it also causes arteriolar constriction which increase afterload and so myocardial work
223
HEART FAILURE Give 3 properties of natriuretic peptides that make them compensatory in heart failure
1. Diuretic 2. Hypotensive 3. Vasodilators
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HEART FAILURE What are the 3 cardinal symptoms of heart failure?
1. SOB 2. Fatigue 3. Peripheral oedema
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HEART FAILURE what are the clinical signs of left heart failure?
1. Pulmonary crackles 2. S3 and S4 and murmurs 3. Displaced apex beat 4. Tachycardia 5. fatigue
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HEART FAILURE what are the clinical features of right HF?
1. Raised JVP 2. Ascites 3. peripheral oedema
227
HEART FAILURE what are the clinical features of heart failure?
SOFA PC - shortness of breath - orthopnea - fatigue - ankle swelling - pulmonary oedema (due to backflow from decreased CO; produced cough with pink frothy sputum) - cold peripheries Raised JVP End respiratory crackles
228
HEART FAILURE What investigations might you do initially do in someone who you suspect has HF?
1. ECG 2. CXR 3. BNP - brain natriuretic peptide
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HEART FAILURE What 4 signs might you see on a CXR taken from someone with HF?
ABCDE A - alveolar oedema (bat wing shadowing) B - Kerley B lines C - cardiomegaly D - dilated upper lobes E - effusions (pleural)
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HEART FAILURE You have done an ECG, CXR and blood tests on a patient who you suspect might have HF. These have come back abnormal. What investigation might you do next?
An echocardiogram - may reveal cause
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HEART FAILURE what is the management for chronic HF?
1st line = ACEi, beta blocker 2nd = ARB + nitrate 3rd = cardiac resynchronization or digoxin 4th = diuretics (furosemide) 5th = aldosterone antagonist (spironolactone)
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HEART FAILURE what is the treatment for acute HF?
OMFG - oxygen - morphine - furosemide - GTN spray
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HEART FAILURE How can chronic HF be prevented?
Stop smoking Eat more healthy Exercise Avoid large meals Vaccinations Treat underlying cause - dysarrhythmias or valve disease
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CONSTIPATION what are the primary and secondary causes?
Primary - disordered regulation of colonic and anorectal neuromuscular function - IBS Secondary - metabolic - hypercalcaemia, hypothyroidism - medicines - opiates, CCBs, antipsychotics - neurological disorders - parkinsons, spinal cord lesions, DM - bowel diseases - cancer, stricture, anal fissure
235
CONSTIPATION what are the red flag symptoms?
Rectal bleeding Haem-positive stool Weight loss Obstructive symptoms Recent onset of symptoms Rectal prolapse Change in stool calibre Age >50 years.
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CONSTIPATION what are the investigations?
- history of bowel habits, consistency - abdominal exam - look for tenderness - DRE - bloods - FBC, U+Es, TFTs, glucose - abdominal x-ray
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CONSTIPATION what is the management?
- treatment of underlying cause - increased dietary fibre - increased fluid intake - exercise - bulk laxatives - stool softeners - osmotic laxatives - lactulose, macrogol
238
SQUAMOUS CELL CARCINOMA OF THE SKIN what is it?
Squamous cell carcinoma is a common variant of skin cancer. Metastases are rare but may occur in 2-5% of patients.
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SQUAMOUS CELL CARCINOMA OF THE SKIN what are the risk factors?
- excessive exposure to sunlight / psoralen UVA therapy - actinic keratoses and Bowen's disease - immunosuppression e.g. following renal transplant, HIV - smoking - long-standing leg ulcers (Marjolin's ulcer) - genetic conditions e.g. xeroderma pigmentosum, oculocutaneous albinism
240
SQUAMOUS CELL CARCINOMA OF THE SKIN what are the clinical features?
- typically on sun-exposed sites such as the head and neck or dorsum of the hands and arms - rapidly expanding painless, ulcerate nodules - may have a cauliflower-like appearance - there may be areas of bleeding
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SQUAMOUS CELL CARCINOMA OF THE SKIN what is the management?
Surgical excision with 4mm margins if lesion <20mm in diameter. If tumour >20mm then margins should be 6mm.
242
SQUAMOUS CELL CARCINOMA OF THE SKIN what factors indicate a good progrosis?
- well differentiated tumours - <20mm diameter - <2mm deep - no associated diseases
243
SQUAMOUS CELL CARCINOMA OF THE SKIN what factors indicates a poor prognosis?
- poorly differentiated tumours - >20mm in diameter - >4mm deep - immunosuppression for whatever reason
244
COTE ASSESSMENT What is frailty?
- 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
245
COTE ASSESSMENT What is the impact of frailty?
- Poor functional reserve (trivial insult to young person = large impact in elderly) - Vulnerable to decompensation when faced with illness, drug SEs + metabolic disturbance - Different type of doctor (geriatricians) - Failure to integrate responses in the face of stress
246
COTE ASSESSMENT What is acopia?
- Social admission – non-specific presentation, not a Dx just describes a patient unable to cope with ADLs - High mortality rate, vast majority have medical pathology.
247
COTE ASSESSMENT What are the geriatric giants? What do they represent?
``` 4Is – - Instability (falls) - Immobility - Intellectual impairment (confusion) - Incontinence They are not diagnoses but more general things that COTE pts present with, often indicator of underlying problem ```
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COTE ASSESSMENT What are the geriatric 5Ms?
- Mind = dementia, delirium, depression - Mobility = impaired gait + balance, falls - Medications = polypharmacy, medication burden, adverse effects, de-prescribing/optimal prescribing - Multi-complexity = multi-morbidity, biopsychosocial - Matters most = individual meaningful health outcomes + preferences
249
COTE ASSESSMENT What is a comprehensive geriatric assessment? What does it focus on? Who is part of the geriatric MDT?
- Multidimensional, MDT diagnostic process in geriatrics. - Determining a frail older person's medical, psychological + functional capability - Geriatrician, social worker, physio, OT, SALT, nurse etc.
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COTE ASSESSMENT What is the role of the comprehensive geriatric assessment? What is the process?
- Development of a coordinated, integrated plan for treatment + long-term support - Assessment > problem list > personalised care plan > intervention > regular planned review > assessment etc.
251
COTE ASSESSMENT What are the components of the comprehensive geriatric assessment and who might be involved?
- Medical assessment = Dr, nurse, pharmacist, dietician, SALT - Functional assessment (OT, physio, SALT) - Psychological assessment (Dr, nurse, OT, psychologist) - Social + environmental assessment (OT, social worker)
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COTE ASSESSMENT What is involved in... i) medical assessment? ii) functional assessment? iii) psychological assessment? iv) social + environmental assessment?
i) Problem list, co-morbid conditions + disease severity, med review, nutritional status ii) ADLs, activity/exercise status, gait + balance iii) Cognitive status testing, mood testing (PHQ-9) iv) Informal support needs + assets, eligibility or need for carers, home safety
253
COTE ASSESSMENT What is rehabilitation?
- Process of restoring a patient to maximum function (need to know pre-morbid function), can happen in variety of settings, involves MDT
254
POLYPHARMACY What is pharmacodynamics? How does this change for the elderly?
- What the DRUG does to the BODY | - In elderly, effects of similar drug conc. may be different to younger so prone to adverse drug reactions
255
POLYPHAMRACY What is pharmacokinetics? How does this change for the elderly?
- What the BODY does to the DRUG - Changes in absorption, distribution, metabolism + excretion of drugs - May mean drugs hang around longer or elderly pts may experience more toxicity from smaller dose
256
POLYPHARMACY Give some specific pharmacokinetic issues in geriatrics.
- Hepatic first pass metabolism declines - Reduced absorption as gastric pH increases due to atrophy - Vascular system less responsive due to calcification of vessels
257
POLYPHARMACY Why might inappropriate drug use occur in geriatrics?
- May not understand instructions - May be unable to read instructions - May make own interpretation of instructions - Could be due to lack of treatment supervision
258
POLYPHARMACY What is polypharmacy? Why are geriatric patients at increased risk?
- Concurrent use of multiple medications by one person (some studies label >5) - Higher rates of chronic illness so more likely to have multiple meds
259
POLYPHARMACY What is multimorbidity?
- ≥2 chronic conditions, often long-term requiring ongoing care.
260
POLYPHARMACY What are some potential problems with polypharmacy?
- Drug interactions + increased SEs - Can affect compliance + lead to decreased pt satisfaction - Pill burden
261
POLYPHARMACY What is appropriate polypharmacy? What can this lead to?
- Prescribing multiple medications for either a complex condition or multiple conditions where medicine has been optimised - Can extend life expectancy + improve QOL
262
POLYPHARMACY What is problematic polypharmacy? How can this be prevented?
- Multiple medications prescribed inappropriately, increasing the risk of SEs - MDT case conferences, computerised support systems, pharmacists
263
POLYPHARMACY What are the reasons for problematic polypharmacy?
- Multimorbidity (increased prevalence with increasing age) - Incremental prescribing (prescribing cascade) = prescribers may not recognise Sx iatrogenic so prescribe more meds to counter SEs of other drugs - End-of-life considerations
264
POLYPHARMACY What is the impact of adverse drug reactions? What specific issue can this impose in geriatrics?
- Increasing fragility means reduced ability to cope with ADRs - May go unnoticed as Sx mimic problems associated with elderly (forgetfulness, weakness, tremor)
265
POLYPHARMACY What are some common adverse drug reactions in geriatrics?
- Falls (postural hypotension with ACEi, beta-blockers) - Confusion (sedation with anticholinergics) - Bowel problems (opioids, PPIs)
266
MENTAL CAPACITY ACT What is the purpose of the Mental Capacity Act, 2005?
- Empower + protect people >16y who lack capacity to make their own decisions about their care + treatment since 1/10/07
267
MENTAL CAPACITY ACT What is the two-step test in MCA?
- 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?
268
MENTAL CAPACITY ACT What are the 4 aspects of assessing capacity?
- 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)
269
MENTAL CAPACITY ACT What are the 5 principles underpinning the MCA?
- Assume capacity until proven otherwise - Maximise decision-making capacity (all practical support to help them make decision given) - Freedom to make seemingly unwise choice (unwise decision ≠ incapacity) - All decisions on behalf of patient in best interests - Least restrictive option should be chosen
270
MENTAL CAPACITY ACT What are some important considerations about a person's capacity status?
- Can fluctuate with time (temporary cognitive impairment like delirium) - Decision specific so may have capacity for some decisions, do not just completely write off
271
MENTAL CAPACITY What is an independent mental capacity advocate (IMCA)?
- Commissioned from independent organisations by the NHS + local authorities to ensure MCA followed
272
MENTAL CAPACITY What is the role of an IMCA?
- Support + represent people who lack capacity + do not have anyone else to represent them in major decision (serious Tx) - Have authority to make enquiries about pt + contribute to decision by representing the patient's interests but cannot make a decision on their behalf
273
BEST INTERESTS What are some important considerations when making best interest decisions?
- Encourage participation of the patient wherever possible - Find out person's views (past + present wishes, feelings, beliefs + values) - Avoid discrimination (don't make assumptions on any personal features) - Regaining capacity (can the decision wait?) - Identify all relevant circumstances to identify what they would have taken into account if they were making this decision
274
BEST INTERESTS Who would you consult when making best interest decisions?
- Anyone previously named by the individual - Anyone engaged in caring for them - Close relatives + friends - Any appointed attorney or deputy appointed by Court of Protection
275
DOLS What is a deprivation of liberty safeguard, DoLS (new name Liberty Protection Safeguards)?
- Amendment of MCA with aim to protect people in care homes + hospitals from being inappropriately deprived of their liberty, meaning safeguards have been put in place to make sure someone's liberty is only restricted safely + correctly
276
DOLS When is a DoLS required?
- When a person does not or cannot consent to care or treatment but are having it anyway (dementia pt not free to leave ward + lacks capacity to consent to this)
277
DOLS What is the acid test for DoLS?
Must meet 3 criteria – - Lack of capacity to consent to the arrangements or their care - Subject to continuous supervision + control - Not free to leave their care setting
278
DOLS How should a DoLS be attained? What are the limitations of an urgent DoLS?
- Officially verified by local DoLS team apart from an urgent DoLS which can be executed without prior formal authorisation - Only if in best interests, up to 7d + must be least restrictive alternative to preventing harm
279
ADVANCED CARE PLANNING What is an advanced directive?
- Written statement that sets down a person's preferences, wishes, beliefs + values regarding their future care
280
ADVANCED CARE PLANNING What are the roles of an advanced directive?
- Aims to provide guide for anyone who might make decisions in their best interests when they lose capacity - Allows people who understand implications of their choices to state wishes in advance
281
ADVANCED CARE PLANNING What can an advanced directive include?
- Where they would like to be cared for (home, nursing home), concerns about practical issues (who will look after pet if ill) - Can authorise or request specific procedures (Where suitable) - Can refuse treatment in a predefined future situation
282
MEDICO-LEGAL ASPECTS What is an advanced refusal of treatments? Is it legally binding?
- A living will - Yes if: – Adult ≥18y – Was competent + fully informed when made decision – Decision is clearly applicable to current circumstances – No reason to believe changed mind
283
MEDICO-LEGAL ASPECTS What is an advanced requests for treatment? Is it legally binding?
- Patient's wish for treatment - Less legal binding but if it's patient's known wish to be kept alive then reasonable efforts (nutrition, hydration) should be considered
284
LASTING POWER OF ATTORNEY What is a Lasting Power of Attorney (LPA)?
- Document which a person can use to nominate someone else to make certain decisions on their behalf when they are unable to do so themselves whilst they still have capacity
285
LASTING POWERR OF ATTORNEY What are the 2 types of LPA? What is needed for it to be valid?
- Health/welfare LPA = make decisions relating to treatment, discharge destination - Financial LPA = make decisions relating to finances (bank accounts) + property - Must be registered with the Office of the Public Guardian
286
ENDURING POWER OF ATTORNEY What is an enduring power of attorney (EPA)?
Under previous law + was restricted to decisions over property + affairs
287
ABUSE What is abuse?
- Single or repeated act or lack of appropriate action that occurs in a relationship where there is an expectation of trust which causes harm or distress
288
ABUSE How should abuse be managed?
- Avoid asking too many questions – LISTEN - Don't agree to keep secret – duty to report to safeguarding - Do NOT confront abuser
289
COTE ASSESSMENT Is frailty inevitable?
- Not inevitable, not irreversible + not simply due to chronic conditions
290
ABUSE Who may the perpetrator be?
- Family, partner, friends, neighbours, carers, strangers
291
ABUSE What are some types?
- Physical, neglect, psychological, financial, sexual, discriminatory
292
MEDICO-LEGAL ASPECTS What is a court appointed deputy?
Alternative from Court of Protection once the person lacks capacity
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POLYPHARMACY What is the impact of multimorbidity?
- Complexity + restrictions with cross-over of Sx - Medication burden (SEs, drug interactions, monitoring, compliance) - Appt burden - Mental health impact
294
ABUSE what are the signs of possible abuse?
cuts or scrapes broken bones bruises burns dislocated joints head injuries sprains a pattern of hospitalisation for the same/similar injuries delayed medical care poor explanations for injuries
My Phase 3a Revision
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