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GERIATRICS Flashcards

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  • Hypoactive = withdrawn, quiet, lethargic, lacks concentration, slow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
Q

DEMENTIA
What are behavioural + psychological symptoms of dementia (BPSD)?
What causes them?

A
  • Heterogenous group of non-cognitive symptoms + behaviours seen in dementia
  • Same causes as delirium
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26
Q

DEMENTIA
How does behavioural + psychological symptoms of dementia (BPSD) present?

A
  • Anxiety/depression, agitation, psychosis (may think nurses out to get them), disinhibition
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27
Q

DEMENTIA
What is the management of behavioural + psychological symptoms of dementia (BPSD)?

A
  • Exclude/Tx underlying cause,
    similar Mx to delirium (supportive environment, meds last line),
    educate family/carer about Sx + causes
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28
Q

DEMENTIA
What are some general investigations for dementia?

A
  • Full Hx + collateral with full physical exam + MSE
  • Check for reversible causes with confusion screen ± CXR ± CT head
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29
Q

DEMENTIA
What might a MMSE score indicate in dementia?

A

MMSE (/30) –
- 21–26 = mild, 14–20 = mod, 10–14 mod-severe, <10 = severe cognitive impairment

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30
Q

DEMENTIA
What might an Addenbrooke’s cognitive examination III (ACE-III) score indicate in dementia?

A

ACE-III (/100) –
- <82 likely dementia + need abnormal scores in ≥2 domains (attention/orientation, memory, language, visuospatial, fluency)

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31
Q

DEMENTIA
What type of imaging may be used in dementia?

A
  • 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
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32
Q

DEMENTIA
What biological treatment can be used in dementia?

A
  • Bio = risperidone for agitation (apart in Lewy-Body)
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33
Q

DEMENTIA
What psychological treatment can be used in dementia?

A
  • Psycho = CBT for depression, counselling, reminiscence therapy + reality orientation, keep stimulated with puzzles, word searches, activities
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34
Q

DEMENTIA
What social treatment can be used in dementia?

A
  • 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
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35
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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36
Q

ALZHEIMER’S DISEASE
What is the onset of Alzheimer’s disease like and why?

A
  • Insidious onset dementia due to generalised deterioration of the brain
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37
Q

ALZHEIMER’S DISEASE
What neurotransmitters are affected?

A
  • ACh, noradrenaline, serotonin, somatostatin
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38
Q

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

A
  • Unknown but most common type of dementia
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39
Q

ALZHEIMER’S DISEASE
What is the epidemiology?

A
  • > 65y, if <65 then early onset + associated with more rapid decline + FHx
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40
Q

ALZHEIMER’S DISEASE
What condition has increased rates of Alzheimer’s?

A
  • Down’s syndrome (most develop by 50)
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41
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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42
Q

ALZHEIMER’S DISEASE
What are some risk factors for Alzheimer’s?

A
  • CVD = HTN, DM, hypercholesterolaemia, smoking
  • FHx
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43
Q

ALZHEIMER’S DISEASE
What is the clinical presentation of Alzheimer’s

A

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

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44
Q

ALZHEIMER’S DISEASE
On CT/MRI head in Alzheimer’s disease, what are the macroscopic pathological changes?

A

Diffuse cerebral atrophy (shrunken brain), increased sulcal widening, enlarged ventricles

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45
Q

ALZHEIMER’S DISEASE
On CT/MRI head in Alzheimer’s disease, what are the microscopic or histological pathological changes?

A

Neuronal loss, neurofibrillary tangles, beta-amyloid plaques

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46
Q

ALZHEIMER’S DISEASE
What is the management of Alzheimer’s?

A
  • 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
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47
Q

VASCULAR DEMENTIA
What causes vascular dementia?

A
  • Any type of vascular disease affecting blood vessels of brain
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48
Q

VASCULAR DEMENTIA
What are the risk factors?

A
  • CVA/TIA = 9x increased risk of dementia
  • CV = HTN, DM, hypercholesterolaemia, smoking
  • Hx of peripheral vascular disease, IHD
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49
Q

VASCULAR DEMENTIA
What is the clinical presentation of vascular dementia?

A
  • Stepwise deterioration with short periods of stability then suddenly decline
  • Patchier cognitive impairment than Alzheimer’s
  • Focal neuro signs if caused by stroke
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50
Q

VASCULAR DEMENTIA
What would a CT head show in vascular dementia?

A
  • ≥1 areas of cortical infarction (white on CT), may show micro-infarcts
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51
Q

VASCULAR DEMENTIA
What is the management of vascular dementia?

A

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)

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52
Q

LEWY-BODY DEMENTIA
What is the pathophysiology of Lewy-Body dementia?

A
  • Presence of Lewy bodies (protein deposits) in the basal ganglia + cerebral cortex, typically presents between 50–80y
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53
Q

LEWY-BODY DEMENTIA
What might it be confused with?

A
  • Delirium due to fluctuating consciousness + hallucinations
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54
Q

LEWY-BODY DEMENTIA
What condition is Lewy-Body dementia closely associated to?

A
  • Parkinson’s disease (25% of PD patients will develop)
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55
Q

LEWY-BODY DEMENTIA
How can you differentiate between lewy-body dementia and parkinsons disease?

A
  • Dementia before movement signs = Lewy-body dementia
  • Movement before dementia signs = Parkinson’s dementia
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56
Q

LEWY-BODY DEMENTIA
What is the clinical presentation of Lewy-Body dementia?

A
  • 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
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57
Q

LEWY-BODY DEMENTIA
What is the management of Lewy-Body dementia?

A
  • Conservative management
  • AChEi used in mild–mod (rivastigmine 1st line), memantine last resort
  • SENSITIVE to antipsychotics, can make worse + lead to neuroleptic malignant syndrome
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58
Q

FT DEMENTIA
What are 2 common features in frontotemporal (FT) dementia?

A
  • Early personality changes + relative intellectual sparing.
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59
Q

FT DEMENTIA
What are some pathological features of frontotemporal dementia?

A
  • Microscopic = ubiquitin + tau deposits
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60
Q

FT DEMENTIA
What causes FT dementia?

A
  • 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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61
Q

FT DEMENTIA
What are the

i) frontal lobe symptoms
ii) temporal lobe symptoms
iii) generic features

of FT dementia?

A

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

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62
Q

FT DEMENTIA
What are the temporal lobe symptoms of FT dementia?

A

Speech disturbances (progressive non-fluent aphasia, may end up mute), expressive dysphasia

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63
Q

FT DEMENTIA
What are the frontal lobe symptoms of FT dementia?

A

i) Euphoria, disinhibition, personality changes + emotional blunting

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64
Q

FT DEMENTIA
What is the management of FT dementia?

A
  • No specific treatment
  • SSRIs may help behavioural symptoms
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65
Q

MILD COG IMPAIRMENT
What is mild cognitive impairment?

A
  • Cognitive impairment without functional impairment (ADLs minimally affected)
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66
Q

MILD COG IMPAIRMENT
How does it present?

A
  • Reduced fluency + some short-term memory difficulties
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67
Q

MILD COG IMPAIRMENT
How does it progress?

A
  • 1/3rd improve, 1/3rd stable, 1/3rd progress to dementia
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68
Q

FALLS
What is a fall?

A
  • Event that results in unintentionally coming to rest at a lower level, usually the floor
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69
Q

FALLS
What are some neurological causes of falls?

A
  • Stroke
  • PD or other movement disorders (Huntington’s)
  • Visual impairment
  • Peripheral neuropathy or myopathy
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70
Q

FALLS
What are some cardiovascular causes of falls?

A
  • Vasovagal or situational syncope
  • Postural hypotension
  • MI, arrhythmias
  • Dehydration or shock
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71
Q

FALLS
What are some iatrogenic causes of falls?

A
  • BDZs (sedative so impairs coordination)
  • Polypharmacy (combination of drugs + interactions)
  • Anti-hypertensives (ACEi, CCB, beta-blockers, diuretics)
  • Anti-depressants + anti-psychotics
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72
Q

FALLS
What are some power causes of falls?

A
  • Inactivity > muscle weakness
  • Dizziness/loss of balance or proprioception (vertigo)
  • Pain/MS > osteoarthritis
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73
Q

FALLS
What are some environmental causes of falls?

A
  • Loose rugs
  • Pets
  • Furniture
  • Unstable footwear
  • Poor lighting
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74
Q

FALLS
What are some other causes of falls?

A
  • Infection or sepsis
  • Delirium
  • Incontinence
  • Hypoglycaemia
  • Alcohol (intoxication, neuropathy, Korsakoff’s or Wernicke’s)
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75
Q

FALLS
What parts of the history are important when assessing falls?

A
  • Collateral Hx
  • Circumstances (timing, physical environment)
  • Sx before + after fall
  • Previous falls, #, syncope or near misses
  • PMH for co-morbidities
  • Functional performance (assess ADLs)
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76
Q

FALLS
What clinical examinations would you perform?

A
  • CVS (LSBP, HR + rhythm, murmurs esp. AS)
  • MSK (assess footwear, joints for deformity + stiffness)
  • Neuro (identify stroke, peripheral neuropathy, ?Parkinson’s)
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77
Q

FALLS
What clinical scale can be used to assess frailty?

A
  • Rockwood clinical frailty scale (from very fit, vulnerable, moderately frail to terminally ill)
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78
Q

FALLS
What investigations would you do for someone presenting with a fall?

A
  • 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
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79
Q

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

A
  • Pressure ulcers
  • Dehydration
  • Rhabdomyolysis
  • Hypothermia
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80
Q

FALLS
What is rhabdomyolysis?

A
  • Skeletal muscle breakdown due to traumatic, chemical or metabolic injury
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81
Q

FALLS
What can cause rhabdomyolysis?

A
  • Crush injuries
  • Prolonged immobilisation following a fall
  • Prolonged seizures
  • Hyperthermia
  • Neuroleptic malignant syndrome
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82
Q

FALLS
How may rhabdomyolysis present?

A
  • Urine may be dark (‘Coca-Cola urine) + urinalysis +ve to Hb but without RBCs
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83
Q

FALLS
What markers are elevated in rhabdomyolysis?
Is that an issue?

A
  • K+, phosphate, myoglobin + creatinine kinase
  • Myoglobin is nephrotoxic as causes acute tubular necrosis
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84
Q

FALLS
What is the management of rhabdomyolysis?

A
  • Measure U+Es, creatinine, CK levels + monitor urine output
  • Supportive with IV fluids, correct electrolytes, ?temporary dialysis
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85
Q

FALLS
How can falls be prevented in a hospital setting?

A
  • 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
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86
Q

FALLS
How can fall frequency be reduced?

A
  • 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
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87
Q

FALLS
How can adverse consequences from falls be reduced?

A
  • Osteoporosis detection + treatment
  • Alarms such as pullcord or pendant alarms to summon help
  • Supervision via visits from carers, family, neighbours
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88
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 + send signals to brain to signal heart to beat faster, pump more blood, cause vasoconstriction + stabilise BP
  • In postural hypotension, something interrupts this mechanism
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89
Q

POSTURAL HYPOTENSION
What are some iatrogenic causes of postural hypotension?

A

Diuretics, anti-hypertensives, antidepressants, polypharmacy

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90
Q

POSTURAL HYPOTENSION
What are some cardiac causes of postural hypotension?

A

Aortic stenosis, arrhythmias, MI, cardiomyopathy, anaemia, CHF

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91
Q

POSTURAL HYPOTENSION
What are some endocrine causes of postural hypotension?

A

DM, hypoadrenalism, hypothyroidism

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92
Q

POSTURAL HYPOTENSION
What are some neuro causes of postural hypotension?

A

PD + PD+ syndromes

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93
Q

POSTURAL HYPOTENSION
What are some other causes of postural hypotension?
How common is it?

A
  • Blood loss, dehydration + shock
  • Occurs in 30% of patients >70y
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94
Q

POSTURAL HYPOTENSION
How may postural hypotension present?

A
  • Postural light-headedness, dizziness, blurred vision
  • Weakness, fatigue, palpitations + headache may be present
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95
Q

POSTURAL HYPOTENSION
What are these patients at risk of?

A

Risk of falls + syncope, CV disease or stroke

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96
Q

POSTURAL HYPOTENSION
What investigations would you do to diagnose postural hypotension?

A

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)

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97
Q

POSTURAL HYPOTENSION
What is the conservative management of postural hypotension?

A
  • Drinks lots of water
  • Avoid alcohol
  • Compression garments (stockings)
  • Stand slowly, elevating head of the person’s bed
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98
Q

POSTURAL HYPOTENSION
What is the pharmacological management of postural hypotension?

A
  • 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
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99
Q

PRESSURE ULCERS
What is an ulcer?

A
  • Open sore caused by a break in the skin or mucous membrane which fails to heal
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100
Q

PRESSURE ULCERS
What is a pressure ulcer?

A

Areas of skin necrosis due to pressure-induced ischaemia

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101
Q

PRESSURE ULCERS
Where would you commonly find a pressure ulcer?

A

Sacrum, heels, greater trochanters, shoulders

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102
Q

PRESSURE ULCERS
How rapidly can a new pressure ulcer develop?

A
  • 2h of tissue ischaemia sufficient for subsequent development of ulcer + there’s a considerable lag between ischaemic insult + resting ulcer
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103
Q

PRESSURE ULCERS
When do they typically occur?

A

Just prior to or at time of admission

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104
Q

PRESSURE ULCERS
How rapidly can an existing pressure ulcer develop?

A

Grade I can progress to deep ulcers over days-weeks without further insult

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105
Q

PRESSURE ULCERS
What are 4 contributing factors to pressure ulcer development?

A
  • Pressure
  • Shear
  • Friction
  • Moisture
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106
Q

PRESSURE ULCERS
Explain how pressure causes pressure ulcers.

A

Capillary pressures >35mmHg compress capillaries + cause ischaemia

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107
Q

PRESSURE ULCERS
Explain how shear causes pressure ulcers.

A

Skin pulled away from fixed axial skeleton so blood vessels can be kinked or torn (may occur during lifts or transfers)

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108
Q

PRESSURE ULCERS
Explain how friction causes pressure ulcers.

A

Rubbing skin decreases integrity

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109
Q

PRESSURE ULCERS
Explain how moisture causes pressure ulcers.

A

Sweat, urine + faeces cause maceration + decrease integrity

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110
Q

PRESSURE ULCERS
What score is used to screen for risk of pressure ulcer development?

A

Waterlow score

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111
Q

PRESSURE ULCERS
What are some risk factors for pressure ulcers?

A
  • Peripheral vascular disease (poor healing, reduced tissue perfusion)
  • Immobility (#, pain)
  • Dehydration + malnourishment
  • Obesity
  • Incontinence
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112
Q

PRESSURE ULCERS
What are the different grades for pressure ulcers?

A
  • 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
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113
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)
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114
Q

PRESSURE ULCERS
How can pressure ulcers be prevented?

A
  • 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
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115
Q

PRESSURE ULCERS
What is involved in a skin assessment?

A
  • Check for areas of pain + discomfort, skin integrity at pressure areas
  • Colour changes
  • Variations in heat, firmness + moisture (incontinence, oedema, dry/inflamed skin)
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116
Q

PRESSURE ULCERS
What is the management of pressure ulcers?

A
  • 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
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117
Q

MALNUTRITION
What is malnutrition?

A
  • State in which a deficiency of energy, protein ± other nutrients causes measurable adverse effects on the body’s form, composition, function + clinical outcome
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118
Q

MALNUTRITION
What patients are at risk of malnutrition?

A
  • 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
Q

MALNUTRITION
What are the 3 broad categories of causes of malnutrition?

A
  • Inadequate nutritional intake
  • Increased nutrient requirements
  • Inability to utilise ingested nutrients (malabsorption)
    (Or a combination)
120
Q

MALNUTRITION
What can cause inadequate nutrient intake?

A

Reduced appetite,
pain,
dysphagia,
starvation,
unfamiliar foods,
mood

121
Q

MALNUTRITION
What can cause increased nutrient requirements?

A

Infection/wound healing,
cancer,
sepsis,
surgery,
trauma,
liver disease

122
Q

MALNUTRITION
What can cause malabsorption?

A
  • Poor gut absorption (IBD, coeliac),
  • increased losses from drains + wounds,
  • D+V,
  • pancreatic insufficiency
123
Q

MALNUTRITION
How is malnutrition defined?

A
  • 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
Q

MALNUTRITION
What investigations would you do in someone with malnutrition?

A
  • U+Es, LFTs + ECG prior to commencing feedings
  • Serum albumin often marker of nutrition (can be inaccurate)
125
Q

MALNUTRITION
What tool should you use on those at risk of malnutrition?

A

Malnutrition Universal Screening Tool (MUST) on admission

126
Q

MALNUTRITION
What are the components of MUST?

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)
127
Q

MALNUTRITION
What do the MUST scores mean?

A
  • 1 = medium risk (observe, if inadequate set goals to improve intake)
  • ≥2 = high risk (refer to dietician, set goals to improve intake)
128
Q

MALNUTRITION
What are some consequences of malnutrition?

A
  • 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
Q

MALNUTRITION
What is the impact of the consequences from malnutrition?

A
  • Lead to poorer prognosis
  • Reduced QOL
  • Greater healthcare needs
130
Q

MALNUTRITION
What is the overall principle for the management of malnutrition?

A
  • Food first – if the gut works, use it
  • Snacks, nourishing drinks, food fortification (add full-fat cream to mashed potato)
131
Q

MALNUTRITION
What is the second line management of malnutrition?
What are they?
Who overviews this care and what is their role?

A
  • 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
Q

MALNUTRITION
What is the second line management of malnutrition?

A
  • Oral nutritional supplements (ONS)
  • Liquid/powder/semi-solid with macro + micronutrients (milkshake, semi-solid, soup)
133
Q

MALNUTRITION
What is the role of a dietician?

A
  • Only qualified HCP that assesses, Dx + Tx nutritional + dietary issues
  • Advice on therapeutic diets, appropriate feeding methods, identifies + advises on managing refeeding syndrome
134
Q

MALNUTRITION
If ONS fails, what two options for feeding are there and what is the difference?

A
  • 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
Q

MALNUTRITION
What are the 4 different types of enteral feeding?

A
  • 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
Q

MALNUTRITION
How do you confirm NG tube position on insertion?

A
  • Check pH aspirate to (<5.5),
  • XR confirmation second line
137
Q

MALNUTRITION
How do you confirm NJ tube position on insertion?

A

Can’t check using pH requires XR

138
Q

MALNUTRITION
What are the indications for PEG?

A
  • Dysphagia (stroke, head + neck surgery, neuro conditions)
  • Cystic fibrosis (high nutritional requirements)
  • Oral nutrition intake inadequate + likely long-term
139
Q

MALNUTRITION
What are the indications for PEJ/surgical JEJ?

A
  • Delayed gastric emptying
  • Upper GI/pancreatic surgery
  • High risk of aspiration or severe acute pancreatitis
140
Q

MALNUTRITION
What are the advantages of enteral feeding?

A
  • Preserves gut mucosa + integrity (NG/NJ),
  • improves nutritional status,
  • inexpensive compared to parenteral nutrition
141
Q

MALNUTRITION
What are the disadvantages of enteral feeding?

A
  • Tolerance (nausea, satiety, bowels both constipation + diarrhoea),
  • tube can be uncomfortable to place,
  • reduced QOL
  • appearance issues
142
Q

MALNUTRITION
What are the indications for parenteral feeding?

A
  • Inadequate absorption (short bowel syndrome)
  • GI fistula
  • Bowel obstruction
  • Prolonged bowel rest
  • Severe malnutrition
  • Significant weight loss ± hypoproteinaemia when enteral therapy not possible
143
Q

MALNUTRITION
What are the advantages of parenteral feeding?

A
  • Easily tolerated
144
Q

MALNUTRITION
What are the disadvantages of parenteral feeding?

A
  • Risk of line infection,
  • expensive
  • invasive procedure
145
Q

OSTEOPOROSIS
What is osteoporosis?

A
  • Systemic skeletal disease characterised by low bone mass + micro-architectural deterioration of bone tissue with consequent increase in bone fragility + susceptibility to fracture
146
Q

OSTEOPOROSIS
What are 2 factors that are important in determining likelihood of an osteoporotic fracture?

A
  • Propensity to fall leading to trauma
  • Bone strength
147
Q

OSTEOPOROSIS
What makes up bone strength?

A
  • Bone mineral density
  • Bone size
  • Bone micro-architecture
  • Bone mineralisation
148
Q

OSTEOPOROSIS
What happens to the bone micro-architecture in osteoporosis?

A
  • Trabecular thickness decreases, especially in the horizontal plane, meaning fewer connections between trabecular + so overall decrease in trabecular strength
149
Q

OSTEOPOROSIS
What is the pathophysiology of osteoporosis?

A
  • 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
Q

OSTEOPOROSIS
What are 2 important components in calcium homeostasis?

A
  • Vitamin D
  • Parathyroid hormone (PTH)
151
Q

OSTEOPOROSIS
What is the role of vitamin D?

A
  • Increased Ca2+ absorption in gut + released from bone
152
Q

OSTEOPOROSIS
What is the role of PTH?

A
  • 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
Q

OSTEOPOROSIS
What are 2 important factors in osteoporosis development/primary causes?

A
  • Increasing age
  • Post-menopause as oestrogen is protective
154
Q

OSTEOPOROSIS
What are the secondary causes/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

155
Q

OSTEOPOROSIS
What is the clinical presentation of osteoporosis?

A
  • 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
Q

OSTEOPOROSIS
What investigations would you do in someone suspected of osteoporosis?

A
  • 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
Q

OSTEOPOROSIS
What does a DEXA scan look at?
What 2 scores are generated?

A
  • 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
158
Q

OSTEOPOROSIS
What DEXA T-scores are significant?

A

≤ -2.5 = osteoporosis (+ current fragility # = severe)
-2.5 < T-score ≤ -1 = osteopenia (low bone mass)
-1 < T-score < 1 = healthy

159
Q

OSTEOPOROSIS
What risk score can be calculated?

A
  • FRAX
160
Q

OSTEOPOROSIS
What does the FRAX score tell you?

A
  • 10-year probability of fragility # (hip, major osteoporotic) for patients aged 40–90
161
Q

OSTEOPOROSIS
What factors are assessed in the FRAX score?

A
  • 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
162
Q

OSTEOPOROSIS
What is the management of the various FRAX score outcomes?

A
  • Low risk = reassure, lifestyle, follow up in 5y
  • Intermediate = offer DEXA scan + Rx if appropriate
  • High risk = Rx
163
Q

OSTEOPOROSIS
What is the overall management of fragility fractures?

A
  • Any patient should have calcium + vitamin D supplementation as well as bisphosphonate regardless of biochemistry as usually normal anyway
164
Q

OSTEOPOROSIS
What is the lifestyle advice for osteoporosis management?

A
  • 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)
165
Q

OSTEOPOROSIS
What pharmacological management is there for osteoporosis?

A
  • 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)
166
Q

OSTEOPOROSIS
What are the benefits of HRT?

A
  • Reduces # risk,
  • stops bone loss
  • prevents menopausal symptoms
167
Q

OSTEOPOROSIS
What are the risks of HRT?

A
  • Increased risk of breast cancer, stroke, CV disease + VTE
168
Q

OSTEOPOROSIS
What is an alternative to HRT?

A
  • Selective oestrogen-receptor modulators (SERMs) like raloxifene
  • Less breast cancer risk as stimulates oestrogen receptors just on bone
169
Q

OSTEOPOROSIS
How do bisphosphonates, denosumab, HRT + SERMs compare to teriparatide?

A
  • First lot are anti-resorptive meds which inhibits osteoclast activity + bone turnover
  • Teriparatide is anabolic which increases osteoblast activity + bone formation
170
Q

OSTEOPOROSIS
Give some examples of bisphosphonate regimes

A
  • PO 70mg alendronate once weekly
  • PO 35mg risedronate once weekly
  • IV 5mg zoledronate once yearly
171
Q

OSTEOPOROSIS
What is the mechanism of action of bisphosphonates?

A
  • Analogues of pyrophosphate, a molecule which decreases demineralisation in bone
  • Inhibit osteoclasts by reducing recruitment + promoting apoptosis
172
Q

OSTEOPOROSIS
What are some important instructions to patients taking bisphosphonates?

A
  • Take on empty stomach with plenty of water
  • Stay upright (sitting/standing for 30m)
173
Q

OSTEOPOROSIS
What are some adverse effects of bisphosphonates?

A
  • Reflux + oesophagitis
  • Osteonecrosis of jaw
  • Atypical stress # (proximal femoral shaft)
174
Q

OSTEOPOROSIS
When should bisphosphonates be reviewed?

A
  • After 5y on PO or 3y on IV
175
Q

OSTEOPOROSIS
What is the process of reviewing bisphosphonates?

A
  • Reassess prescription,
  • update FRAX score + DEXA scan
176
Q

OSTEOPOROSIS
When should bisphosphonates be stopped?

A
  • Consider holiday (18m-3y) if BMD improved + no fragility fractures
177
Q

OSTEOPOROSIS
What factors would make you have to continue bisphosphonate treatment?

A
  • On steroids
  • > 75y
  • Previous hip/vertebral # or further # on Rx
  • High risk FRAX
  • DEXA T score -2.5 or less after Rx
178
Q

PHARMACOLOGY
What is the mechanism of action of acetylcholinesterase inhibitors?

A
  • Increase ACh as ACh is depleted in Alzheimer’s to slow disease progression + aid cognitive issues
179
Q

PHARMACOLOGY
Give some examples of acetylcholinesterase inhibitors

A

Donepezil, rivastigmine

180
Q

PHARMACOLOGY
What are the side effects of acetylcholinesterase inhibitors?

A
  • D+V,
  • nausea,
  • abdo pain (work systemically so GI upset)
  • bradycardia
181
Q

PHARMACOLOGY
What is the mechanism of action of N-methyl D receptor antagonists (NMDA)?

A
  • Protects brain cells from excess glutamate (excitatory neurotransmitter) released from cells affected by Alzheimer’s to prevent further damage, good for agitation + BPSD
182
Q

PHARMACOLOGY
Give an example of NMDA?

A
  • Memantine
183
Q

PHARMACOLOGY
What are some side effects of NMDA?

A
  • Confusion,
  • hallucinations,
  • agitation,
  • paranoid delusions
184
Q

PHARMACOLOGY
When should NMDA be avoided?

A

Do not give in renal failure (low GFR) as nephrotoxic

185
Q

INCONTINENCE
What is incontinence?

A
  • Involuntary leakage of urine/faeces at a time which is not socially acceptable
186
Q

INCONTINENCE
What are some causes of incontinence?

A
  • MS
  • Stroke
  • Parkinson’s
  • Spinal trauma
  • Cauda equina/cord compression
  • Brian tumour
  • Normal pressure hydrocephalus
187
Q

INCONTINENCE
What investigations would you do for incontinence?

A
  • Urine MC&S for infections
  • MRI spine of ?cord compression
  • MRI head if ?MS or Parkinson’s
  • Treat underlying cause if find one
188
Q

INCONTINENCE
What is the management of incontinence?

A
  • Pads, intermittent self-catheterisation or indwelling catheter
  • Permanent catheter if spinal cord damage/paralysis, surgery option if severe
189
Q

URINARY RETENTION
What is urinary retention?

A
  • Inability to empty the bladder due to obstruction or decreased detrusor power
190
Q

URINARY RETENTION
What are some causes of urinary retention?

A
  • BPH (#1 cause in men)
  • Urethral strictures
  • Anticholinergics
  • Alcohol
  • Constipation
  • Infection
  • Cancer
191
Q

URINARY RETENTION
How does acute urinary retention present?

A
  • Inability to pass urine, elderly may become agitated
  • Bladder tender on abdo exam
  • Contains around 600ml urine
192
Q

URINARY RETENTION
How does chronic urinary retention present?

A
  • 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
193
Q

URINARY RETENTION
What might you find on clinical examination in urinary retention?

A
  • Abdo = palpate + percuss bladder to assess extent of retention + if tender
  • PR = ?enlarged prostate, check tone for ?cauda equina
194
Q

URINARY RETENTION
What other investigations would you do in urinary retention?

A
  • FBC, U+E, CRP/ESR, LFTs, TFTs, PSA
  • Urine MC&S for infections
  • CT if concerned about cancer
195
Q

URINARY RETENTION
What is the conservative management of urinary retention?

A

(Tips to aid voiding)
- Analgesia
- Walk around
- Stand to void
- Sound of running water
- Hot bath

196
Q

URINARY RETENTION
What other management is there for urinary retention?

A
  • 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
Q

END OF LIFE CARE
What is palliative care?

A
  • Holistic management of a pt in whom death is likely to be soon + where curative treatment no longer possible
198
Q

END OF LIFE CARE
What are the aims of palliative care?

A

Help pt + relatives come to terms with death whilst optimising the quality of time left

199
Q

END OF LIFE CARE
What does palliative care involve?

A

MDT approach – physical Sx relief, social, psychological, spiritual + family support

200
Q

END OF LIFE CARE
What care should be given to an end of life patient?

A
  • 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
Q

END OF LIFE CARE
How does a patient at the end of their life present?

A
  • 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
Q

END OF LIFE CARE
What is the death rattle?
Is this dangerous?

A
  • Reduced ability to clear saliva + mucous from back of throat + hypersecretion leading to noisy airway
  • No, not painful or uncomfortable
203
Q

END OF LIFE CARE
How is the death rattle managed?

A
  • Hyoscine butylbromide if distressing
204
Q

END OF LIFE CARE
What issues presenting at the end of life can be managed pharmacologically?

A
  • Pain
  • Dyspnoea
  • Agitation + anxiety
  • Nausea
  • Constipation
205
Q

END OF LIFE CARE
In terms of managing end of life care, what should be given for regular medication?

A

Syringe driver

206
Q

END OF LIFE CARE
In terms of managing end of life care, what should be given for pain + dyspnoea?

A

Morphine or oxycodone

207
Q

END OF LIFE CARE
In terms of managing end of life care, what should be given for agitation, anxiety, or dyspnoea?

A

Midazolam

208
Q

END OF LIFE CARE
In terms of managing end of life care, what should be given for nausea or agitation?

A

Haloperidol (other anti-emetics can be used like ondansetron)

209
Q

END OF LIFE CARE
In terms of managing end of life care, what should be given for constipation?

A

Start with stimulant laxative (senna) as opiates decrease peristalsis or stool softener if not on opiates, if not suppositories, enemas, PR evacuation

210
Q

BPPV
what is benign paroxysmal positional vertigo (BPPV)?

A

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
Q

BPPV
what is the pathophysiology?

A
  • calcium deposits (canaliths) floating in the semicircular canals which activates the vesticulo-ocular reflex
212
Q

BPPV
what are the causes?

A

50-70% = primary (idiopathic)

secondary
- head trauma
- labyrinthitis
- vestibular neuronitis
- Meniere’s disease
- migraines

213
Q

BPPV
what are the investigations?

A
  • 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
214
Q

BPPV
what is the management?

A
  • patient education and reassurance
  • repositioning manoeuvres - 3 position particular repositioning manoeuvre (PRM)
  • if manoeuvres are ineffective surgery may be helpful
215
Q

HEART FAILURE
what is it?

A

Inability of the heart to deliver blood and thus oxygen at a rate that is commensurate with the requirements of the body

216
Q

HEART FAILURE
what are the different categories of heart failure?

A
  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
Q

HEART FAILURE
what are the risk factors for heart failure?

A
  1. > 65 y/o
  2. African descent
  3. Men
  4. Obesity
  5. Previous MI
218
Q

HEART FAILURE
Why are men more commonly effected by heart failure than women?

A

Women have ‘protective hormones’ meaning they are less at risk of developing HF

219
Q

HEART FAILURE
what is the pathophysiology?

A

When the heart fails, compensatory mechanisms attempt to maintain CO
As HF progresses, these mechanism are exhausted and become pathophysiological

220
Q

HEART FAILURE
What are the compensatory mechanisms in heart failure?

A
  1. Sympathetic system
  2. RAAS
  3. Natriuretic peptides
  4. Ventricular dilation
  5. Ventricular hypertrophy
221
Q

HEART FAILURE
Explain how the sympathetic system is compensatory in heart failure and give one disadvantage of sympathetic activation

A

Improves ventricular function by increasing HR and contractility = CO maintained
BUT it also causes arteriolar constriction which increases afterload and so myocardial work

222
Q

HEART FAILURE
Explain how the RAAS system is compensatory in heart failure and give one disadvantage of RAAS activation

A

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
Q

HEART FAILURE
Give 3 properties of natriuretic peptides that make them compensatory in heart failure

A
  1. Diuretic
  2. Hypotensive
  3. Vasodilators
224
Q

HEART FAILURE
What are the 3 cardinal symptoms of heart failure?

A
  1. SOB
  2. Fatigue
  3. Peripheral oedema
225
Q

HEART FAILURE
what are the clinical signs of left heart failure?

A
  1. Pulmonary crackles
  2. S3 and S4 and murmurs
  3. Displaced apex beat
  4. Tachycardia
  5. fatigue
226
Q

HEART FAILURE
what are the clinical features of right HF?

A
  1. Raised JVP
  2. Ascites
  3. peripheral oedema
227
Q

HEART FAILURE
what are the clinical features of heart failure?

A

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
Q

HEART FAILURE
What investigations might you do initially do in someone who you suspect has HF?

A
  1. ECG
  2. CXR
  3. BNP - brain natriuretic peptide
229
Q

HEART FAILURE
What 4 signs might you see on a CXR taken from someone with HF?

A

ABCDE
A - alveolar oedema (bat wing shadowing)
B - Kerley B lines
C - cardiomegaly
D - dilated upper lobes
E - effusions (pleural)

230
Q

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?

A

An echocardiogram - may reveal cause

231
Q

HEART FAILURE
what is the management for chronic HF?

A

1st line = ACEi, beta blocker
2nd = ARB + nitrate
3rd = cardiac resynchronization or digoxin
4th = diuretics (furosemide)
5th = aldosterone antagonist (spironolactone)

232
Q

HEART FAILURE
what is the treatment for acute HF?

A

OMFG
- oxygen
- morphine
- furosemide
- GTN spray

233
Q

HEART FAILURE
How can chronic HF be prevented?

A

Stop smoking
Eat more healthy
Exercise
Avoid large meals
Vaccinations
Treat underlying cause - dysarrhythmias or valve disease

234
Q

CONSTIPATION
what are the primary and secondary causes?

A

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
Q

CONSTIPATION
what are the red flag symptoms?

A

Rectal bleeding
Haem-positive stool
Weight loss
Obstructive symptoms
Recent onset of symptoms
Rectal prolapse
Change in stool calibre
Age >50 years.

236
Q

CONSTIPATION
what are the investigations?

A
  • history of bowel habits, consistency
  • abdominal exam - look for tenderness
  • DRE
  • bloods - FBC, U+Es, TFTs, glucose
  • abdominal x-ray
237
Q

CONSTIPATION
what is the management?

A
  • treatment of underlying cause
  • increased dietary fibre
  • increased fluid intake
  • exercise
  • bulk laxatives
  • stool softeners
  • osmotic laxatives - lactulose, macrogol
238
Q

SQUAMOUS CELL CARCINOMA OF THE SKIN
what is it?

A

Squamous cell carcinoma is a common variant of skin cancer. Metastases are rare but may occur in 2-5% of patients.

239
Q

SQUAMOUS CELL CARCINOMA OF THE SKIN
what are the risk factors?

A
  • 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
Q

SQUAMOUS CELL CARCINOMA OF THE SKIN
what are the clinical features?

A
  • 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
241
Q

SQUAMOUS CELL CARCINOMA OF THE SKIN
what is the management?

A

Surgical excision with 4mm margins if lesion <20mm in diameter.

If tumour >20mm then margins should be 6mm.

242
Q

SQUAMOUS CELL CARCINOMA OF THE SKIN
what factors indicate a good progrosis?

A
  • well differentiated tumours
  • <20mm diameter
  • <2mm deep
  • no associated diseases
243
Q

SQUAMOUS CELL CARCINOMA OF THE SKIN
what factors indicates a poor prognosis?

A
  • poorly differentiated tumours
  • > 20mm in diameter
  • > 4mm deep
  • immunosuppression for whatever reason
244
Q

COTE ASSESSMENT
What is frailty?

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
245
Q

COTE ASSESSMENT
What is the impact of frailty?

A
  • 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
Q

COTE ASSESSMENT
What is acopia?

A
  • 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
Q

COTE ASSESSMENT
What are the geriatric giants?
What do they represent?

A 
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
248
Q

COTE ASSESSMENT
What are the geriatric 5Ms?

A
  • 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
Q

COTE ASSESSMENT
What is a comprehensive geriatric assessment?
What does it focus on?
Who is part of the geriatric MDT?

A
  • Multidimensional, MDT diagnostic process in geriatrics.
  • Determining a frail older person’s medical, psychological + functional capability
  • Geriatrician, social worker, physio, OT, SALT, nurse etc.
250
Q

COTE ASSESSMENT
What is the role of the 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.
251
Q

COTE ASSESSMENT
What are the components of the comprehensive geriatric assessment and who might be involved?

A
  • Medical assessment = Dr, nurse, pharmacist, dietician, SALT
  • Functional assessment (OT, physio, SALT)
  • Psychological assessment (Dr, nurse, OT, psychologist)
  • Social + environmental assessment (OT, social worker)
252
Q

COTE ASSESSMENT
What is involved in…

i) medical assessment?
ii) functional assessment?
iii) psychological assessment?
iv) social + environmental assessment?

A

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
Q

COTE ASSESSMENT
What is rehabilitation?

A
  • Process of restoring a patient to maximum function (need to know pre-morbid function), can happen in variety of settings, involves MDT
254
Q

POLYPHARMACY
What is pharmacodynamics?
How does this change for the elderly?

A
  • 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
Q

POLYPHAMRACY
What is pharmacokinetics?
How does this change for the elderly?

A
  • 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
Q

POLYPHARMACY
Give some specific pharmacokinetic issues in geriatrics.

A
  • Hepatic first pass metabolism declines
  • Reduced absorption as gastric pH increases due to atrophy
  • Vascular system less responsive due to calcification of vessels
257
Q

POLYPHARMACY
Why might inappropriate drug use occur in geriatrics?

A
  • 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
Q

POLYPHARMACY
What is polypharmacy?
Why are geriatric patients at increased risk?

A
  • 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
Q

POLYPHARMACY
What is multimorbidity?

A
  • ≥2 chronic conditions, often long-term requiring ongoing care.
260
Q

POLYPHARMACY
What are some potential problems with polypharmacy?

A
  • Drug interactions + increased SEs
  • Can affect compliance + lead to decreased pt satisfaction
  • Pill burden
261
Q

POLYPHARMACY
What is appropriate polypharmacy?
What can this lead to?

A
  • Prescribing multiple medications for either a complex condition or multiple conditions where medicine has been optimised
  • Can extend life expectancy + improve QOL
262
Q

POLYPHARMACY
What is problematic polypharmacy?
How can this be prevented?

A
  • Multiple medications prescribed inappropriately, increasing the risk of SEs
  • MDT case conferences, computerised support systems, pharmacists
263
Q

POLYPHARMACY
What are the reasons for problematic polypharmacy?

A
  • 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
Q

POLYPHARMACY
What is the impact of adverse drug reactions?
What specific issue can this impose in geriatrics?

A
  • Increasing fragility means reduced ability to cope with ADRs
  • May go unnoticed as Sx mimic problems associated with elderly (forgetfulness, weakness, tremor)
265
Q

POLYPHARMACY
What are some common adverse drug reactions in geriatrics?

A
  • Falls (postural hypotension with ACEi, beta-blockers)
  • Confusion (sedation with anticholinergics)
  • Bowel problems (opioids, PPIs)
266
Q

MENTAL CAPACITY ACT
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
267
Q

MENTAL CAPACITY ACT
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?
268
Q

MENTAL CAPACITY ACT
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)
269
Q

MENTAL CAPACITY ACT
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)
  • 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
Q

MENTAL CAPACITY ACT
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
271
Q

MENTAL CAPACITY
What is an independent mental capacity advocate (IMCA)?

A
  • Commissioned from independent organisations by the NHS + local authorities to ensure MCA followed
272
Q

MENTAL CAPACITY
What is the role of an IMCA?

A
  • 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
Q

BEST INTERESTS
What are some important considerations when making best interest decisions?

A
  • 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
Q

BEST INTERESTS
Who would you consult when making best interest decisions?

A
  • 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
Q

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

A
  • 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
Q

DOLS
When is a DoLS required?

A
  • 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
Q

DOLS
What is the acid test for DoLS?

A

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
Q

DOLS
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
  • Only if in best interests, up to 7d + must be least restrictive alternative to preventing harm
279
Q

ADVANCED CARE PLANNING
What is an advanced directive?

A
  • Written statement that sets down a person’s preferences, wishes, beliefs + values regarding their future care
280
Q

ADVANCED CARE PLANNING
What are the roles of an advanced directive?

A
  • 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
Q

ADVANCED CARE PLANNING
What can an advanced directive include?

A
  • 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
Q

MEDICO-LEGAL ASPECTS
What is an advanced refusal of treatments?
Is it legally binding?

A
  • 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
Q

MEDICO-LEGAL ASPECTS
What is an advanced requests for treatment?
Is it legally binding?

A
  • 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
Q

LASTING POWER OF ATTORNEY
What is a Lasting Power of Attorney (LPA)?

A
  • 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
Q

LASTING POWERR OF ATTORNEY
What are the 2 types of LPA?
What is needed for it to be valid?

A
  • 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
Q

ENDURING POWER OF ATTORNEY
What is an enduring power of attorney (EPA)?

A

Under previous law + was restricted to decisions over property + affairs

287
Q

ABUSE
What is abuse?

A
  • 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
Q

ABUSE
How should abuse be managed?

A
  • Avoid asking too many questions – LISTEN
  • Don’t agree to keep secret –duty to report to safeguarding
  • Do NOT confront abuser
289
Q

COTE ASSESSMENT
Is frailty inevitable?

A
  • Not inevitable, not irreversible + not simply due to chronic conditions
290
Q

ABUSE
Who may the perpetrator be?

A
  • Family, partner, friends, neighbours, carers, strangers
291
Q

ABUSE
What are some types?

A
  • Physical, neglect, psychological, financial, sexual, discriminatory
292
Q

MEDICO-LEGAL ASPECTS
What is a court appointed deputy?

A

Alternative from Court of Protection once the person lacks capacity

293
Q

POLYPHARMACY
What is the impact of multimorbidity?

A
  • Complexity + restrictions with cross-over of Sx
  • Medication burden (SEs, drug interactions, monitoring, compliance)
  • Appt burden
  • Mental health impact
294
Q

ABUSE
what are the signs of possible abuse?

A

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

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