TO DO GERIATRICS Flashcards

1
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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2
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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3
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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4
Q

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

A
  • FBC
  • blood glucose
  • LFTs
  • bone profile
  • TFTs
  • U&Es
  • folate + B12
  • drug levels (digoxin, lithium, alcohol)
  • inflammatory markers

to consider
- CXR

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5
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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6
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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7
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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8
Q

DEMENTIA
What biological treatment can be used in dementia?

A
  • Bio = risperidone for agitation (apart in Lewy-Body)
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9
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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10
Q

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

A

Diffuse cerebral atrophy (shrunken brain) particularly involving the cortex and hippocampus,
increased sulcal widening, enlarged ventricles

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11
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
  • 1st line = AChEi (donepezil, rivastigmine) for mild–mod
  • 2nd line = NMDA antagonist (memantine) for mod–severe
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12
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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13
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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14
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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15
Q

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

A
  • Conservative management
  • mild/mod = donepezil or rivastigmine (galantamine if both are contraindicated)
  • severe = donepezil or rivastigmine (memantine if both are contraindicated)
  • SENSITIVE to antipsychotics, can make worse + lead to neuroleptic malignant syndrome
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16
Q

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

A
  • Early personality changes + relative intellectual sparing.
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17
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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18
Q

FT DEMENTIA
What is the management of FT dementia?

A
  • No specific treatment
  • SSRIs may help behavioural symptoms
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19
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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20
Q

FALLS
What can cause rhabdomyolysis?

A
  • Crush injuries
  • Prolonged immobilisation following a fall
  • Prolonged seizures
  • Hyperthermia
  • Neuroleptic malignant syndrome
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21
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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22
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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23
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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24
Q

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

A
  • Pressure
  • Shear
  • Friction
  • Moisture
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25
Q

PRESSURE ULCERS
Explain how friction causes pressure ulcers.

A

Rubbing skin decreases integrity

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26
Q

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

A

Waterlow score

27
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
28
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
29
Q

PHARMACOLOGY
Give an example of NMDA?

30
Q

INCONTINENCE
What are some causes of incontinence?

A
  • MS
  • Stroke
  • Parkinson’s
  • Spinal trauma
  • Cauda equina/cord compression
  • Brian tumour
  • Normal pressure hydrocephalus
31
Q

URINARY RETENTION
What are some causes of urinary retention?

A
  • BPH (#1 cause in men)
  • Urethral strictures
  • Anticholinergics
  • Alcohol
  • Constipation
  • Infection
  • Cancer
32
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)
33
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)

34
Q

ALZHEIMER’S DISEASE
What neurotransmitters are affected?

A
  • ACh, noradrenaline, serotonin, somatostatin
35
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

36
Q

FT DEMENTIA
What are some pathological features of frontotemporal dementia?

A
  • Microscopic = ubiquitin + tau deposits (pick bodies)
37
Q

FT DEMENTIA
What are the symptoms of FT dementia?

A

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

FRONTAL LOBE
Euphoria, disinhibition, personality changes + emotional blunting

38
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)
39
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)

40
Q

PRESSURE ULCERS
Explain how moisture causes pressure ulcers.

A

Sweat, urine + faeces cause maceration + decrease integrity

41
Q

PHARMACOLOGY
Give some examples of acetylcholinesterase inhibitors

A

Donepezil, rivastigmine

42
Q

PHARMACOLOGY
What are the side effects of acetylcholinesterase inhibitors?

A
  • D+V,
  • nausea,
  • abdo pain (work systemically so GI upset)
  • bradycardia
43
Q

PHARMACOLOGY
When should NMDA be avoided?

A

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

44
Q

PHARMACOLOGY
What are some side effects of NMDA?

A
  • Confusion,
  • hallucinations,
  • agitation,
  • paranoid delusions
45
Q

BPPV
what are the causes?

A

50-70% = primary (idiopathic)

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

46
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

47
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
48
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
49
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
50
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

51
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
52
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
53
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
54
Q

POLYPHARMACY
What are some potential problems with polypharmacy?

A
  • Drug interactions + increased SEs
  • Can affect compliance + lead to decreased pt satisfaction
  • Pill burden
55
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
56
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)
57
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
58
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
59
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
60
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
61
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
62
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
63
Q

ALZHEIMER’S DISEASE
what are the microscopic pathological changes?

A

beta amyloid plaques
neurofibrillary tangles

64
Q

FT DEMENTIA
what is FT dementia also known as?

A

Pick’s disease