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Phase 3a > Geriatrics > Flashcards

Geriatrics Flashcards

1
Q

What is Benign paroxysmal positional vertigo?

A

Common peripheral cause of recurrent episodes of vertigo triggered by head movement because of problems in the inner ear. More common in older adults.

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2
Q

Describe the presentation of BPPV

A
  • Asymptomatic between attacks
  • Common trigger is turning over in bed
  • Symptoms usually last 20-60 seconds
  • Episodes can come and go
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3
Q

Describe the pathophysiology of BPPV

A
  • Crystals of calcium carbonate called otoconia become displaced into the semicircular canals most often in the posterior semicircular canal.
  • Cause can be viral infection, head trauma, ageing or idiopathic
  • Otoconia disrupt the normal flow of endolymph through canals confusing the vestibular system
  • Head movement creates flow of endolymph in canals triggering episodes of vertigo
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4
Q

Describe Dix-Hallpike Manoeuvre

A
  • Diagnostic for BPPV - moves head in a way that moves endolymph through semicircular canals and triggers vertigo
  • Patient sits upright head 45 degrees to one side, support head and rapidly lower patient so head hangs off bed 20-30 degrees
  • Watch eyes for 30-60 secs for rotational beats of nystagmus towards affected ear
  • Repeat on other side
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5
Q

What is the Epley Manoeuvre?

A

Treats BPPV - moves crystals into a positional that doesn’t disrupt endolymph flow

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6
Q

Describe Brandt-Daroff Exercises

A
  • Performed at home by patient to treat BPPV
  • Roll from side to side on the bed facing the ceiling
  • Repeat several times a day
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7
Q

State 5 causes of Cardiac Failure

A
  • IHD
  • Hypertension
  • Cardiomyopathy
  • VHD
  • CHD
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8
Q

Describe the types of cardiac failure

A
  • Systolic - failure to contract, ejection fraction <40%
  • Diastolic - inability to relax and fill, ejection fraction >50%
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9
Q

Describe the pathology of cardiac failure

A

Compensatory changes - sympathetic stimulation |(increases HR), increased RAAS (due to fall in CO, leads to increased water retention and oedema), cardiac changes (ventricular dilation and myocyte hypertrophy)

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10
Q

Describe left cardiac failure and symptoms

A
  • Reduced ejection fraction (systolic)
  • Symptoms - pulmonary oedema, tachycardia, pleural effusion
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11
Q

Describe right cardiac failure and symptoms

A
  • Can be caused by left ventricular failure
  • Symptoms - pitting oedema, ascites, weight gain (fluids)
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12
Q

State 3 investigations for cardiac failure

A
  • ECG - may show underlying causes
  • Bloods - Brain Natriuretic Peptide (released by ventricles with mycocardial wall stress)
  • Cardiac enzymes - creatinine kinase, Troponin I, Troponin T, Myoglobulin
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13
Q

State the management for cardiac failure

A
  • Lifestyle changes
  • ACE inhibitors - dilates blood vessels
  • Beta blockers
  • Diuretics
  • Heart transplant
  • Oxygen (acute)
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14
Q

Describe the presentation of delirium

A
  • Acute onset
  • Fluctuating course
  • Inattention
  • Altered level of consciousness
  • Usually reversible
  • Associated with underlying medical cause
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15
Q

State the causes of delirium

A

Drug use (introduction, dose adjustments)

Electrolyte and physiological abnormalities

Lack of drug (withdrawal)

Infection

Reduced sensory input (deaf, blind, changing environment)

Intracranial problems (stroke, post-ictal, meningitis, subdural haematoma)

Urinary retention and faecal impaction

Myocardial (MI, Arrhythmias, HF)

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16
Q

Describe the treatment for delirium

A
  • Treat the cause - meds review, infection, pain relief, low dose haloperidol/lorazepam
  • Manage the environment - soft lighting, clocks and calendars, sleep hygiene, avoid room/ward moves, minimise provocation
  • Capacity assessment - MHA, MCA
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17
Q

Describe the types of delirium

A
  • Hyperactive - agitation, inappropriate behaviour, hallucinations
  • Hypoactive - lethargy, reduced concentration
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18
Q

How would you assess delirium?

A
  • History - collateral, cognitive screening, previous level of function, social circumstances, risk factors
  • Bedside tests - 02 sats, bp, temp, ABG/VBG
  • Investigations - FBC, LFT, U&E, CRP/ESR Sputum culture, Folate, B12, HbA1c, TFT, CXR, ECG, urinalysis
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19
Q

State some delirium differentials

A
  • Depression
  • Dementia
  • Mental illness
  • Anxiety
  • Thyroid disease
  • Temporal lobe epilepsy
  • Charles Bonnet syndrome
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20
Q

Dementia Investigations

A

Mini-Mental State Examination - out of 30. 25-30 normal. 21-24 mild. 10-20 moderate. <10 severe

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21
Q

Dementia management

A
  • Healthier lifestyle
  • Social support
  • ACh inhibitor - rivastigmine
  • Control CV risk factors
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22
Q

Differences between delirium and dementia

A

Delirium - acute onset, fluctuating course, lasts hours to weeks, altered consciousness
Dementia - insidious onset, progressive course, lasts months to years, normal consciousness unless severe

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23
Q

Describe Alzheimer’s history, symptoms and pathology

A

History - gradual onset
Symptoms - aphasia, agnosia, apraxia, amnesia
Pathology - degeneration of cerebral cortex with cortical atrophy

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24
Q

Describe vascular dementia history, symptoms and pathology

A

History - abrupt or gradual onset
Symptoms - stepwise deterioration with short periods of stability, raise BP
Pathology - brain damage from cerebrovascular disease

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25
Q

Describe Lewy-Body dementia history, symptoms and pathology

A

History - Insidious onset
Symptoms - fluctuating cognition, impairment with visuospatial ability
Pathology - deposition of abnormal proteins, associated with Parkinsons

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26
Q

Describe fronto-temporal dementia history, symptoms and pathology

A

History - insidious onset with rapid progression
Symptoms - behavioural and personality changes
Pathology - atrophy of fronto-temporal lobes

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27
Q

Malnutrition causes

A
  • Decreased nutrient intake (starvation)
  • Increased nutrient requirements (sepsis or injury)
  • Inability to utilise ingested nutrients (malabsorption)
  • Or combination of above
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28
Q

Risks for developing malnutrition

A
  • Eaten little or nothing for >5 days
  • Poor absorptive capacity
  • High nutrient losses
  • Increased nutritional needs from causes such as catabolism
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29
Q

How to diagnose malnutrition

A
  • BMI <18.5kg/m2
  • Unintentional weight loss >10% last 3-6months
  • BMI <20 AND unintentional weight loss >5% within last 3-6 months
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30
Q

Consequences of malnutrition

A
    • Impaired immunity
    • Impaired wound healing
    • Muscle mass loss
    • Respiratory function loss
    • Cardiac function loss
    • Impaired skin integrity
    • Impaired recovery from illness
    • Worsening prognosis
    • Low quality of life
    • Prolonged hospital stay
    • More hospital admissions
    • Greater healthcare needs
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31
Q

Describe refeeding syndrome and pathology

A
  • Prolonged starvation followed by provision of nutritional supplementation from any route
  • Chronic malnutrition leads to decreased insulin levels, energy source switch, normal serum phsophate levels, low intracellular phosphate levels
  • Refeeding leads to insulin increase, movement of electrolytes into cell results in decreased serum electrolyte levels
32
Q

Refeeding syndrome clinical features

A
  • CVS: arrhythmia, HT, CHF
  • GI: abdo pain, constipation, vomiting, anorexia
  • MUSC: weakness, myalgias, rhabdomyolysis, osteomalacia
  • NEURO: weakness, paraesthesia, ataxia
  • METABOLIC: infections, thrombocytopaenia, haemolysis, anaemia
  • OTHER: ATN, wernicke’s encephalopathy, liver failure
33
Q

Refeeding syndrome investigations

A

Bloods:

  • Hypophosphataemia
  • Hypokalaemia
  • Hypomagnesaemia
  • Hyperglycaemia
  • Thiamine deficiency
  • Trace elements deficiencies
34
Q

Refeeding syndrome management

A
  • Recognise patients at risk
  • Replace electrolytes
  • Supportive care
  • Monitor glucose and Na levels
  • Feeds, vitamins (B6, B12), folate
  • Refer to nutritional support team/dietician
35
Q

What does a patient need to be able to do to have capacity

A
  • Understand the information relevant to the decision
  • Retain the information
  • Weigh up the information
  • Communicate the decision
36
Q

Things to consider with Mental Capacity Act

A
  • Assume capacity - until proven otherwise
  • Maximise decision making capacity - all support to help person make a decision should be given
  • Freedom to make seemingly unwise decisions - unwise decisions do not prove incapacity
  • Best interests - all decisions taken on behalf of the person must be in their best interests
  • Least restrictive option - care that achieves the necessary goal and interferes the least with the person’s rights and freedom of action must be chosen
37
Q

Describe different types of Mental Health Acts

A
  • Section 2 - 28 days for assessment, not renewable, done by an Approved Mental Health Professional and 2 Drs.
  • Section 3 - Treatment for up to 6 months, can be renewed
  • Section 4 - 72 hour assessment order, used in emergency when section 2 would cause delay
  • Section 5(2) - a voluntary patient in hospital detained by a doctor for 72 hours
  • Section 5(4) - a voluntary patient in hospital detained by a nurse for 6 hours
  • Section 135 - a court order obtained allows police to break into property to remove a person to a Place of Safety
  • Section 136 - someone found in a public place with mental disorder taken by police to a Place of Safety
38
Q

Things to consider with best interests

A

Consider:

  • Whether the person is likely to regain capacity and can the decision wait
  • How to encourage and optimise the participation of the person in the decision
  • The past and present wishes, feelings, beliefs, values of the person and any other relevant factors
  • Views of other relevant people
39
Q

Describe advanced directives

A
  • Can state treatment wishes in advance e.g.
    • authorise or request specific procedures
    • Refuse treatment in a predefined future situation
  • Advance refusals of treatment are legally binding if:
    • The person is an adult
    • Was competent and fully informed when making the decision
    • The decision is clearly applicable to current circumstances
    • There is no reason to believe that they have since changed their mind
  • Advance requests for treatment don’t have same legal binding status but should be considered when assessing best interests
40
Q

Describe DoLs

A

Deprivation of Liberty

Occurs when a person does not consent to care or treatment, for example, a person with dementia who is not free to leave a care home and lacks capacity to consent to this

41
Q

Describe LPAs

A

Lasting power of attorney

A document which a person can nominate someone else to make certain decisions on their behalf e.g. finances, health, personal welfare when they are unable to do so themselves.

To be valid it needs to be registered with the Office of the public Guardian

42
Q

Describe IMCAs

A

Independent mental capacity advocate

- Commissioned from independent organisations by the NHS and local authorities to ensure that MCA is being followed
- Role: to support and represent people who lack capacity and they do not have anyone else to represent them in decisions about changes in long-term accomadation or serious medical treamtent. They can also be present for decisions regarding care reviews or adult protection.
43
Q

Osteoporosis description

A

A systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue with a consequent increase in bone fragility and susceptibility to fracture

44
Q

Osteopenia description

A

Precursor to osteoporosis characterised by low bone density. Defined as bone mineral density 1-2.5 SD below mean

45
Q

Osteomalacia description

A

Poor bone mineralisation leading to soft bones due to lack of calcium (adult form of rickets)

46
Q

Osteoporosis causes

A
  • Primary - post-menopausal
  • Secondary - SHATTERED
    • Steroid use
    • Hyperthyroidism/hyperparathyroidism
    • Alcohol
    • Thin (low BMI)
    • Testosterone low
    • Early menopause
    • Renal or liver failure
    • Erosive/inflammatory bone disease
    • Dietary calcium low
47
Q

Osteoporosis risk factors

A
  • Patient - old, female, low BMI, diet, athletes
  • Disease - RA, SLE, Hyperthyroidism, Hyperparathyroidism, Cushing’s, Hypogonadism, Renal disease
  • Medication - Corticosteroids, Hormonal (depo-provera, androgen deprivation, aromatase inhibitors, GnRH analogues)
48
Q

Osteoporosis patholgy

A
  • Increased resorption by oesteoclasts and decreased formation by osteoblasts → inadequate peak bone mass
  • With ageing comes decrease in trabecular thickness + decrease in connections between horizontal trabeculae = decrease in trabecular strength and increased susceptibility to fracture
  • Oestrogen deficiency → loss of restraining effects of oestrogen on bone turnover → cancellous bone loss and microarchitectual disruption
  • Eular buckling theory says that trabeculae make bones stronger
49
Q

Osteoporosis symptoms

A
  • Asymptomatic until fracture
  • Hip - neck of femure after fall on side or back
  • Wrist - distal radius (Colle/Smith’s fracture from fall on outstretched arm)
  • Vertebra - shorter and stooping posture, can lead to kyphosis (curvature of spine)
50
Q

Osteoporosis investigations

A
  • DEXA BMD (Dual Energy XR and Absoptiometry) - T score (standard deviation). < -2.5 = OP, -1—2.5 = Osteopenia, > -1 = normal
  • FRAX (fracture risk assessment) - age, sex, BMI, previous fractures, steroids
51
Q

Osteoporosis treatment

A
  • Lifestyle - smoking, alcohol, Vit D supplements
  • Alendronate daily (1st line) - oral bisphosphonate, inhibits bone resorption through inhibition of Farnesyl Prophosphate synthase (in cholesterol pathway) which reduces osteoclast activity by removing their ruffled border
  • Different Bisphosphonate (2nd line) - e.g. Risedronate (daily), Idandronate (weekly)
  • Strontium ranelate (3rd line) - reduces fracture rate
  • Recombinant human parathyroid peptide (3rd line) - e.g. Teriparatide. Increases osteoblast activity and bone formation
52
Q

Osteoporosis primary prevention

A
  • Adcak D3 - Vit D + Calcium
  • HRT - menopausal women
  • Corticosteroids
  • Smoking and alcohol cessation
  • DEXA scans
53
Q

Bisphosphonates clinical uses

A
  • Prevention and treatment of osteoporosis
  • Hypercalcaemia
  • Paget’s disease
  • Pain from bone metastases
54
Q

Bisphosphonates adverse effects

A
  • Oesophageal reactions: oesophagitis, oesophageal ulcers
  • Osteonecrosis of the jaw
  • Increased risk of atypical stress fractures of the proximal femoral shaft in patients taking alendronate
55
Q

When should you stop taking bisphosphonates

A

After 5 years if the patient is:
- <75
- Femoral neck T-store of > -2.5
- Low risk according to FRAX/NOGG

56
Q

Parkinson’s epidemiology

A

More common in men

Mean age of diagnosis is 65 years

57
Q

Parkinson’s pathology

A
  • Neurodegenerative loss of dopamine secreting cells from the pars compacta of the substantia nigra that project to the striatum → reduced striatal dopamine levels
  • Less dopamine inhibits thalamus → decreased movement
  • Under microscopy there are Lewy bodies (intracytoplasmic intrusion bodies in remaining neurones)
58
Q

Parkinson’s diagnostic criteria

A
  • 4 diagnostic criteria:
  • Bradykinesia - slowness or absence of movement
  • Resting tremor - may be unilateral
  • Rigidity - pain, increased tone in limbs and trunk
  • Postural instability - impaired balance
  • Gait - small shuffling steps, reduced arm swing, slow start
  • Mental health - Depression (20-40%), dementia
59
Q

Parkinson’s differentials

A
  • If incontinence, dementia, symmetry, early falls, tremor in action are present in early stages think:
  • Normal pressure hydrocephalus - increase CSF → enlarged ventricles. Magnetic gait, incontinence, dementia. Treat with surgical correction
  • Essential tremor - very common. No rest tremor, no increased tone, better after alcohol. Treat with deep brain stimulation or beta blockers (primidone)
60
Q

Parkinson’s investigations

A
  • DaTSCAN - imaging of dopaminergic terminals of nigrostriatal neurons in striatum, shows reduced dopamine supply
  • CT/MRI shows substantia nigra atrophy
  • Microscopy shows Lewy bodies
  • Diagnosis mostly made off history and exam
61
Q

Describe bradykinesia

A
    • Poverty of movement also seen (hypokinesia)
    • Slow, shuffling steps
    • Reduced arm swinging
    • Difficulty in intiating movement
62
Q

Describe parkinson’s tremor

A
  • Most marked at rest, reduced on movement
  • Worse when stressed or tired
  • Typically pill-rolling, asymmetrical
63
Q

Describe Parkinson’s rigidity

A
  • Lead-pipe - hypertonic in limb throughout the range of movements of a joint
  • Cogwheel - muscular stiffness through the range of passive movement due to superimposed tremor
64
Q

Dopamine receptor agonists side effects

A
  • Ergot-derived dopamine receptor agonists (bromocriptine, cabergoline) have been associated with pulmonary, retroperitoneal and cardiac fibrosis - do ECG, ESR, creatinine and chest X-ray prior to treatment and close monitoring
  • Can cause impulse control disorders and excessive daytime sleepiness
  • More likely than levodopa to cause hallucinations in older patients
  • Nasal congestion and postural hypotension are also seen in some patients
65
Q

Describe levodopa and side effects

A
  • Usually combined with a decarboxylase inhibitor (carbidopa or benserazide) to prevent peripheral metabolism of levodopa to dopamine
  • Reduced effectiveness with time (2 years)
  • Unwanted effects: dyskinesia (writhing movements), on-off effect, dry mouth, anorexia, palpitations, postural hypotension, psychosis, drowsiness
66
Q

Medications other than Levodopa used for Parkinson’s

A
  • MAO-B inhibitors - inhibits dopamine breakdown
  • COMT inhibitors - inhibits dopamine breakdwon, adjunct to Levodopa
  • Antimuscarinins - help with tremor and rigidity
  • Amantidine - thought to increase dopamine release and prevent reuptake at synapses
67
Q

Describe stroke types

A
  • TIA - if symptoms and signs last less than 24 hours
  • Thrombotic stroke - thrombosis from large vessels e.g. carotid
  • Embolic stroke - usually a blood clot but fat, air or clumps of bacteria may act as an embolus. AF is an important cause of emboli forming in the heart
  • Cerebral hemisphere infarcts - contralateral hemiplegia: initially flaccid then spastic, contralateral sensory loss, homonymous hemianopia, dysphasia
  • Brainstem infarction - may result in more severe symptoms including quadriplegia and lock-in-syndrome
  • Lacunar infarcts - small infarcts around the basal ganglia, internal capsule, thalamus and pons. May result in pure motor, pure sensory, mixed motor and sensory signs or ataxia
68
Q

Features of stroke

A
  • Motor weakness
  • Speech problems
  • Swallowing problems
  • Visual field defects - homonymous hemianopia
  • Balance problems
69
Q

Describe the acute stroke management

A
  • ABCDE assessment
  • Urgent neuroimaging to rule out haemorrhagic stroke
  • Thrombolysis (alteplase) - withing 4,5h of symptom onset, not had a previous intracranial haemorrhage, uncontrolled hypertension, pregnant
  • Aspiring 300mg - ASAP and antiplatelet therapy should be continued
70
Q

What is the management for a TIA with ABCD2 score >= 4

A
  • Aspirin - 300mg daily, started immediately
  • Specialist referral within 24 hours of onset of symptoms
  • Secondary prevention measures
71
Q

What is the management for a TIA with ABCD2 score <= 3

A
  • Specialist referral withing 1 week of symptom onset, including decision on brain imaging
  • If vascular territory or pathology is uncertain, refer for brain imaging
  • Crescendo TIAs (two or more episodes in a week) should be treated as being at high risk, regardless of ABCD2 score.
72
Q

Stroke differentials

A
  • Hypoglycaemia
  • Migrainous aura
  • Mass lesions
  • Syncope due to arrhythmia
  • Simple partial seizures
73
Q

What questions should you ask patient/ witness presenting with syncope

A
  • Precipitating factors?
  • Activity the patient was involved in before the event?
  • Position the patient was in when the event occurred? (i.e. detailed account by eyewitnesses)
  • Was loss of consciousness complete?
  • Was loss of consciousness with rapid onset and short duration?
  • Was recovery spontaneous, complete, and without sequelae?
  • Were there seizures? If so, describe it.
  • Was postural tone lost?
  • Patient’s medical history, esp cardiac disease.
  • Family history of cardiac disease?
74
Q

Red flags with syncope

A
  • Exertional onset
  • Chest pain
  • Dyspnoea
  • Low back pain
  • Palpitations
  • Severe headache
  • Focal neurological deficits, diplopia, ataxia or dysarthia
75
Q
A

Phase 3a (11 decks)

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