Geriatrics Flashcards

1
Q

Define delirium

A

An acute fluctuating syndrome of encephalopathy, causing disturbed consciousness, attention, cognition, or perception, usually developing over hours to days

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2
Q

What are the risk factors for delirium?

A
  • Older age (over 65)
  • Cognitive impairment (e.g. dementia)
  • Frailty/multiple comorbidities
  • Significant injuries (e.g. hip fracture)
  • Functional impairment (e.g. immobility)
  • Iatrogenic events (e.g. surgery, catheterisation, polypharmacy)
  • Substance misuse
  • Hearing or visual impairment
  • Poor nutrition
  • Lack of stimulation or social isolation
  • Terminal phase of illness
  • Movement to a new environment
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3
Q

What are the causes/precipitating factors of delirium?

A

PINCH ME
- Pain (severe, uncontrolled)
- Infection (UTI, pneumonia, sepsis, viral infections, pressure sore)
- Nutrition (inadequate nutrition, vitamin deficiencies)
- Constipation/continence (urinary retention)
- Hydration (dehydration)
- Medications (benzodiazepines, anticholinergics, anticonvulsants, steroids, opioids, anti-Parkinson’s)
- Environment (new, disorientation, sensory impairment, poor sleep)

Others:
- surgery
- toxic substances (alcohol, drug misuse or withdrawal, CO poisoning)
- vascular disorders (stroke, intracranial haemorrhage, vasculitis, cardiac failure or ischemia)
- metabolic (hypoxia, hyponatraemia, hypercalcaemia, hypo/hyperglycaemia, hepatic/renal impairment)
- endocrine (hypo/hyperthyroid, hypo/hyperparathyroid, hypopituitarism, cushing’s)
- neurological (trauma, tumours, epilepsy, cognitive impairment)
- emotional stress/trauma

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4
Q

What are the clinical features of delirium?

A
  • Altered cognition: disorientated, memory and language impairment, slow responses, confusion
  • Inattention: worsened concentration, easily distractable, unable to maintain conversations/follow commands
  • Disorganised thinking: rambling or irrelevant conversation, unclear/illogical flow of ideas, difficulty expressing needs
  • Altered perception: paranoid delusions, misperceptions, visual or auditory hallucinations
  • Altered physical function: hyperactive (agitation, restlessness, increased sensitivity), hypoactive (lethargic, reduced mobility/appetite , lack of interest, withdrawn), mixed
  • Altered behaviour: intermittent and liable changes in mood/emotion, non-cooperative or inappropriate behaviour
  • Altered level of consciousness: reduced awareness, sleep disturbances (daytime drowsiness, insomnia, complete sleep cycle reversal)
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5
Q

How is delirium assessed and investigated?

A
  • Gain collateral history of events and background (will provide onset and details of their baseline cognition)
  • Physical examination: vital signs, and all systems
  • 4AT (four-item test of alertness, cognition, attention, and presence of acute change/fluctuating course)
  • Bloods: FBC, U&E, creatinine, glucose, calcium, magnesium, LFTs, TFTs, vitamin B12, cardiac enzymes, cultures (if indicated)
  • MSU
  • ECG
  • Bladder scan/stool chart (if indicated)
  • CXR (if indicated)
  • Further imaging e.g. head CT (if indicated)
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6
Q

What are the supportive and environmental managements of delirium?

A

Supportive:
- clear communication (adapted if needed)
- reorientation with reminders of day, time, location, people
- access to familiar objects (especially glasses, hearing aids, mobility aids)
- involvement of family
- consistency of staff
- relaxation

Environmental:
- avoid sensory extremes (over/under stimulation of noise, light, temperature etc.)
- adequate sleep (encourage a normal sleep/wake cycle)
- private space if possible or near to nurses station
- maintain competence e.g. walking
- adequate nutrition (assistance with oral intake, calorie rich foods, monitor weight)

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7
Q

What are the supportive and environmental managements of delirium?

A

Medical: (correct underlying precipitants)
- infection (antibiotics)
- constipation (laxatives)
- urinary retention (catheterisation, address any anticholinergics/immobility)
- dehydration and electrolyte abnormalities (monitor fluids, offer oral rehydration, correction of severe electrolyte imbalances)
- pain (regular and adequate analgesia, with careful monitoring with opiates)
- regular medications (consider recent changes)

Pharmacological:
- in patients who are aggressive or not responding to verbal de-escalation techniques (antipsychotics haloperidol or olanzapine may be used at the lowest possible dose for the shortest time)
- in delirium tremens (benzodiazepines diazepam or chlordiazepoxide are used)

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8
Q

Define vertigo and its causes

A

The hallucination of movement, and sensation of rotatory motion with respect to the patient and their environment, described as…
- peripheral: problems with the vestibular system, presenting as abrupt onset with nausea/vomiting and tinnitus (e.g. viral labyrinthitis, benign paroxysmal positional vertigo, Meniere’s disease, ototoxicity)
- central: problems with cerebral cortex, cerebellum or brain stem, presenting more gradually with less positional episodes, usually with other neurological signs (acoustic neuroma, stroke, vestibular migraine, MS)

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9
Q

Define benign paroxysmal positional vertigo

A

Most common cause of vertigo, occurring due to inner ear dysfunction when otoliths become detached from the macula into the semi-circular canals, causing hair cells on the detatched otoliths to be stimulated after the head as stopped moving which gives conflicting sensory inputs

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10
Q

What are the causes of benign paroxysmal postural vertigo?

A
  • Idiopathic (in 60%)
  • Head injury
  • Spontaneous degeneration of the labyrinth
  • Post-viral illness
  • Complication of stapes surgery
  • Chronic middle ear disease
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11
Q

What are the clinical features of benign paroxysmal positional vertigo?

A
  • Vertigo provoked by head movements (often worse on a particular side)
  • Sudden onset lasting 20-60 seconds, with a 5-20 second delay after the provocative movement
  • Commonly associated with nausea, but not vomiting, tinnitus, hearing loss, or pain
  • May present as a fall or non-specific dizziness in the elderly
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12
Q

What investigations are needed for benign paroxysmal postural vertigo?

A
  • Examination of external ear and tympanic membrane
  • Examine eye movements for nystagmus and saccades
  • Hearing test
  • Neurological examination (e.g. cranial nerves)
  • Hallpike manoeuvre (50-80% sensitive for BPPV)
  • Neuroimaging if any diagnostic uncertainty
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13
Q

What is the management of benign paroxysmal positional vertigo?

A
  • General advise: limit symptoms by getting out of bed slowly and reducing head movements
  • Consider safety e.g. driving, occupational hazards, risks of falls
  • Repositing techniques (e.g. Epley’s manoeuvre, or Brandt-Daroff exercises)
  • Avoid vestibular suppressant medications or surgery
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14
Q

What factors increase the frequency and severity of falls?

A

Frequency:
- intrinsic factors (balance, muscle strength, sensory input, peripheral and central nervous system)
- extrinsic factors (environment, lighting, obstacles, grab rails, height of steps, softness and grip of floor)
- lower threshold of stressors (e.g. pre-existing orthostatic hypotension, syncope)

Severity:
- multiple system impairments (leading to less effective saving mechanisms)
- osteoporosis
- secondary injury due to post-fall immobility (e.g. pressure sores, dehydration, pneumonia)
- psychological adverse effects (e.g. loss of confidence)

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15
Q

What medicals conditions associated with falls?

A
  • Affecting mobility, strength or balance (benign paroxysmal positional vertigo, Parkinson’s, orthostatic hypotension, arthritis
  • Affecting cognition: dementia, neurological conditions
  • Affecting sensory elements: visual impairment, peripheral neuropathy
  • Affecting bone health: osteoporosis (increased fracture risk)
  • Leading to urgent movement: urinary frequency, incontinence, infection
  • Cardiac conditions: aortic stenosis, atrial fibrillation, pacemakers, arrhythmias
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16
Q

What medications are associated with falls?

A
  • Antihypertensives e.g. ramipril, amlodipine (increased risk of hypotension)
  • Sedating drugs e.g. benzodiazepines, antipsychotics, opioids, anti-epileptics (increasing risk of drowsiness causing fall)
  • Diuretics e.g. furosemide, indapamide (increased risk of hypotension and electrolyte disturbances)
  • Antidepressants e.g. SSRIs, TCAs (increased risk of postural hypotension, sedation, and electrolyte disturbances)
  • Skeletal muscle relaxants e.g. baclofen (increased muscle weakness)
  • Diabetic medication e.g. insulin, SGLT2 inhibitors (increased risk of hypoglycaemia)
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17
Q

What investigations are needed for falls?

A
  • Functional assessment (e.g. stand from chair, walk, turn around)
  • Cardiovascular examination (lying and standing BP, pulse rate and rhythm, murmurs)
  • Neurological examination (identify stroke, Parkinson’s, vestibular disease, cognitive impairment, etc.)
  • Bloods (FBC, B12, folate, U&Es, calcium, phosphate, glucose, TFT)
  • ECG (24hr if patient has frequent near-syncope)
  • Echo (if systolic murmur)
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18
Q

Define syncope and presyncope

A
  • Syncope is a sudden transient loss of consciousness due to reduced cerebral perfusion, where the patient is unresponsive and loses postural control (falls)
  • Presyncope is a feeling of light-headedness that would lead to syncope if corrective measures were not taken (e.g. sitting or lying down)
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19
Q

What are the causes of syncope?

A

Neurally mediated syncope (reflex syncope)…
- vasovagal (simple faint): caused by emotional stress (fear, pain etc.) or orthostatic stress (prolonged standing, crowded, hot places)
- situational syncope: caused by cough, sneeze, GI stimulation, micturition
- carotid sinus hypersensitivity: occurs when rotating head, if collar is tight, if neck tumour present

Orthostatic hypotension…
- autonomic: Parkinson’s, multi system atrophy, diabetic neuropathy, medications, post-exercise, postprandial
- hypovolaemia: haemorrhage, vomiting, diarrhoea, dehydration, Addison’s disease

Cardiac causes…
- arrhythmias: VT, SVT, fast AF, complete heart block, long QT syndrome
- structural cardiopulmonary causes: acute coronary syndrome, obstructive cardiac valve disease, PE, pulmonary hypertension

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20
Q

What are the additional features in a history of syncope?

A
  • Was there loss of consciousness? (syncope has brief complete LOC lasting usually under 30 seconds, but may be several minutes)
  • What was the situation? (standing = orthostatic hypotension, exercise = cardiac, in pain/frightened = vasovagal, on the toilet = defecation/micturition syncope)
  • Was there a prodrome? (palpitations = arrhythmia, chest pain or SOB = ischemia, light-headedness = hypotension)
  • Description of the attack from eye witness (pale/clammy = systemic hypoperfusion, ictal features = seizure)
  • How was recovery? (long recovery, with prolonged drowsiness and confusion suggests seizure)
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21
Q

What is the management of falls?

A
  • Treat the underlying cause (often not found, multifactorial)
  • Drug review (reduce polypharmacy, reduce dose or stop medications that could contribute)
  • Treatment of orthostatic hypotension (advise to stand slowly, lie down at prodrome, fluid and salt replacement if needed, consider fludrocortisone or alpha-agonist)
  • Physiotherapy (strength and balance training, walking aids)
  • Occupational therapy (environmental assessment and modification)
  • Prevent adverse consequences (osteoporosis treatment, alarms, supervision, change of accommodation)
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22
Q

Define osteoporosis

A

Reduction in the bone mass density and disruption of the bone architecture, due to a prolonged imbalance of bone remodelling where resorption exceeds deposition, resulting in increased bone fragility and fracture risk

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23
Q

What are the risk factors for a fragility fracture?

A
  • Increasing age
  • Female
  • Low BMI
  • Parental history of hip fracture
  • Past history of fragility fractures
  • Corticosteroid therapy
  • Cushing’s syndrome
  • Alcohol intake of more than 3 units/day
  • Smoking
  • Conditions which increase falls risks (e.g. visual impairment, lack of neuromuscular co-ordination and strength, cognitive impairment, sedatives)
  • Secondary osteoporosis (rheumatoid arthritis, type 1 diabetes, premature menopause, chronic liver disease, IBD, coeliac, hyperthyroidism, hypogonadism)
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24
Q

What are the clinical features of osteoporosis?

A
  • The pathological process itself is asymptomatic
  • Often presents with fragility fractures (e.g. wrist, femoral neck, vertebral body)
  • Wedging of the vertebrae caused by higher load bearing by the anterior potion of the vertebral body, presenting as acute painful fracture, progressive kyphosis, or incidental findings
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25
Q

What are the investigations for osteoporosis?

A
  • DEXA scan: gives T score which compare BMD to peak bone mass (<-2.5 indicated osteoporosis)
  • X-ray: shows fractures
  • Bloods: identify treatable cause and rule out other causes (FBC, CRP, U+Es, LFTs, TFTs, calcium, testosterone in men)
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26
Q

What is the management of osteoporosis?

A
  • Calcium and vitamin D supplements if required

Antiresorptive therapy…
- oral bisphosphonates: e.g. alendronate, once weekly, taken 30 minutes before food/drink remaining upright for 30 mins, SE of GI issues, CI in oesophageal issues and hypocalcaemia
- IV bisphosphonates: e.g. zoledronate, 1st line in hip fractures, given as yearly infusion, possible SE of acute phase reaction, CI in hypocalcaemia and severe renal impairment
- monoclonal antibodies: e.g. denosumab, given as s/c injection every 6 months, SE of skin reactions, hypocalcaemia

Anabolic therapy…
- teriparatide: recombinant PTH, 1st line in postmenopausal women or men >50 at very high risk, given as daily s/c injection, SE of nausea, dizziness, postural hypotension, CI in hypercalcaemia, severe renal impairment, bone malignancy, pregnancy

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27
Q

What factors support a diagnosis of normal aging rather than pathological cognitive decline?

A
  • Ability to maintain function in normal life through aids (e.g. lists, calendars), or adaptation (e.g. of the environment, of one’s expectations)
  • A very long time scale of decline (10-30 years, rather than months-short years)
  • A relative decline to the person’s previous cognition
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28
Q

Define dementia

A

A syndrome of generalised decline of memory, intellect and personality, without impairment of consciousness, leading to functional impairment

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29
Q

Describe the difference between delirium and dementia

A
  • Onset: delirium has an acute onset, dementia has a more chronic onset
  • Reversibility: delirium is often reversible, dementia is rarely reversible
  • Fluctuation: delirium can fluctuate hour-to hour or diurnal, dementia has little fluctuation but have have diurnal variation (sundowning)
  • Attention and conscious level: both are affected and variable in delirium, not affected in dementia unless severe
  • Hallucinations: common in delirium, usually occurs in late stages of dementia and more likely to be visual
  • Short and long term memory: both are poor in delirium, but long term memory is often normal until the late stages of dementia
30
Q

Describe some different types of dementia

A
  • Alzheimer’s disease: degeneration of cholinergic neurons leading to a deficiency of acetylcholine in the cerebral cortex, with changes including cortical atrophy, neurofibrillary tangles, amyloid plaque formation
  • Vascular dementia: damage from cerebrovascular disease due to a major stroke, multi-infarcts (smaller unrecognised strokes), or chronic changes to small vessels (arteriosclerosis)
  • Lewy-body dementia: abnormal deposition of a protein (Lewy body) within the neurons of the brain stem, neocortex, and substantia nigra
  • Fronto-temporal dementia: specific degeneration (atrophy) of the frontal and temporal lobes, with a specific type being Pick’s disease (deposition of protein tangles/Pick’s bodies)
  • Other causes of dementia include Parkinson’s, infections (syphilis, HIV, CJD), substance misuse, folate/B12 deficiencies, normal pressure hydrocephalus, space-occupying lesions
31
Q

What are the clinical features of Alzheimer’s disease?

A
  • most common type, insidious onset with slow progression over years
  • Loss of memory (commonest presenting symptom, first short then long-term)
  • Disorientation to time and place
  • Impaired executive functions (problem solving, abstract thinking, decision making, judgement, organisation, processing)
  • Language disturbance (word finding difficulties, decreased vocabulary, perseveration, global aphasia)
  • Apraxia (difficulty with previously learned purposeful movements e.g. dressing, buttons, despite normal coordination and strength)
  • Visuospatial abilities (getting lost, impaired driving)
  • Non-cognitive symptoms: (hallucinations, delusions, emotional changes, abnormal behaviour)
32
Q

What are the clinical features of vascular dementia?

A
  • associated with vascular risk factors (diabetes, hypertension, smoking)
  • Stepwise and abrupt deterioration of cognition (including memory, orientation, executive function, attention, language function)
  • Emotional and personality changes (depressions, apathy), earliest symptoms
  • Neurological symptoms (e.g. unilateral spastic weakness, increased tendon reflexes, focal upper motor neuron signs, abnormal gait, urinary incontinence, dysphagia)
33
Q

What are the clinical features of Lewy body dementia?

A
  • Background of gradually progressive dementia, with insidious onset
  • Day to day fluctuations in cognitive performance
  • Recurrent visual hallucinations, often with paranoia and delusions
  • Parkinsonism motor signs (tremor, rigidity, bradykinesia)
  • Severe sensitivity to typical antipsychotics and dopamine agonists, which worsen confusion and parkinsonism
34
Q

What are the clinical features of front-temporal dementia?

A
  • Usual insidious onset aged 35-75, with slow progression
  • Behavioural changes (e.g. disinhibition, inflexibility, apathy, repetitive behaviours/compulsions, impaired executive functions, decreased personal care, lack of insight)
  • Language impairment (e.g. loss of vocabulary, difficulty finding words, loosing meaning/recognition of words/objects, slow or hesitant speech, loss of literacy skills)
  • Memory and other cognitive impairments may only be affected in later stages
35
Q

Describe normal pressure hydrocephalus

A
  • Condition of ventricular dilatation in the absence of raised CSF pressure on lumbar puncture
  • May be idiopathic, or have a secondary cause (head injury, meningitis, subarachnoid haemorrhage, CNS tumour)
  • Presents with triad of gait disturbance (wide-based), urinary incontinence, cognitive impairment
  • Investigations: neuroimaging, lumbar puncture (normal opening pressure, remove CSF to check for improved symptoms)
  • Treated with CSF shunt (to peritoneum, right atrium, or external drainage)
36
Q

What investigations are needed for cognitive impairment?

A
  • Bloods: FBC (infection, anaemia), CRP (infection, inflammation), U&Es (renal disease), LFTs (liver disease), calcium (hypercalcaemia), glucose (hypoglycaemia), vitamin B12 and folate (nutritional deficiencies)
  • Urinalysis (UTI)
  • Chest X-ray (pneumonia, tumour)
  • Syphilis and HIV testing (only if specific risk)
  • Brain imaging (indicated in early/sudden onset, risk of structural pathology, focal CNS signs): CT (can identify cortical atrophy), MRI (identifies posterior circulation pathology), SPECT (only in specialist centres, differentiate between types)
  • EEG: if fronto-temporal dementia, CJD, or seizure activity is suspected
  • Lumbar puncture: if meningitis or CJD is suspected
  • Genetic testing: for Huntington’s or familial dementia
  • Cognitive assessment: MMSE, AMT, 4AT etc
37
Q

What is the management for dementia?

A

Non-pharmacological:
- social support (support groups)
- assistance with ADLs (OT, carers)
- information and education
- community services (meals-on-wheels, day centres, respite care)
- alternative therapies (aromatherapy, massage, music, art, animal)
- carers support

Pharmacological:
- Acetylcholinesterase inhibitors e.g. donepezil, rivastigmine (cognitive enhancers for Alzheimer’s and Lewy body dementia
- Memantine (N-methyl-D-aspartate receptor antagonist), for severe Alzheimer’s on where AChE inhibitors are not tolerated/contraindicated
- Management of behavioural changes: short course antipsychotics (not Lewy body dementia), antidepressants for low mood

38
Q

Define Parkinson’s disease

A

Parkinson’s disease is an idiopathic movement disorder associated characterised by a resting tremor, rigidity, and bradykinesia, caused by degeneration of the dopaminergic pathways in the substantia nigra

39
Q

What are the clinical feature of Parkinson’s disease?

A
  • Tremor: worse at rest, pin-rolling movements
  • Rigidity: cogwheeling (due to tremor superimposed on rigidity)
  • Bradykinesia: slowness of voluntary movements, seen as reduced arm swinging, expressionless face, fatigability of repetitive movements)
  • Gait disturbances: small shuffling steps, difficulty rising from sitting, difficulty turning/stopping
  • Postural instability: tendency to fall
  • Non-motor features: late autonomic features (weight loss, dysphagia, orthostatic hypotension, drooling, constipation), sleep disturbance, depression, psychosis (related to medications)
    • signs are initially unilateral, then become generalised
40
Q

What investigations are needed for Parkinson’s disease?

A
  • Diagnosis is clinical
  • Neuroimaging (CT/MRI): exclude other causes, if fails to respond to L-dopa
  • SPECT scan can assist diagnosis
41
Q

Describe Parkinson’s disease with dementia

A
  • Defined as dementia occurring more than one year after a diagnosis of Parkinson’s disease
  • Similar to Alzheimer-type dementia, but with Parkinsonism in the limbs and frequent hallucinations and fluctuations in lucidity
  • Difficult to treat as confusion and hallucination may be worsened by Parkinson’s medication
    • if Parkinsonism develops after dementia, this is Lewy body dementia
42
Q

What investigations are needed for Parkinson’s disease?

A
  • Diagnosis is clinical
  • Neuroimaging (CT/MRI): exclude other causes, if not responded to L-dopa
  • SPECT: can assist diagnosis
43
Q

What is the management for Parkinson’s disease?

A

Non-pharmacological:
- physio and OT
- speech and language therapy
- care package

Drugs for motor symptoms:
- levodopa (plus decarboxylase inhibitor, prevent breakdown of drug, e.g. Madopar)
- dopamine agonists (ropinirole, pergolide, cabergoline)
- monoamine oxidase-B inhibitors (selegiline, rasagiline
- catechol-O-methyltransferase inhibitors (inhibit peripheral breakdown of L-dopa, e.g. entacapone)

Drugs for non-motor symptoms:
- SSRI for depression
- cholinesterase inhibitors (rivastigmine) for dementia
- modafinil for daytime sleepiness
- midodrine or fludrocortisone for orthostatic hypotension

Surgery:
- deep brain stimulation

44
Q

Define heart failure

A

A clinical syndrome resulting in reduced cardiac output and/or elevated intracardiac pressures, characterised by classical signs/symptoms and objective evidence of a structural/functional abnormality

45
Q

Describe the classification of heart failure

A

Acute and chronic:
- describes time rather than severity
- acute heart failure can present as new-onset, or acute decomposition, managed as an inpatient
- chronic heart failure describes a long-standing condition managed in the community

Ejection fraction:
- describes the percentage of blood in the left ventricle which is pumped with each heartbeat, which determines severity
- reduced LVEF (HFrEF) = 40% or less, significant reduction in LV systolic function
- mildly reduced LVEF = 41-49%
- preserved ejection fraction (HFpEF) = 50% of higher

46
Q

Describe the New York Heart Association staging of heart failure

A
  • Class I: no physical limitation, ordinary activity does not cause fatigue, breathlessness, or palpitations
  • Class II: slight physical limitation, comfortable at rest but ordinary activity causes fatigue, breathlessness, or palpitations
  • Class III: marked physical limitation, comfortable at rest but less than ordinary activity causes fatigue, breathlessness, or palpitations
  • Class IV: unable to carry out physical activity without discomfort, symptoms present at rest
47
Q

What are the causes of heart failure?

A
  • Coronary heart disease (especially Caucasians)
  • Hypertension (especially African Caribbeans)
  • Valvular heart disease
  • Cardiomyopathies
  • Pericardial disease (pericarditis, effusion)
  • Arrhythmias
  • Conditions that increase peripheral demand (e.g. anaemia, pregnancy, hyperthyroid, Paget’s disease, sepsis)
48
Q

What are the clinical features of heart failure?

A

Symptoms:
- Exertional dyspnoea and fatigue (limits exercise tolerance)
- Orthopnoea
- Paroxysmal nocturnal dyspnoea
- Fluid retention (causing pulmonary or peripheral oedema
- Nocturnal cough or wheeze (+/- pink frothy sputum)
- Light-headedness or syncope
- Anorexia

Signs:
- tachycardia
- low systolic blood pressure
- narrow pulse pressure
- displaced apex beat
- gallop rhythm (presence of S3)
- raised JVP
- bilateral basal end-inspiratory crackles +/- wheeze
- tachypnoea
- pleural effusions
- tender hepatomegaly (pulsatile in tricuspid regurgitation)
- peripheral oedema (ankles, sacral, ascites)

49
Q

What investigations are needed for heart failure?

A
  • Routine bloods: FBC (anaemia), U&Es (renal function, electrolyte abnormalities in fluid overload, LFTs (hepatic congestion, troponin (recent MI), lipids/HbA1c (ischemic risk profile)
  • N-terminal pro-B-type natriuretic peptide (NT-proBNP): increased with pressure overload on heart (can be raised/reduced in other causes)
  • ECG: abnormal in most cases (AF, left axis deviation due to LVH, prolonged PR interval, wide QRS, abnormal P waves)
  • CXR: (ABCDE) alveolar oedema, Kerley B lines, cardiomegaly, dilated upper lobe vessel, pleural effusions
  • Echocardiography: for all patients with suspected heart failure, identifies ventricular dysfunction, valve disease, cardiomyopathy, estimates ejection fraction
50
Q

What is the management of heart failure?

A

Lifestyle changes:
- smoking cessation
- encourage good nutrition (low salt)
- avoid excessive alcohol
- weight loss if obese
- exercise (as part of supervised cardiac rehab)

Pharmacological:
- diuretics (loop diuretics e.g. furosemide for symptoms control, thiazide diuretics added in end stage)
- ACE inhibitors (e.g. ramipril, started in all patients, use ARB as an alternative)
- beta blockers (e.g. bisoprolol, started in all patients)
- spironolactone (for continuing symptoms despite diuretic and ACEi)
- SGLT2 inhibitor ( e.g. empagliflozin, for continuing symptoms despite other therapy)
- digoxin (for continuing symptoms despite other therapy in sinus rhythm)
- ivabradine (for continuing symptoms despite other therapy in sinus rhythm)
- DOAC/warfarin (for AF, or intracardiac thrombus on echo)
- statins (for secondary prevention where the cause is IHD)

51
Q

What is end-stage heart failure, and when is it suspected?

A
  • End-stage heart failure = high risk of dying within 6-12 months
  • Frequent hospital admissions
  • Poor response to treatment and severe breathlessness at rest
  • Acute deterioration and frequent admissions from comorbid conditions (e.g. chest infection)
  • Poor QOL and dependence on others for ADLs
  • Low serum albumin, deterioration in eGFR and hypotension
52
Q

What should an advanced care plan address?

A
  • Sensitive, open, and honest information on prognosis
  • The person’s preferences regarding location they wish to be cared for in and resuscitation status
  • Anticipatory prescribing of medication to manage symptoms
  • When, who, and how to call for help in a crisis or acute exacerbation
  • The needs for psychological and spiritual care
  • Care for the family (before and after the person’s death)
53
Q

What pre-emptive medications are used in end of life care?

A
  • Analgesia/dyspnoea: morphine (oxycodone in renal impairment)
  • Antisecretory: hyoscine (antimuscarinic)
  • Antiemetic: haloperidol
  • Sedative: midazolam (benzodiazepine)
54
Q

Describe malnutrition in the elderly

A
  • Normal aging includes reduced calorie requirements, reduction in appetite, and lower reserves of macro and micronutrients
  • Malnutrition therefore occurs quickly in the presence of disease, and nutritional status declines further if hospitalised
55
Q

How is nutrition assessed?

A
  • BMI (approximations can be made using ulnar length and mid-arm circumference
  • Screening tools (e.g. MUST)
  • Biochemical measurements (e.g. anaemia, hypoalbuminaemia, hypocholesterolaemia)
56
Q

What does nutritional support involve?

A
  • Early identification and involvement of MDT including dietician
  • Record food intake
  • Prioritise mealtimes (protected times, provide assistance)
  • Establish food preferences and offer high-calorie foods
  • Prescribe dietary supplements according to patient preferences (e.g. milky/fruity drinks, soups, yogurts, puddings)
  • Consider role of enteral feeding
57
Q

Describe enteral feeding

A
  • Considered if there is dysphagia (e.g. stroke, MND) or failure of oral feeding (anorexia, ICU) with a functioning GI tract
  • Common methods are NG tube (preferred short term but risks of self-removal), PEG (more complicated insertion, but better tolerated and discrete)
  • Complications include aspiration pneumonia, refeeding syndrome, fluid overload, diarrhoea
58
Q

Define constipation

A

The term constipation can be used to describe one or more of…
- the time between bowel evacuations being longer than normal
- the stool being harder, dryer, or smaller than normal
- an increase of total faecal mass within the abdomen

58
Q

Describe parenteral feeding

A
  • Consider when the gut is not functioning, usually as a temporary measure
  • Requires central venous access, and only under supervision of specialist nutritional team
  • Complications include fluid overload, electrolyte disturbance, IV catheter sepsis
59
Q

What are the causes of constipation in the elderly?

A

Reduced bowel motility:
- drugs (opiates, iron, anticholinergics, antidepressants, calcium channel blockers)
- immobility
- electrolyte disturbances (hypercalcaemia, hypokalaemia)
- hypothyroidism
- dehydration
- lack of fibre

Failure to evacuate bowels fully:
- anorectal disease (haemorrhoids, fissure, stricture, prolapse)
- difficulty accessing toilet
- post operative pain
- lack of privacy
- altered daily routine

Neuromuscular:
- Parkinson’s disease
- diabetic neuropathy
- spinal or pelvic nerve injury

Mechanical obstruction:
- malignancy
- diverticular disease
- pelvic mass (e.g. fibroids)
- pseudo-obstruction

60
Q

How is constipation assessed?

A
  • Suspect in elderly patients presenting with confusion, nausea, loss of appetite, overflow diarrhoea, urinary retention
  • Rectal examination may be diagnostic, but empty rectum may indicate high impaction (confirmed with adnominal X-ray)
  • Investigations needed if age >40, recent change in bowel habit, associated symptoms (FBC, U&E, Ca, TFTs, sigmoidoscopy)
61
Q

How is constipation managed?

A

Supportive management:
- treat cause
- mobilise patient
- increase fluid intake
- increase intake of high-fibre foods (fruit, veg, whole wheat, bran)
- improve access to toilet

Drug therapy:
- bulking agents (bran powder, ispaghula husk, methylcellulose)
- osmotic agents (macrogols, lactulose, laxido)
- stimulants (oral - senna, bisacodyl, suppositories - bisacodyl, glycerol, enemas - docusate sodium, sodium phosphate,
- stool softeners (arachis oil enema)

62
Q

Define pressure sores

A

Skin damage occurring due to pressure-induced ischemia, presenting as red, blistered, broken, or necrotic areas that may extend to underlying structures

63
Q

What are the risk factors for pressure sores?

A
  • Older age
  • Immobility (especially postoperatively)
  • Low or high body wight
  • Malnutrition
  • Dehydration
  • Incontinence
  • Decreased consciousness
  • Cognitive impairment
  • Neuropathy
  • Vascular impairment
  • Peripheral oedema
64
Q

Describe the grading of pressure sores

A
  • 0: skin hyperaemia (redness)
  • 1: non-blanching erythema of intact skin
  • 2: partial-thickness skin loss (epidermis +/- dermis)
  • 3: full-thickness skin loss (down to subcutaneous fat
  • 4: tissue necrosis and ulceration down to muscle/bone
65
Q

What is the management of pressure sores?

A
  • Mobility and positioning (encourage mobilising, reposition regularly, avoid direct pressure)
  • Pressure relief (high specification foam/alternating pressure mattresses, cushions)
  • Wound management (wound dressings and topical treatments)
  • Promote healing (good nutrition, glycaemic control, manage incontinence)
  • Pain relief
  • Infection control (antibiotics needed if signs of cellulitis or sepsis)
  • Debridement (removal of necrotic tissue, can be autolytic using bodies own enzymes, or surgical)
66
Q

Define rhabdomyolysis

A

A clinical syndrome associated with the breakdown of skeletal muscle and release of myoglobin which is nephrotoxic in high levels, causing acute renal failure

67
Q

What are the causes of rhabdomyolysis?

A

Anything that leads to muscle necrosis:
- trauma
- significant prolonged pressure (e.g. long lie after fall)
- burns
- compartment syndrome
- alcohol misuse
- over exertion
- status epilepticus
- heat stroke
- neuroleptic malignant syndrome
- drugs (e.g. statins)

68
Q

What are the clinical features of rhabdomyolysis?

A
  • Non-specific (e.g. fever, malaise, nausea, vomiting, anorexia)
  • Muscle pain and weakness
  • Signs of clinical dehydration
  • Confusion, agitation, delirium (in elderly)
  • Dark urine
69
Q

What investigations are needed for rhabdomyolysis?

A
  • CK levels: raised at least 5 times normal
  • Potassium: raised
  • Calcium: low
  • Urine dipstick: positive for blood (haemoglobin present, but no RBCs)
70
Q

What is the management of rhabdomyolysis?

A
  • Aggressive rehydration (with monitoring of urine output and renal function)
  • Treat hyperkalaemia (calcium gluconate and dextrose-insulin infusion)
  • Haemodialysis if renal failure