COTE Flashcards
Define delirium
An acute and fluctuating disturbance in consciousness
Describe the key features of delirium
-change in cognition: widespread memory impairment, disorientation, language disturbance, hallucinations
-acute onset/fluctuating: onset over hours or a few days with severity worsening throughout the day
-disturbance of consciousness: decreased ability to focus or sustain attention, distractibility, losing track of conversations
Other: sleep disturbance, emotional disturbance, delusions and restless or listless
What are the two main types of delirium?
Hyperactive: agitation, aggression, psychotic symptoms, oversensitive to stimuli, repeatedly getting out of bed/trying to wander
Hypoactive: lethargic, quiet, few psychotic symptoms, slower speech/not talking (less commonly diagnosed so worse prognosis)
can be mixed
What are the predisposing factors for someone developing delirium?
Old age <65 years old
Cognitive impairment eg dementia
Frailty/multiple comorbidities
Significant injuries eg hip fracture
Surgery
History of (or current) alcohol excess
Sensory impairment eg deaf or blind
Lack of stimulation
Terminal phase of illness
Surgery
Polypharmacy
What are the causes of delirium?
Infection: viral/bacterial eg UTI, pneumonia, biliary infection
Drugs: changes to medication/new medication OR illegal drugs eg in a younger person
Electrolyte/Fluid imbalance: dehydration, hypercalcaemia
Alcohol or drug withdrawal
Organ failure eg cardiac
Endocrine: hypo or hyperthyroid or low/high blood sugars
Epilepsy
Intercranial pathology: have they had recent head trauma?
Pain
CONSTIPATION (in elderly people)
Changes to environment eg home –> hospital, family/carers not around, overstimulation in hospital environment
Give the drug classes and examples of drugs that can cause delirium
Anticholinergics: atropine
Antipsychotics: chlorpromazine, thioridazine
Antidepressants: tricyclics
Opiates: codeine, tramadol
Corticosteroids: prednisolone
Investigations for delirium
Basic obs at bedside: are they in pain, BP, pulse ox, last time BO
Bloods:
-confusion screen= U&Es (dehydration/hypercalc), B12, TFTs, glucose
-FBC
-Coagulation eg intercranial bleed?
CXR- pneumonia?
Mid-stream urine/urinalysis- UTI
Management for delirium
Non-Medical: quiet environment, ensure patient gets enough sleep, presence of family/carers, use of clocks to orient to time, familiar objects, calm manner when dealing with the patients, keep routine as similar as possible
Medical: treat cause if possible eg
-antibiotics: pneumonia or UTI
-plenty of fluids and nutrition to avoid patient becoming dry
-laxatives for constipation
-pain relief if in pain
Drug management for delirium
-only if patient is threatening safety of themselves/others or interfering in medical treatment
-should be used as a last resort
-minimum effective dose
-dose PRN
-short acting benzodiazepines eg lorazepam
Differences between delirium and dementia
Delirium:
-acute/subacute
-often reversible
-fluctuation common throughout the day
-poor attention
-conscious level usually affected but may be subtle
-hallucinations and misinterpretations common
-agitation and aggression common
-disorganised thought and unreal ideas
-motor signs inc tremor or asterixis
-poor short AND long term memory
-dysgraphia
Dementia:
-chronic onset
-rarely reversible
-little diurnal variation
-poor attention in severe dementia
-normal conscious level
-hallucinations in later disease
-agitation and aggression uncommon in early disease
-disorganised thought in later disease
-motor signs only later
-speech normal
-dysgraphia present later
-long term memory often normal till later
Define dementia
Progressive and acquired decline in the memory and cognitive functioning of an alert person with daily life significantly affected
Describe the pathology of Alzheimer’s disease
Pathological changes:
-deposits of beta-amyloid plaques occur outside of neurons. Amyloid precursor protein (APP) helps neurones grown and repair. Normally broken down by alpha secretase and gamma secretase into a soluble peptide. If beta secretase breaks down APP, it creates a monomer called amyloid beta, which is sticky. They can bind together to form the beta amyloid plaques.
-Neurofibrillary tangles made of the protein tau which holds the tubules of the neuron cytoskeleton together. The beta amyloid plaque build up leads to the activation of kinase inside the neuron. This leads to phosphorylation of the tau protein, changing its shape and clumping with other tau proteins.
Neurones with tangles do not function as well and end up apoptosing and the brain begins to atrophy.
What are two most common types of dementia?
Vascular dementia and Alzheimer’s
Describe the symptoms and progression of Alzheimer’s
Insidious onset, with progressive but slow decline.
-poor memory
-language problems
-disorientation
-agitation
-sleep disturbance
-anxiety and depression
-withdrawal/apathy
-motor disturbance
-loss of independence
Early stages begin with profound short term memory loss and issues with high functioning eg finances leasing to later stages of broad cognitive dysfunction and behavioural changes
Describe the investigations and their findings in Alzheimer’s
Physical exam- normal
Neuroimaging- shows no other causes of dementia eg infarct with disproportionate medial temporal lobe atrophy
Cognitive assessment: MMSE assesses different areas of higher cortical functioning
Describe the pathology of vascular dementia
Vascular dementia is a progressive loss of brain function caused by long term poor blood flow to the brain usually because of a series of strokes
Atherosclerosis in arteries to the brain leads to plaques breaking off and blocking smaller arteries or small arteries can get completely blocked with plaque growing inside them
Once blood flow to parts of the brain is stopped, the tissue becomes damaged leading to necrosis and a loss of mental functions governed by that area
Describe the symptoms and progression of vascular dementia
Progression is often a sudden decline in function and appears stepwise, with cognitive impairment patchy vs the uniform impairments of Alzheimer’s
-front lobe symptoms: falls, depression, reduced creativity, impaired judgement
-extrapyramidal symptoms: parkinsonism, restlessness, involuntary muscle contractions
-pseudobulbar features: involuntary outbursts of emotion
-other features mimic Alzheimer’s eg memory issues, language problems etc
-depression and apathy also common symptoms
Urinary incontinence and falls without other explanation are often early features
Describe the investigations and their results in vascular dementia
Physical exam: focal neurology showing hyperreflexia, extensor plantars, abnormal gait
Neuroimaging: multiple large vessel infarcts OR a single critical infarct eg thalamus OR white matter infarcts or periventricular white matter changes OR microvascular disease that may be too fine to be seen on neuroimaging
Describe the general dementia management
General: modify reversible aggravating factors eg constipation, drug side effects, mild anaemia and treat depression with SSRIs. Carers for helping with ADLs, medications etc
Social: encouraging physical and mental activity, creating a safe and caring environment with a predictable routine PLUS respite and support for caregivers/family.
Practical: simple interventions eg alarms & calendars and simplifying medication eg with dosette boxes
Contraindications for starting anti-cholinesterase inhibitors?
QT prolongations, second or third degree heart block in an unpaced patient, sinus bradycardia of <50bpm
May make incontinence worse
Describe the medical management of Alzheimers & Lewy Body dementia
Acetylcholinesterase inhibitors: they work by blocking acetylcholinesterase which breaks down acetylcholine
-mostly useful in Alzheimer’s, Lewy body and Parkinson’s disease dementia as they have the greatest cholinergic deficits- rivastigamine, galantamine, donepezil
Memantine: blocker of NMDA receptors that may reduce glutamate mediated destruction of cholinergic neurons
What are the factors that influence fall frequency?
Intrinsic factors: maintaining balance is complex- requires good muscle strength, stable joints, multiple sensory modalities and a functional peripheral/central nervous system.
Extrinsic factors: environmental factors eg lighting, steps, shoes, floor surface, presence of rails
What are the factors that influence fall severity?
-multiple system impairments leading to less effective saving mechanisms
-osteoporosis and increased facture rates
-secondary injury due to post fall immobility eg bed sores, pneumonia and dehydration
-psychological adverse effects eg loss of confidence
List some possible causes of falls
cardiovascular: arrhythmias, orthostatic hypotension, bradycardia, valvular heart disease
Neurological: stroke, peripheral neuropathy
GU: UTI, incontinence
Endocrine: hypoglycaemia
MSK: arthritis, disuse atrophy
ENT: benign paroxysmal positional vertigo, ear wax
Polypharmacy
What drugs are associated with falls?
Drugs can be either directly psychoactive or may lead to systemic hypotension and cerebral hypoperfusion —>
-benzodiazepines
-antidepressants eg SSRIs
-Opiates
-diuretics
-anti HTN esp ACE-i and alpha blockers
-antiarrhythmics
-hypoglycaemics
Describe the investigations for falls
Bedside: vital signs
BP lying and standing: orthostatic hypotension
Urine dipstick: infection & rhabdomyolysis
ECG: bradycardia and arrhythmias
Cognitive screening eg AMT: cognitive impairment
Blood glucose: hypoglycaemia
FBC: anaemia/ raised WBC
U&Es: dehydration and electrolyte abnormalities eg hypocalc
LFT: alcohol use
Bone profile: calcium abnormalities
CXR: pneumonia
CT head: chronic or acute subdural, stroke
Echo: valvular heart disease
How is fall frequency reduced?
-Drug review
-Treatment of orthostatic hypotension
-Strength and balance training
-Walking aids
-Environmental assessment and modification eg by OT
-Vision
What is orthostatic hypotension?
When someone experiences a drop in BP of >20mmHg systolic or 10mmHg diastolic when going from lying/sitting to standing
What are the causes of orthostatic hypotension?
Drugs: vasodilators, diuretics, B blockers, CCB, opiates
Chronic hypertension
Volume depletion eg dehydration or haemorrhage
Sepsis leading to vasodilation
Autonomic failure eg diabetes, Parkinson’s, dementia
Prolonged bed rest
Adrenal insufficiency
Raised intrathoracic pressure
What is the first line investigation into orthostatic hypotension?
Posture Test
BP should be measure on sitting/lying and after standing for 3 minutes.
Multiple BP measurements should be taken
If the HR doesn’t raise as much as expected eg <15pbm cause of the hypotension is probably neurogenic eg peripheral neuropathy
What is the treatment for orthostatic hypotension?
-treat the cause eg changing/reducing drugs
-reduce consequences of falls eg pendant alarms
-modify behaviour eg getting up slowly, reduce dehydration
-consider starting drugs eg fludrocortisone to raise BP or desmopressin
What is syncope?
Sudden, transient loss of consciousness due to a reduced cerebral perfusion
What is presyncope?
A feeling of light-headedness that would lead to syncope if corrective measures were not taken
What are the causes of syncope?
Peripheral factors: eg orthostatic hypotension, low circulating volume eg dehydration
Vasovagal syncope: common in young and old people. Vagal stimulation eg pain, fright, emotion leads to hypotension. Prodrome eg pale, clammy and light headed followed by nausea and abdo pain and then syncope
Carotid sinus syndrome
Pump problem: myocardial infarction or ischaemia/arrhythmia
Outflow obstruction eg aortic stenosis
Pulmonary embolism
What are the investigations for syncope?
Bloods: check for anaemia, sepsis, kidney function
ECG: look at PR interval, QT interval, ischaemic changes, LVH
Holter monitor: if arrhythmias suspected
Lying and standing BP
Define Parkinson’s Disease
A neurodegenerative disorder characterised by loss of dopaminergic neurones within the substantia nigra pars compacta of the basal ganglia. There may also be Lewy Body formation in the substantia nigra as well.
What is the pathophysiology of Parkinson’s?
There is a progressive reduction of dopamine in the basal ganglia of the brain which leads to disorders of movement.
What are the motor signs and symptoms of Parkinson’s?
Bradykinesia: slowness in initiation of voluntary movement. Increased repetitive actions
OR hypokinesia: reduced facial expression/arm swing and difficulty with fine movements eg buttoning clothes and opening jars
-cogwheel rigidity
-rest tremor which improves on sleeping/moving/increased concentration
-balance problems
Describe some of the non-motor signs and symptoms of Parkinson’s?
-depression/anxiety/fatigue
-reduced sense of smell
-cognitive impairment
-sleep disturbance
-constipation
How is Parkinson’s diagnosed?
PD is mainly a clinical diagnosis –> should be suspected in patients with tremor, rigidity, postural instability and bradykinesia
What is the management of PD?
A dopamine agonist eg levodopa
OR a monoamine oxidase-B inhibitor eg rasagiline
PLUS physical and non-pharmacological therapies
Define osteoporosis
A bone disease characterised by low bone mass and structural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture. It is normally asymptomatic until a fragility fracture occurs. Older people who have had a fragility fracture almost certainly have osteoporosis
What is an osteoporotic fracture?
A fragility fracture occurring as a consequence of osteoporosis. Fractures usually occur in the wrist, spine and hip- can occur in ribs/pelvis
What is a fragility fracture?
A fractures following a fall from standing height or less as a result of routine activities eg bending or lifting
What are the risk factors for osteoporosis?
SHATTTERED
Steroid use
Hyperthyroidism, hyperparathyroidism
Alcohol use
Thin BMI <18.5
Testosterone decrease
Early menopause
Renal or live failure
Erosive/inflammatory bone disease eg rheumatoid arthritis
Dietary eg reduced Ca, malabsorption, DM
What are the investigations for osteoporosis?
Blood tests: normal (unless after a fracture)
DEXA scan- usually used in younger people and rarely used in older population
Secondary causes:
TSH for all
Testosterone levels in men
What is a DEXA scan and what scores does it produce?
Measures bone mineral density (BMD) by measuring how much radiation is absorbed by the bones. Reading at hip is key.
Two scores:
Z score - represents the number of standard deviations the patient’s bone density falls below the mean for their age
T score - represent the number of standard deviations below the mean for a healthy young adult their bone density is
What is the pathophysiology for osteoporosis?
The activity of osteoclasts increases and is not matched by the osteoblasts so bone mass decreases.
Glucocorticoids increase bone turnover
Oestrogen is protective
How is osteoporosis managed?
Not steroid induced : bisphosphonate eg alendronic acid or IV zol, calcium and vitamin D supplementation
Steroid induced: stop steroids, bisphosphonate and calcium/vitamin D supplementation
