Geriatrics Flashcards
Common causes of delirium
PINCHME
Pain
Infection
Nutrition
Constipation
Hydration
Medication
Environment
What is dementia?
the decline in memory with impairment of at least one other cognitive function - eg skilled movements, language or executive function
Hypoactive delirium vs Hyperactive delirium
Hypoactive = more common, lethargy, drowsiness, reduced appetite and concentration
Hyperactive = agitation, restlessness and confusion that can vary throughout the day
Give a definition of TIA
Transient (< 24 hrs) neurological dysfunction caused by focal brain, spinal cord, or retinol ischaemia, w/out evidence of acute infarction
ABCD2 score factors
Age >60
Blood pressure
Clinical presentation (unilateral leg weakness, speech impairment)
Diabetes
Give a definition for stroke
What are the 2 types and their prevalence?
sudden onset of rapidly developing focal or global neurological disturbance which lasts for >24hrs or leads to death, w/ no other apparent cause other than of vascular origin
Ischaemic = 85%
Haemorrhagic = 15%
Causes of ischaemic stroke
atherosclerosis
cardio-embolic
dissection
Investigations for stroke
Brain imaging - non contrast CT (rule out haemorrhagic), MRI w/ diffusion-weighted imaging
Blood tests - FBC, coag profile, renal, electrolytes, LFT, lipid and glucose
further = echo, carotid imaging, ECG, cerebral angiography
Management of ischaemic stroke
short term = anti-platelets (aspirin, clopidogrel), manage bp, thrombectomy
long term = lifestyle (diet, SEA), reduce lipids, longterm bp
Can you drive after a stroke?
not for a month. Might need assessment to be able to drive again
What is thrombolysis?
A drug (eg alteplase) used as a clot buster after a stroke or PE
considered if pt presents w/in 4.5hr of stroke
Causes of haemorrhagic stroke
CAA - amyloid beta peptide deposits in walls of blood vessels
HTN
aneurysms
AV malformations
trauma
blood thinners - antiplatelet and anticoagulants
Management of haemorrhagic stroke
bp management - 140/80
reverse coagulation
neurosurgical referral
if develop hydrocephalus - consider insertion of external ventricular drain
Causes of dementia
Common = Alzheimer’s, cerebrovascular disease, Lewy body
Rarer = Huntington’s, CJD, Pick’s disease, HIV
What is CJD?
Creutzfeldt-Jakob disease
rare and fatal condition that affects the brain, causes brain damage that worsens rapidly over time
What is Pick’s disease?
rare, progressive, degenerative brain disease atrophy of frontal and temporal lobes
Dementia differentials
hypothyroidism - Addison’s
B12 / folate / thiamine deficiency
syphilis
brain tumour
normal pressure hydrocephalus
subdural haematoma
depression
chronic drug use
Main subtypes of vascular dementia
stroke-related VD (multi-infarct or single-infarct dementia)
subcortical VD (caused by small vessel disease)
mixed dementia (both VD and Alzheimer’s)
Risk factors of Vascular dementia
history of stroke or TIA
AF
HTN
DM
hyperlipidaemia
smoking
obesity
coronary heart disease
FH of stroke or CVD
How does Vascular dementia present?
several months or several years of a history of a sudden or STEPWISE DETERIORATION of cognitive function
Vascular dementia symptoms
focal neuro abnormalities
difficulty w/ concentration and attention
seizures
memory disturbance
gait disturbance
speech disturbance
emotional disturbance
How to diagnose vascular dementia?
comprehensive history and physical exam
formal screen for cognitive impairment
med review to exclude medication cause
MRI scan
Non-pharmacological management of vascular dementia
cognitive stimulation programmes
multisensory stimulation
music and art therapy
animal-assisted therapy
managing challenging behaviours - address pain, clear communication, avoid overcrowding
Pharmacological management of vascular dementia
no specific treatment approved
only consider AChE inhibitors for ppl w/ VD if suspected comorbid AD, Parkinson’s or Dw/LB
Memory Screening Tests
6CIT - 6 item cognitive impairment test
10-CS - 10 point cognitive screener
mini-cog
general practitioner assessment of cognition - GPCOG
MoCA
What is the ACE-III?
Addenbrooke’s cognitive examination
tool for memory impairment
tests: attention, memory, language, visuospatial function, verbal fluency
/ 100
<88 indicates dementia
Characteristic pathology of Lewy bodies dementia
alpha-synuclein cytoplasmic inclusions (Lewy bodies) in substantia nigra, paralimbic and neocortical areas
Features of Lewy body dementia
- progressive cognitive impairment - typically occurs before parkinsonism but usually both features occur w/in a year of eachother
- parkinsonism
- visual hallucinations
Diagnosis of Lewy body dementia
usually clinical
SPECT / DaTscan (single-photon emission computed tomography)
Lewy body dementia management
acetylcholinesterase inhibitors (eg donepezil, rivastigmine) and memantine
neuroleptics should be avoided as pts may develop irreversible parkinsonism
Risk factors of Alzheimer’s disease
increasing age
family history
autosomal dominant trait
caucasian
Down’s syndrome
apoprotein E allele E4
Pathological changes in Alzheimer’s disease
Macroscopic = widespread cerebral atrophy, particularly cortex and hippocampus
Microscopic = cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of tau protein
Biochemical = acetylcholine deficit from damage to an ascending forebrain projection
What are neurofibrillary tangles?
paired helical filaments are partly made from tau protein - tau interacts w/ tubulin to stabilise microtubules and promote tubulin assembly into microtubules.
Tau protein and Alzheimer’s disease
tau proteins are extremely phosphorylated, impairing its function
Management of mild to moderate Alzheimer’s disease
acetylcholinesterase inhibitors eg donepezil, galantamine and rivastigmine
second-line treatment of Alzheimer’s disease
memantine - NMDA receptor antagonist
Donepezil contraindication and adverse effect
contraindicated in pts w/ bradycardia
adverse effects include insomnia
What is Parkinson’s disease?
progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra
Triad of features of Parksinson’s disease
Bradykinesia - difficulty initiating movement, short shuffling steps w/ arm swinging
‘Pill rolling’ Resting Tremor - 3-5 Hz, worse when stressed/tired
Rigidity - lead pipe, cogwheel - due to superimposed tremor
characteristically asymmetrical
Other characteristic features of Parkinson’s disease
mask-like facies
flexed posture
micrographia
drooling
depression
impaired olfaction
fatigue
postural htn
How does drug-induced parkinsonism differ to Parkinson’s disease?
motor symptoms are generally rapid onset and bilateral
rigidity and rest tremor are uncommon
Diagnosis of Parkinson’s disease
usually clinical
could use SPECT - discolouration of substantia nigra or +ve staining for alpha-synuclein
Parkinson’s disease first-line treatment
if motor symptoms affecting pt’s qol = levodopa
if motor symptoms not affecting pt’s qol = dopamine agonist - levodopa or monoamine oxidase B (MAO-B) inhibitor
Risk if Parkinson’s medication isn’t taken / absorbed eg due to gastroenteritis
risk of acute akinesia or neuroleptic malignant syndrome
Side effects of levodopa
dry mouth
anorexia
palpitations
postural htn
psychosis
What should be prescribed w/ levodopa?
decarboxylase inhibitor eg carbidopa or benserazide
prevents peripheral metabolism of levodopa to dopamine outside brain, reduce side effects
adverse effects due to lack of steady dose of levodopa
end-of-dose wearing off = symptoms worsen towards end, results in decline of motor activity
‘on-off’ phenomenon = large variations in motor performance, normal function in ‘on’ period, weakness and restricted mobility in ‘off’ period
dopamine receptor agonists examples
bromocriptine
ropinirole
cabergoline
apomorphine
MAO-B inhibitors examples
selegiline - inhibits breakdown of dopamine secreted by dopaminergic neurons
What is amantadine? What are the side effects?
used to treat dyskinesia and Parkinsons symptoms
side effects = ataxia, slurred speech, confusion, dizziness, livedo reticularis
COMT inhibitors
entacapone, tolcapone
COMT is an enzyme involved in dopamine breakdown, may be used to adjunct levodopa therapy, used in conjunction w/ levodopa in established PD pts
Antimuscarinics
procyclidine, benzotropine, trihexyphenidyl
block cholinergic receptors
now used more to treat drug-induced parkinsonism
helps tremor and rigidity
Causes of Parkinsonism
Parkinson’s disease
drug-induced eg antipsychotics, metoclopramide
progressive supranuclear palsy
multiple system atrophy
Wilson’s disease
post-encephalitis
dementia pugilistica
toxins - carbon monoxide, MPTP
How does the prevalence of osteoporosis increase in women?
from 2% at 50yrs to
>25% at 80yrs
Risk factors of osteoporosis (used in FRAX)
history of glucocorticoid use
rheumatoid arthritis
previous fragility fracture
alcohol excess
history of parental hip fracture
low BMI
current smoker
Other risk factors of osteoporosis
sedentary lifestyle
premature menopause
caucasians and asians
endo disorders (hyperthyroidism, hypogonadism)
multiple myeloma, lymphoma
GI disorders
chronic kidney disease
osteogenesis imperfecta
What medications may worsen osteoporosis?
SSRIs
antiepileptics
proton pump inhibitors
glitazones
long term heparin therapy
aromatase inhibitors eg anastrozole
Tests for osteoporosis
history and physical exam
FBC
urea and electrolytes
LFT
bone profile
CRP
thyroid function test
When would a DEXA scan be offered w/out calculating fragility risk score?
> 50 yrs w/ fragility fracture history
<40yrs w/ major fragility fracture risk (depends on T-score)
before starting treatments that may have a rapid adverse effect on bone density
Qfracture score meaning
if 10yr fracture risk is ≥ 10% then DEXA scan should be arranged
FRAX score meaning
green, orange or red
orange = DEXA scan if not already to further refine 10yr risk
red = DEXA scan to act as baseline and guide drug treatment
When should FRAX / Qfracture be recalculated?
original calculated risk was in region of intervention threshold for proposed treatment and only after minimum 2yrs
when there’s been a change in person’s risk factors
What is a T score?
based on bone mass of young reference population
What is Z score?
bone density adjusted for age, gender and ethnic factors
What would a T score of -1 mean?
bone mass of 1 std dev below that of young reference population
T score results meanings
> -1 = normal
-1 to -2.5 = osteopaenia
< -2.5 = osteoporosis
Bisphosphonates function
inhibit osteoclasts by reducing recruitment and promoting apoptosis
Clinical uses of bisphosphonates
prevention and treatment of osteoporosis
hypercalcaemia
Paget’s disease
pain from bone metastases
adverse effects of bisphosphonates
oesophageal reactions - oesophagitis, ulcers
osteonecrosis of jaw
increased risk of atypical stress fractures of proximal femoral shaft (alendronate)
acute phase response - fever, myalgia and arthralgia
hypocalcaemia
Counselling for pts taking oral bisphosphonates
tablets should be swallowed w/ plenty of water
while sitting or standing
empty stomach
at least 30 mins before breakfast
stand or sit upright for at least 30 mins after taking tablet
What may a person become deficient in due to bisphonates?
vitamin D - hypocalcaemia should be corrected before treatment
calcium only prescribed if dietary intake is inadequate
vitamin D supplements also given
Why might bisphosphonates be stopped after 5 years?
pt <75yrs
femoral neck T-score > -2.5
low risk according to FRAX / NOGG
What is denosumab?
new treatment for osteoprosis
human monoclonal antibody that prevents osteoclast development by inhibiting RANKL
How is denosumab given?
subcutaneous injection every 6 months, 60mg
larger dose 120mg may be given every 4wks for prevention of skeletal-related events in adults w/ bone metastases from solid tumours
First line treatment of osteoporosis
oral bisphosphonates - alendronate
alternative = risedronate or etidronate
Denosumab side effects
dyspnoea
diarrhoea
hypocalcaemia
upper resp tract infections
Risk in hip fractures
avascular necrosis - blood supply to femoral head runs up neck
Features of a hip fracture
pain
shortened and externally rotated leg
pts w/ non-displaced or incomplete neck of femur fractures may be able to weight bear
Classifying hip fractures by location
intracapsular (subcapital) - from edge of femoral head to insertion of capsule of hip joint
extracapsular - can be either trochanteric or subtrochanteric (lesser trochanter is dividing line)
Garden System Classification
classifies hip fractures
TI = incomplete fracture and non-displaced
TII = complete fracture but non-displaced
TIII = partial displacement - trabeculae at angle
TIV = full displacement - trabeculae parallel
When is bloody supply disruption most common in terms of the Garden system classification of hip fractures?
Types III and IV
Intracapsular hip fracture management
Undisplaced = internal fixation, or hemiarthroplasty if unfit
Displaced = replacement arthroplasty (ttl hip replacement or hemiarthroplasty)
Extracapsular hip fracture management
for stable intertrochanteric fractures = dynamic hip screw
if reverse oblique, transverse or subtrochanteric features = intramedullary device
What is osteopetrosis?
marble bone disease
rare disorder of defective osteoclast function resulting in failure of normal bone resorption
results in dense, thick bones that are prone to fracture
bone pains and neuropathies are common
calcium, phosphate and ALP are normal
treatment = stem cell transplant and interferon-gamma
What is osteomyelitis? How can it be subclassified?
infection of the bone
subclassified into haematogenous osteomyelitis and non-haematogenous osteomyelitis
What is haematogenous osteomyelitis?
results from bacteraemia
usually monomicrobial
most common form in children
in adults most common is vertebral osteomyeltis
RF = sickle cell anaemia, IVDU, immunosupressed, infective endocarditis
What is non-haematogenous osteomyelitis?
results from contiguous spread of infection from adjacent soft tissues to bone or from direct injury / trauma to bone
often polymicrobial
most common form in adults
RF = diabetic foot ulcers / pressure sores, DM, periph. arterial disease
Most common cause of osteomyelitis?
staph aureus
(except in pts w/ sickle cell anaemia where salmonella species predominate)
Investigations and management of osteomyelitis
investigations = MRI
management = flucloxacillin for 6wks
clindamycin if penicillin allergic
Risk factors of hip oesteoarthritis
increasing age
female (2x more common)
obesity
developmental dysplasia of hip
Features of osteoarthritis of hip
chronic history of groin ache following exercise and relieved by rest
locking, sticking or grinding
stiffness and weakness
Oxford Hip score used to assess severity
Investigations of osteoarthritis of hip
clinical diagnosis
x-ray
Management of osteoarthritis of hip
oral analgesia
intra-articular injections - short term benefit
total hip replacement
Complications of total hip replacement
aseptic loosening - prosthetic joint infection
leg length discrepancy
posterior dislocation
perioperative - VTE, intraoperative fracture, nerve injury, surgical site infection
What is osteomalacia?
softening of bones secondary to low vitamin D lvls that in turn lead to decreased bone mineral content
called rickets in growing children
Causes of osteomalacia
vit D deficiency (malabsorption, lack of sunlight, diet)
CKD
drug induced eg anticonvulsants
inherited - hypophosphatemic rickets
liver disease eg cirrhosis
coeliac disease
Features of osteomalacia
bone pain
bone / muscle tenderness
fractures - especially femoral neck
proximal myopathy - may lead to waddling gait
Investigations and treatment of osteomalacia
Investigations = bloods - low vitD, low calcium, phosphate and raised alkaline phosphatase (ALP
X-ray - translucent bands
Treatment = vitD supplementation - loading dose needed initially
calcium supplementation if dietary is inadequate
Describe the process of bone fracture healing
- bleeding vessels in bone and periosteum
- clot and haematoma formation
- clot organises over a week
- periosteum contains osteoblasts - produce new bone
- mesenchymal cells produce cartilage (fibrocartilage and hyaline) in soft tissue around fracture
- connective tissue + hyaline cartilage = callus
- as new bone approaches new cartilage, endochondral ossification occurs to bridge gap
- trabecular bone forms
- trabecular bone resorbed by osteoclasts and replaced w/ compact bone
Factors affecting fracture healing
- age
- malnutrition
- bone disorders - osteoporosis
- systemic disorders - DM, Marfan’s, Ehlers-Danos
- drugs - steroids, NSAIDs
- bone type
- degree of trauma
- vascular injury
- degree of immobilisation
- intra-articular fractures
- separation of bone ends
- infection
What is a fragility fracture?
occur due to weakness in bone, usually due to osteoporosis
often occur w/out appropriate trauma typically required to break a bone
Osteopenia and osteoporosis WHO criteria
T-score:
> -1 = normal
-1 to -2.5 = osteopenia
< -2.5 = osteoporosis
< -2.5 plus a fracture = severe osteoporosis
What is fat embolism?
can occur following fracture of long bones
fat globules released into circulation following fracture, globules can become lodged in blood vessels and cause flow obstruction
can cause systemic inflammatory response, resulting in fat embolism syndrome
presents 24-72hrs after fracture
What is Gurd’s criteria?
used to diagnose fat embolism
Major criteria - resp distress, petechial rash, cerebral involvement
Minor criteria - jaundice, thrombocytopenia, fever, tachycardia
Risk factors of urinary incontinence
advancing age
previous pregnancy and childbirth
high BMI
hysterectomy
family history
Classification of urinary incontinence
- overactive bladder / urge incontinence - urge followed by uncontrollable leakage
- stress incontinence - small amounts when coughing or laughing
- mixed incontinence - both urge and stress
- overflow incontinence - bladder outlet obstruction
- functional incontinence - impaired ability to get to bathroom in time
Investigations of urinary incontinence
bladder diaries minimum 3 days
vaginal exam
urine dipstick and culture
urodynamic studies
Urge continence management
bladder retraining
antimuscarinics - bladder stabilisng eg oxybutynin or darifenacin
mirabegron (beta 3 agonist) - concerns about anticholinergic side effects in frail elderly
Stress incontinence management
pelvic floor muscle training
surgical procedures - retropubic mid-urethral tape procedur
duloxetine may be offered to women if they decline surgical procedures (combined noradrenaline and serotonin re-uptake inhibitor)
What medications are prescribed for end of life care?
opioid - pain eg morphine
breathlessness - midazolam / opioid
anxiety - midazolam
nausea and vomiting eg cyclizine, metoclopramide
chest secretions - hyoscine
What does a straight line on an ECG indicate?
a pacemaker - paced rhythm, difficult to tell other issues on ECG
What drugs can lead to parkinsonism?
anti-psychotics
neuroleptic drugs - blocks the action of dopamine
What are the types of ischaemic stroke?
Thrombotic - clot forms in artery supplying blood to brain, usually due to atherosclerosis
Embolic - blood clot or other debris from another part of body travels and becomes lodged in artery supplying blood to brain
What are the types of haemorrhagic stroke?
Intracerebral haemorrhage - rupture of blood vessel w/in brain parenchyma, often due to HTN, cerebral amyloid angiopathy or vascular malformations
Subarachnoid haemmorhage - bleeding into subarachnoid space, typically due to rupture of intracranial aneurysm or arteriovenous malformation
Describe cerebral ischaemia
reduction in blood flow to affected brain region = inadequate oxygen and glucose delivery = energy failure and disruption of cellular ion homeostasis = exctitoxicity, oxidative stress, inflammation, apoptosis = irreversible neuronal damage
Describe cerebral oedema
in both stroke types
accumulation of fluid w/in brain tissue
increase intracranial pressure, further intracranial pressure, further compromise cerebral blood flow and cause secondary neuronal damage
Describe cerebral haemorrhage
rupture of blood vessel causes blood to accumulate w/in brain tissue or subarachnoid space
increased intracranial pressure, compression of brain tissue, disruption of cerebral blood flow
can trigger local inflammatory response = further neuronal damage
How are strokes classified?
using Oxford Stroke Classification (Bamford Classification) - based on initial symptoms:
1. unilateral hemiparesis and/or hemisensory loss of face, arm and leg
2. homonymous hemianopia
3. higher cognitive dysfunction eg dysphagia
What are total anterior circulation infarctions?
15%
middle and anterior cerebral arteries
all 3 of criteria are present
What are partial anterior circulation infarctions?
25%
involves smaller arteries of anterior circulation eg upper or lower division of middle cerebral artery
2 of criteria present
What are lacunar infarctions?
25%
Involves perforating arteries around internal capsule, thalamus and basal ganglia
presents w/ one of:
- unilateral weakness
- pure sensory stroke
- ataxic hemiparesis
What are posterior circulation infarctions?
25%
involves vertebrobasilar arteries
presents with one of:
- cerebellar of brainstem syndromes
- loss of consciousness
- isolated homonymous hemianopia
Patterns of Weber’s syndrome
ipsilateral third nerve palsy
contralateral weakness
How to differentiate a stroke and Bell’s palsy?
Bell’s typically affects only lower motor neurones of facial nerve leading to unilateral weakness including forehead
stroke more commonly is forehead sparing due to bilat UMN innervation
Ball’s pts also experience hyperacusis or altered taste
Stroke differentials
migraine w/ aura
Bell’s palsy
hypoglycaemia
Acute stroke management
maintain blood glucose, hydration, oxygen sat and temp
BP - not lowered in acute phase of ischaemic unless complications, BP considered for pts presenting w/ ischaemic, present w/in 6hrs and have bp > 150
aspirin 300mg
if cholesterol > 3.5mmol/l = statin
What should bp be lowered to before thrombolysis?
185/110 mmHg
Absolute contraindications of thrombolysis
- previous intracranial haemorrhage
- seizure at onset of stroke
- intracranial neoplasm
- suspected subarachnoid haemorrhage
- stroke or traumatic brain injury in preceding 3 months
- lumbar puncture in preceding 7 days
- GI haemorrhage in preceding 3 days
- active bleeding
- oesophageal varices
- uncontrolled HTN
Relative contraindications of thrombolysis
- pregnancy
- concurrent anticoagulation
- haemorrhagic diathesis
- active diabetic haemorrhagic retinopathy
- suspected intracardiac thrombus
- major surgery / trauma in previous 2wks
Secondary prevention for stroke
clopidogrel ahead of combo use of aspirin + modified-release dipyridamole
aspirin recommended after ischaemic if clopidogrel contraindicated or not tolerated
carotid endarterectomy if stroke in carotid territory
Complications of stroke
physical - falls, pain, incontinence
vascular - VTE, CV events
psychological - depression, anxiety, emotional liability
infection - pneumonia, UTIs
What is frailty?
multidimensional syndrome
diminished strength, endurance and physiological function
increases individual’s vulnerability for developing increased dependency and/or mortality when exposed to stressor
2 types of frailty
physical - based on wt loss, exhaustion, low physical activity, slowness and weakness
frailty phenotype - cognitive and social aspects
Clinical implications of frailty
higher risk of adverse health outcomes eg falls, delirium, disability and hospitalisation
Assessment tools of frailty
Fried frailty Index
Groningen frailty Indicator
Factors of a fall
Intrinsic - age-related physiological changes, comorbidities eg Parkinson’s or stroke
Extrinsic - environmental hazards
Investigations after a fall
detailed history about fall circumstances, meds, visual impairment, cognitive function and gait analysis
orthostatic bp, ECG and imaging
Management after a fall
treating any fracture or intracranial injury
risk factor modification eg med review, physical therapy for strength and balance training, vision correction and home safety evaluation
What are the two broad types of falls?
Accidental - environmental and occupational
Non-Accidental - syncope related, gait/balance related, muscle weakness related
What assessments should be done after a fall?
environmental
physical health
mental health
medication
functional ability
any specific investigations
Fall differentials
Neuro - stroke, Parkinson’s, MS, cerebellar disorders
CV - arrhythmias, vasovagal syncope, orthostatic htn
MSK - osteoarthritis, RA, osteoporosis
Sensory - visual impairment, hearing loss
Med related
Endo - hypoglycaemia, hypocalcaemia
Typical areas for pressure sores
bony prominences - sacrum, coccyx, heels or hips
Pathophysiology of pressure sores
ischaemic damage due to compression of capillaries leading to cell death and ulceration
What are the 4 stages of pressure sores?
1 = non-blanchable erythema w/out skin loss
2 = partial thickness skin loss affecting epidermis or dermis
3 = full thickness skin loss extending into subcutaneous tissue but not through underlying fascia
4 = full thickness skin loss w/ extensive destruction involving muscle, bone or supporting structures
Pressure sore risk factors
immobility
malnutrition and dehydration
incontinence
sensory impairment
Underlying causes of pressure sores
prolonged pressure
shearing forces
foisture
ageing skin
Investigations of pressure sores
wound swabs - Levine technique
blood test - FBC, U&E, CRP and albumin
tissue biopsy
radiological imaging
Pressure ulcer differentials
diabetic ulcers
venous stasis ulcers
ischaemic ulcers
Pressure sore management
Risk assessment - Braden or Waterlow scale
Prevention strategies
Treatment - dressings, pressure relieving devices, abx if infected
Pain relief
Types of syncope
vasovagal - drop in bp and heart rate
cardiac - heart electrical system
orthostatic htn
neurological - eg stroke or seizure disorder
hypoglycaemia
Forms of reflex syncope
- vasovagal - most common, stress or pain related
- situational - micturition, defecation or coughing, abrupt drop in bp
- carotid sinus hypersensitivity -
- atypical reflex syncope - lacks triggers
Syncope differentials
arrhythmias
structural heart disease
vasovagal syncope
seizures
cerebrovascular disease
pulmonary embolism
anaemia
metabolic disorders
panic attacks
pseudosyncope
Symptoms preceding syncope
lightheadedness
weakness
blurred vision
palpitations
Management of syncope
immediate stabilisation - ABCDE
identify any reversible causes
symptomatic relief
plan for further diagnostic
Forms of cardiac syncope
- structural disease eg aortic stenosis, pulmonary HTN, acute MI
- arrhythmias
Symptoms during syncope
pallor
diaphoresis
convulsive moments that can be mistaken for seizures
Consequences of overnutrition
increases risk of non-communicable diseases eg T2DM, CVD, HTN and certain cancers
Syncope investigations
orthostatic vitals - bp and heart rate
cardiac auscultation - murmurs or heart disease
carotid sinus massage
ECG
echo
tilt-table testing
Malnutrition biochemical abnormalities
anaemia
hypoalbuminaemia
electrolyte imbalances
What is malnutrition?
multifaced condition of both undernutrition (stunting, wasting and deficiencies of micro- and macronutrients) and overnutrition (overweight or obesity due to excessive nutrient intakes)
What is protein-energy malnutrition (PEM)?
severe form of undernutrition characterised by insufficient intake of protein and energy
can lead to marasmus - presents as significant weight loss or kwashiorkor w/ oedema and skin changes
Causes of constipation
functional - lack of fibre, fluids or due to sedentary lifestyle
medication induced - eg opioids, antacids, antidepressants
IBS-C
colorectal cancer
hypothyroidism
Give a definition of constipation
defecation that is unsatisfactory because of infrequent stools (<3 times weekly), difficult stool passage (w/ straining or discomfort) or seemingly incomplete defecation
Management of constipation
lifestyle modifications
dietary requirements
pharmacological interventions - laxatives
follow-up
Depression differentials
bipolar disorder
dysthymia
anxiety disorders
thyroid disorders
neuro conditions eg Parkinsons
nutritional deficiency eg B12, folate and VitD
endo disorders eg Cushing’s
alcohol and drug related issues
Examination of pt presenting w/ constipation
abdominal examination - percussion
DRE
anorectal manometry
if red flags, blood tests eg FBC, coeliac, TFT, calcium and glucose
stool tests eg FIT, calprotectin
x-rays
What is depression?
characterised by persistent feelings of sadness, hopelessness and loss of interest in activities that were once enjoyable
can cause physical symptoms such as fatigue, change in appetite and sleep disturbances
Complications of constipation
overflow diarrhoea
acute urinary retention
haemorrhoids
delirium
anal fissures
Constipation symptoms
infrequent bowel movements (<3 per wk)
hard / lumpy stools
straining
sensation of incomplete emptying
bloating and abdominal discomfort
Types of depression
major depressive episode
persistent depressie disorder
seasonal affective disorder
Depression diagnosis
Major depressive disorder DSM-5 criteria:
presence of at least 5: low mood, loss of interest in activities, decreased energy, increased fatigue, cognitive changes, sleep disturbance, appetite changes, psychomotor agitation / retardation, suicidal ideation
for at least 2 wks
Classification of depression
‘less severe’ = PHQ-9 <16
‘more severe’ = PHQ-9 ≥ 16
Management of less severe depression
guided self-help
CBT
behavioural action
exercise
mindfullness and meditation
interpersonal psychotherapy
selective serotonin re-uptake inhibitors - SSRIs
counselling
short term psychodynamic psychotherapy (STPP)
Management of more severe depression
combo of CBT and antidepressant
behavioural activation
antidepressants - SSRI or seretonin-noriepinephrine reuptake inhibitor (SNRI)
counselling
short term psychodynamic psychotherapy
guided self-help
grp exercise
Depression screening questions
‘During the last month, have you often been bothered by feeling down, depressed or hopeless?’
‘During the last month, have you often been bothered by having little interest or pleasure in doing things?’
What is benign paroxysmal positional vertigo?
most common causes
sudden onset of dizziness and vertigo triggered by changes in head position
average age of onset = 55
Management of benign paroxysmal positional vertigo
usually resolves spontaneously after a few wks = months
symptomatic relief - Epley manoeuvre, exercises to relieve
meds eg betahistine
Types of lower limb fractures
Hip = intrascapular and extrascapular
Femur = shaft and distal shaft
Knee = tibial plateau and patellar
Tibia/ Fibula = tibial shaft and fibular shaft
Ankle = malleolar and pilon
Foot = metatarsal and phalangeal
Risk factors of lower limb fractures
Intrinsic = age, sex, genetics, nutritional status, disease status, bone density
Extrinsic = trauma, lifestyle choices, mechanical stressors, medications
Pathophysiology of lower limb
External force exerted on bone that exceeds structural integrity - bone undergoes elastic deformation initially. If stress persists and surpasses yield point, plastic deformation occurs, leading to microscopic cracks w/in bone structure.
Inflammatory response - damaged cells release inflammatory mediators eg cytokines and growth factors - attract immune cells which clear debris and initiate healing
A few days post injury, fibroblasts and chondrocytes proliferate around fracture site forming soft, cartilagenous callus. Process facilitated by angiogeneses promoting factors
soft callus gradually mineralises into hard callus over several wks due to osteoblast activity - provides stabilisation
remodelling - hard callus replaced by lamellar bone restoring og shape and function
Presentation of lower limb fracture
acute onset of pain, deformity, inability to bear weight, swelling, bruising
crepitus, nerve injury, vasc injury, compartment syndrome, fat embolism syndrome
Investigations of lower limb fractures
X-ray
CT
MRI
ultrasound
Lower limb fracture management
Initial assessment
Pain management
Immobilisation
Definitive treatment - Conservative or surgical
Rehabilitation
Follow-up
Causes of acute heart failure
reduced cardiac output that results from a functional or structural abnormality
ACS
hypertensive crisis eg bilat renal artery stenosis
acute arrhythmia
valvular disease
De-novo heart failure causes
increased cardiac filling pressures and myocardial dysfunction usually as a result of ischaemia
reduced cardiac output = hypoperfusion = pulmonary oedema
less common causes = viral myopathy, toxins, valve dysfunction
Symptoms of acute heart failure
breathlessness
reduced exercise tolerance
oedema
fatigue
chest pain
viral infection
Is blood pressure affected by acute heart failure?
over 90% of pts have a normal or raised bp
Signs of acute heart failure
cyanosis
tachycardia
elevated JVP
displaced apex beat
chest signs - bibasal crackles, wheeze
S3 heart sound
Acute heart failure investigations
bloods - anaemia, electrolytes, infection
chest x-ray - pulmonary venous congestion, interstitial oedema, cardiomegaly
echo - pericardial effusion and cardiac tamponade
B-type natriuretic peptide - raised
Management of acute heart failure
IV loop diuretics eg furosemide or bumetanide
oxygen to 94 - 98%
vasodilators eg nitrates
if resp failure = CPAP
Should heart failure meds be stopped in acute heart failure?
regular meds eg beta blockers or ACE inhibitors should be continued. Only stop beta blockers if pt heart rate <50 bpm, 2nd or 3rd AV block or shock
Risk factors of chronic heart failure
Coronary artery disease
HTN
valvular heart diseases
cardiomyopathies
DM
renal dysfunction
obesity
aging
smoking
alcohol
sedentary lifestyle
First stage of chronic heart failure
Initial Insult to myocardium - triggers pathogenesis of chf
can include MI, HTN, valvular heart disease or cardiomyopathy
result in decrease in cardiac output and increase in ventricular filling pressures
Second stage of chronic heart failure
Compensatory Mechanisms:
- neurohormonal activation - in response to cardiac output, sympathetic NS and RAAS activate. Lead to vasoconstriction, fluid retention and increased heart rate to maintain bp and perfusion
- ventricular remodelling - over time, persistent neurohormonal activation causes changes in structure and function of heart. Includes hypertrophy of myocardium, dilation of ventricles and alteration in chamber geometry
- Frank-Sterling mechanism - allows for increased stroke vol via enhanced end-diastolic volume. However, over time this mechanism becomes less efficient due to structural changes w/in myocardium.
Third stage of chronic heart failure
Decompensated phase - compensatory mechanisms no longer sufficient to maintain adequate cardiac output leading to symptomatic heart failure.
Pts may present w/ dsypnoea, fatigue and fluid retenetion
progression from compensated to decompensated influenced by several factors: ongoing MI due to ischaemia or pressure overload, further activation o neurohormonal systems causing increased preload or afterload, and progressive ventricular remodelling leading to systolic and diastolic dysfunction
Classification of chronic heart failure
NYHA
Class 1 = no symptoms, no limitation
Class 2 = mild symptom, slight limitation of physical activity - comfy at rest but ordinary activity results in fatigue, palpitations or dyspnoea
Class 3 = moderate symptoms, marked limitation of physical activity - comfy at rest but less than ordinary activity results in symptoms
Class 4 = severe symptoms, unable to carry out any physical activity w/out discomfort
Clinical features of chronic heart failure
dyspnoea - exacerbated by exertion or lying flat. Due to pulmonary congestion from L.vent dysfunction
fatigue - reduced CO leading to inadequate perfusion of tissues
fluid retention - periph. oedema, elevated JVP, chest pain, nocturia, cachexia, pallor or cyanosis, tachycardia
Investigations of chronic heart failure
N-terminal pro-B-type natriuretic peptide blood test
hormone produced by mainly L. vent myocardium in response to strain
What increases BNP levels?
L. ventricular hypertrophy
ischaemia
tachycardia
R. ventricular overload
hypoxaemia
GFR < 60
Sepsis
COPD
diabetes
age > 70
liver cirrhosis
What decreases BNP levels?
obesity
diuretics
ACE inhibitors
beta blockers
angiotensin 2 receptor blockers
aldosterone antagonists
Chronic heart failure diagnosis
echo - evaluate L. vent ejection fraction
natriuretic peptides
chest x-ray - cargiomegaly and signs of pulmonary congestion
ECG
Chronic heart failure differentials
COPD
anaemia
renal impairment
Chronic heart failure management
treat underlying cause
lifestyle modifications
ACE inhibitor or ARBs
beta blockers
mineralcorticoid receptor antagonists (MRAs) eg spironolactone
implantable devices eg cardioverter defibs, resynchronisation therapy
surgical intervention
regular monitoring and follow up
ECG changes in hypothermia
bradycardia
‘J’ wave - small hump at end of QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias
What happens in the body in hypothermia?
initial stages: thermoreceptors in skin and subcutaneous tissues sense low temp and cause regional vasoconstriction.
Causes hypothalamus to stimulate TSH and ACTH release
Also stimulates heat production by promoting shivering
Mild, moderate and severe hypothermia temps
mild = 32-35 degrees
moderate or severe <32 degrees
Causes of hypothermia
exposure to cold
inadequate insulation in operating room
cardiopulmonary bypass
newborn babies
Hypothermia risk factors
general anaesthesia
substance abuse
hypothyroidism
impaired mental status
homelessness
extremes of age
signs of hypothermia
shivering
cold and pale skin
slurred speech
tachypnoea, tachycardia and HTN (if mild)
resp depression, bradycardia and htn (if moderate)
confusion / impaired mental state
Hypothermia investigations
temp
12 lead ecgs - ST elevation and J waves or Osborn waves as temp = 32-33
FBC, serum electrolytes - haemoglobin and haematocrit can be elevated, platelets and WBCs are low
blood glucose
ABG
coag factors
CX
Hypothermia management
remove pt from cold environment
warm body w/ blankets
secure airway and monitor breathing
can use warm IV fluids or apply warm air directly
What may be seen on an ECG in a hypothermia pt?
bradycardia
J wave - Osborne waves - small hump at end of QRS complex
first degree heart block
longQT interval
atrial and ventricular arrhythmias
Squamous cell carcinoma risk factors
excessive exposure to sunlight
actinic keratoses and Bowen’s disease
immunosuppression eg following renal transplant
smoking
long standing leg ulcers
genetic conditions
Features of squamous cell carcinoma
typically on sun exposed sites eg head and neck or dorsum of hands / arms
rapidly expanding painless, ulcerate nodules
may have cauliflower-like appearance
may be areas of bleeding
Treatment of squamous cell carcinoma
lesion <20mm in diameter = surgical excision w/ 4mm margin
tumour >20mm = excision w/ 6mm
Squamous cell carcinoma w/ good prognosis
well differentiated tumours
<20mm in diameter
<2mm deep
no associated symptoms
Squamous cell carcinoma poor prognosis
poorly differentiated
>20mm in diameter
>4mm deep
immunosuppression
What is Wells score?
predicts likelihood of DVT
Info:
- Unilateral swelling >3cm, whole leg swelling
- Pitting oedema of symptomatic side
- Localised tenderness, paralysis / weakness, leg immobilisation
- Superficial veins present
- Bed ridden >3 days or surgery in last 12wks
- Previous DVT, active malignancy
Score:
0 = low risk - d-dimer US if +ve
1 - 2 = moderate - highly sensitive d-dimer then US
3 = high risk - US
What is FRAX score?
predicts risk of osteoporosis fracture in 10yrs, greater score = higher risk
Info:
- Age, Sex, Height
- Smoking, Alcohol >3units/day
- Previous low force fracture
- Bone mineral density
- RA
- Steroid use
- 2ndary osteoporosis
Score:
Low risk (green) - lifestyle advice, reassess in 5yrs
Intermediate risk (yellow) - measure BMD, recalculate risk, treat if above threshold
>10%, High risk (red) - bisphosphonates, calcium/vitD supplements
V.High risk (dark red) - refer to specialist treatment
What is Q-risk score?
Predicts MI/stroke risk in 10yrs
Info:
- Age, Sex, Ethnicity
- Smoking
- 1st degree relative under 60 w/ MI/angina
- Comorbidities (DM, RA, AF, CKD 4/5, SLE, migraines etc)
- Medications (steroids, antihypertensives, atypical anti-psychotics)
- Others (height, weight, systolic BP, cholesterol / HDL ratio)
Score:
<10% = lifestyle changes, review comorbidities, review in 5yrs
>10% = as above and statin
What is CHA2DS2-VASc score?
To predict stroke risk in AF pts
Info:
Congestive HF
HTN
Age > 75 (2 points)
Diabetes
Stroke / TIA (2 points)
Vasc disease
Age 65-74
Sex (female)
Score:
Low risk 0(m) or 1(f) = no treatment, lifestyle advice
Moderate risk 1(m) or 2(f) - consider anticoag
High risk 2(m) or 3(f) = offer anticoag
What is ABCD2 score?
for TIA, estimates risk of stroke after TIA
Info:
Age >60
BP
Clinical TIA features (unilat weakness, speech disturbance)
Duration of symptoms <10mins >60mins
Diabetes history
Score:
Low risk 0-3 = outpt management - eval w/in 1 wk
Moderate risk 4-5 = hospitalisation recommended
High risk 6-7 = hospitalisation, dual antiplatelet therapy eg aspirin and clopidogrel
What is diabetes risk?
Predicts likelikood of having undiagnosed T2DM
Info:
- Age, Sex, Ethnicity
- Height, Weight, Waist circumference
- Antihypertensives, steroids, smoking
- 1st degree relative w/ T2DM
Score:
Low risk = reassurance/encouragement, lifestyle advice
Moderate risk = explore RFs, offer brief lifestyle intervention, weight management
High risk = explore RFs, offer intensive lifestyle and WL intervention
