Geratology Flashcards
Define Benign Paroxysmal Positional Vertigo
BPPV - MC cause of vertigo.
sudden onset dizziness and vertigo triggered by head position change.
Average Age onset of BPPV
55- less common in younger pts.
Features of BPPV
Vertigo triggered by head position change - rolling over in bed/gazing upwards
associated with nausea
10-20 sec episode
DIX-HALLPIKE MANOEUVRE -
lower pt to supine position and extend neck - should recreate symptoms if they have it.
ROTARY NYSTAGMUS - rapid repetitive uncontrollable movement in a circle around visual axis.
Treatment of BPPV
usually resolves spontaneously after few weeks
Symptomatic Relief:
Epley Manoeuvre - 80% success
teach pts vestibular rehab exercises : BRANDT-DAROFF
Betahistine (anti-vertigo) often prescribed - limited value
Recurrence of BPPV
half pts have recurrence of symptoms 3-5 yrs after diagnosis
Define Malnutrition (according to nice)
BMI less than 18.5 or unintentional weight loss over 10% within last 3-6 months
or
BMI less than 20 and unintentional weight loss over 5% within last 3-6 months
Epidemiology of Malnourished patients
10% over 65
most living independently - ie: not in hospital or care/nursing home.
Screening Tool for Malnutrition
MUST - Malnutrition universal screen tool
done on admission or if concern. eg: old, thin woman with pressure sores
takes into account:
BMI
recent weight change
acute disease
categories:
low
medium
high risk
Managing Malnourished Patient
dietician support - high risk
FOOD FIRST - add full fat cream to mash rather than oral nutritional supplements (ons) eg: ensure
if ONS - give between meals not instead of meals.
What Systems are involved in achieving normal gait?
neurological system - basal ganglia and cortical basal ganglia loop.
MSK - appropriate tone and strength.
Effective processing of senses eg: sight, sound, sensation (fine touch, proprioception)
as pt gets older, medical problems, systems affected, gait abnormalities = falls
Name Some Risk Factors for Falling
previous falls
vision problem
polypharmacy - 4+
incontinence
over 65
fear of falling
depression
postural hypotension
psychoactive drugs
cognitive impairement
lower limb muscle weakness
balance/gait disturbances (diabetes, rheumatoid arthritis, parkinsons)
Pt has 4 or more risk factors of falling, what is the likelihood?
78%
what questions can you ask for risk assessment for fall patient?
where was the patient when the fall happened?
when did they fall?
PMH
SOCIAL HX
Systems review
have they fallen before?
why do they think they fell?
anyone see the fall? (collateral history)
what happened? any associated features before/during/after?
You are required to do a medication review for a fall patient, what medications can cause postural hypotension?
nitrates
diuretics
anticholinergic medications
antidepressants
beta-blockers
l-dopa
angiotensin-converting enzyme inhibitors (ACE)
You are required to do a medication review for a fall patient, which medications are associated with falls due to other mechanisms other than postural hypotension?
benzodiazepines
antipsychotics
opiates
anticonvulsants
codeine
digoxin
other sedative agents
what approach should you use when examination of a fall patient?
A - E
Which Bedside tests to do for a fall patient?
basic obs
BP
BG
URINE DIP
ECG
what bloods should you do for a fall patient?
FBC
U+E
LFT
BONE PROFILE
What imaging should you do for fall patient?
X-ray of chest/injured limbs
CT head
cardiac echo
what tests do NICE recommend you to do for a fall patient?
for all fallen in last year
do investigations (all)
medication review
risk assessment
TURN 180 TEST - STAND UP AND STEP AROUND UNTIL OPP DIRECTION - 4 OR MORE STEPS - HIGHER RISK OF FALL.
TIMED UP AND GO TEST - STAND UP WALK 3M AND WALK BACK SIT DOWN. - 12-15 SECONDS OR MORE SHOWS HIGHER RISK OF FALL
Based on NICE recommendations, when should you do a multidisplinary assessment for a fall patient?
all pts over 65 with:
over 2 falls in last 12 months
fall requiring medical treatment
poor performance/failure to complete turn 180 test/timed up and go test
if criteria not met, review criteria annually.
What is Squamous Cell Carcinoma?
Skin Cancer Variant.
Metastases rare but in 2-5% of patients.
Risk Factors of SCC
excessive exposure to sunlight/ psoralen UVA therapy
smoking
long-standing leg ulcers (Marjolin’s Ulcer)
actinic keratoses and Bowen’s Disease
immunosuppresion eg following renal transplant, HIV
genetics: xeroderma pigmentosum, oculocutaneous albinism
What is the most common malignancy secondary to immunosuppression due to renal transplant?
Squamous Cell Carcinoma
Features of SCC
areas of bleeding
cauliflower like appearance
rapidly expanding, painless, ulcerate nodules
typical on sun-exposed sites eg head,neck,dorsum of hands and arms
Treatment of SCC
surgical excision 4mm margins if lesion <20mm in diameter.
if tumour over 20mm - margins should be 6mm.
MOHS micrographic surgery - high risk pts and cosmetically important sites.
prognosis of SCC
Good prognosis:
well differentiated.
less than 20mm diameter. less than 2mm deep.
no associated diseases
Poor prognosis:
poor differentiated tumours
over 20mm in diameter. over 4mm deep.
immunosuppression for whatever reason
What is constipation?
primary functional disorder of bowel. could be secondary to another condition.
unsatisfactory defaecation because of infrequent stools - less than 3 times weekly, difficult stool passage (straining or discomfort)
seemingly incomplete defecation
features of constipation
passage of infrequent hard stools
How to Manage Constipation?
1st line laxative: bulk-forming laxative - ISPAGHULA HUSK
2ND: OSMOTIC LAXATIVE - MACROGOL
investigate and exclude secondary causes, red flag sx
exclude faecal impaction (dry stool stuck in rectum)
Lifestyle advice for constipated patients
increasing dietary fibre
ensuring adequate fluid intake
ensuring adequate activity levels
complications of constipation
haemorrhoids
acute urinary retention
overflow diarrhoea (due to faecal impaction)
what is overflow diarhoea?
faecal impacting - stuck stool in rectum
weakened rectum muscles
watery stools leak around stool and out the bottom.
Risk Factors of Urinary Incontinence
Advancing Age
previous pregnancy and childbirth
high BMI
FHx
hysterectomy (remove the womb (uterus)
Classifications of Urinary Incontinence
overactive bladder/urge incontinence - detrusor overactivity. urge to urinate followed by uncontrollable leakage from few drops to complete emptying
stress incontinence - leak when cough/laugh
mixed incontinence - urge + stress
overflow incontinence - bladder outlet obstruction e.g.: due to prostate enlargement - bladder palpable post urination.
functional incontinence: comorbid physical condition cant walk in time. e.g. : dementia, sedating meds, injury/illness = decreased ambulation (ability to walk/move around)
How would you investigate urinary incontinence patient?
Bladder diaries - min 3 days
urine dip + culture
urodynamic studies
vaginal exam : exclude pelvic organ prolapse and ability to initiate voluntary contraction of pelvic floor muscles (Kegel exercises)
How to manage urge incontinence predominant urinary incontinence?
1st line: bladder retraining - min 6 weeks. - gradually increase intervals between voiding.
1st line: antimuscarinics - bladder stabilising drugs : OXYBUTININ/TOLTERODINE (immediate release), or DARIFENACIN - once daily preparation
possible: mirabegron - beta-3 agonist - concern on anticholinergic side-effects on frail-elderly pts
Who should you avoid oxybutinin/mirabegron in?
frail older woman
oxybutinin - antimuscarinic
mirabegron - beta - 3 agonist
Name some anticholinergic side effects
dry mouth
constipation
urinary retention
bowel obstruction
dilated pupils/blurred vision.
less sweating
increased hr
How would you manage stress incontinence predominant urinary incontinence?
1st line: pelvic floor muscle training - min 8 contractions 3 times a day for 3 months
surgery: retropubic mid-urethral tape
DULOXETINE - women if decline surgery.
class of drug for duloxetine and mechanism of action
combined noradrenaline and serotonin reuptake inhibitor
MoA : increased synaptic concentration of noradrenaline + serotonin within pudendal nerve (major nerve in pelvic region control movement/sensation in genitals anus) =
increased stimulation of urethral striated muscles within the sphincter = enhanced contraction.
Who are pressure sores/ulcers more likely to develop in?
pts unable to move parts of body due to illness,paralysis, increased age.
where do pressure sores/ulcers typically develop?
bone prominences eg : sacrum or heel
factors predisposing to development of pressure ulcers?
malnourishment
incontinence - urinary and faecal
lack of mobility
pain - mobility reduction
Screening tool for pts at risk of developing pressure areas?
Waterlow Score :
factors :
bmi
nutritional status
skin type
mobility
continence
Grading System for pressure sores/ulcers
GRADE 1 : non blanchable erythema of intact skin. discolouration, warmth, hardness/induration possible - particularly on pts with darker skin
GRADE 2 : partial thickness skin loss - involves epidermis or dermis or both. ulcer superficial - presents clinically as abrasion/blister.
GRADE 3 : full thickness skin loss - damage to or necrosis of subcutaneous tissue may extend to not through underlying fascia
GRADE 4: extensive destruction - tissue necrosis - damage to muscle bone or supporting structures with/without full thickness skin loss
How would you manage pressure sores/ulcers?
referral to tissue viability nurse
moist wound environment - hydrocolloid dressings/hydrogels. - avoid soap to avoid drying wound.
wound swabs not routinely as most will have bacteria colonisation. - use systemic abx based on clinicasl exam eg: evidence of cellulitis.
surgical debridement - possible for some wounds.
what is delirium?
acute confusional state/ acute organic brain syndrome.
30% of hospitalised elderly
predisposing factors to delirium
over 65
dementia background
polypharmacy
frailty or multimorbidity
significant injury eg: hip fracture
possible precipitating factors for delirium (most probs multifactorial)
constipation !!!
alcohol withdrawal
severe pain
infection: UTI particularly
Metabolic: hypercalcaemia , hypoglycaemia, hyperglycaemia, dehydration
any cardio,resp, neuro, endo condition
environment change in cognitively impaired patients
features of delirium
memory disturbances - loss of short term> long term
agitated/withdrawen
disorientation
mood change
visual hallucinations
disturbed sleep cycle
poor attention
how would you manage delirium?
tx - underlying cause
modify environment
haloperidol 0.5mg - 1st line sedative
could use olanzapine
BE CAREFUL FOR PARKINSONS PTS - ANTIPSYCHOTICS WORSE PARKINSONIAN SX. - reduce Parkinson meds carefully.
if require urgent tx - atypical antipsychotics can be used: quetiapine/clozapine
MC cause of dementia
Alzheimers
then
vascular and lewy body.
these conditions can co-exist
Assessment Tools for dementia
non -specialist setting : 10-cs and 6CIT
others (not recommended by nice) : AMTS, GPCOG, MMSE (24 OR LESS/30 = DEMENTIA)
amts - abbreviated mental score test
cs - cognitive screener
cit - cognitive impairement test
What initial tests would you do when you suspect dementia?
blood screen : fbc, u+e, lft , calcium, glucose, esr crp, tft, vit b12, folate. EXCLUDE REVERSIBLE CAUSES LIKE HYPOTHYROIDISM.
secondary care: neuroimaging - exclude reversible cause : subdural haematoma, normal pressure hydrocephalus. - help with aetiology and management.
Delirium vs Dementia : favouring delirium
acute onset
delusions
agitation
fear
impairment of consciousness (possible psychotic sx)
fluctuating sx : worse @ night, periods of normality
abnormal perception : illusions and hallucinations
Causes of dementia
common : alzheimers, cerebrovascular disease (multi-infarct dementia 10-20%) , lewy body (10-20%)
Rarer: huntingtons, CJD, picks(atrophy of frontal and temporal lobes). HIV (50% of aids patients)
important differentials (potentially treatable) of dementia
hypothyroidism, addisons
b12/folate/thiamine deficiency
syphilis
brain tumour
normal pressure hydrocephalus
subdural haematoma
depression
chronic drug use eg alcohol, barbiturates
Depression vs Dementia favouring depression
short history, rapid onset
pt worried about poor memory
MMSE: variable
global memory loss -dementia is usually short term loss
reluctant to take tests, dissapointed with results
biological sx: weight loss, sleep disturbance
sleep disturbance , normal mmse, and stress trigger = depression
What is Alzheimers Disease?
progressive degenerative disease of the brain.
Risk Factors of Alzheimers
increasing age
fhx
5% genetic - autosomal dominant. - mutation in amyloid precursor protein (chr 21), presenilin 1 (chr 14), presenilin 2 (chr 1)
apoprotein E allele E4 - encodes a cholesterol transport protein
caucasian
downs syndrome
Pathological Changes Alzheimers - Macroscopic
widespread cerebral atrophy - involving cortex and hippocampus
Pathological Changes Alzheimer’s - Microscopic
cortical plaques due to deposition of type A beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein.
hyperphosphorylation of tau protein
Pathological Changes Alzheimer’s - Biochemical
deficit of acetylcholine from damage to an ascending forebrain projection
What are neurofibrillary tangles and what is tau ? (AD)
paired helical filaments partly made from tau protein.
tau = protein interacting with tubulin to stabilize microtubules.
promote tubulin assembly into microtubules.
in ad, tau hyperphosphorylated, impairing its function
What is the non pharmacological management of Alzheimer’s?
range of activities to promote wellbeing tailored.
group cognitive stimulation therapy : mild-moderate AD.
group reminiscence therapy and cognitive rehabilitation
What is the pharmacological management of Alzheimers?
1st line: acetylcholinesterase inhibitor : DONEPEZIL, GALANTAMINE, RIVASTIGMINE - mild -moderate disease
MEMANTINE - NMDA RECEPTOR ANTAGONIST - 2nd line.
use memantine for:
1. moderate AD intolerant/CI to acetylcholinesterase inhibitor
2. add-on drug to acetylcholinesterase inhibitor for mod-severe
3. monotherapy in severe AD
How would you manage non-cognitive symptoms of AD?
don’t give antidepressants for mild-moderate depression in dementia pts.
only give anytipsychotics for pts risk of harming themselves/others or when they agitated, hallucinating, delusional - severe distress
Negative of giving antipsychotic in AD patient
significant increase in mortality in dementia pts
Contraindications of donepezil
bradycardia
adverse effects include insomnia!!
Pathological Feature of Lewy Body Dementia
Alpha-synuclein cytoplasmic inclusions (Lewy bodies) in substantia nigra, paralimbic and neocortical areas.
Relationship between Parkinson’s Disease and Lewy Body Dementia?
40% of patients with AD have lewy bodies.
dementia is often seen in Parkinsons patients so its complicated
Features of Lewy Body Dementia
parkinsonisms (PARKINSON+DEMENTIA = LEWY BODY)
visual hallucinations - also delusions and non-visual hallucinations
progressive cognitive impairment: typically BEFORE parkinsonism, both within a yr of each other though.
PARKINSONS HAS MOTOR SYMPTOMS A YEAR BEFORE THEN COGNITIVE.
fluctuating cognition
early impairments in attention and cognitive function rather than just memory loss compared to AD
How would you diagnose Lewy Body Dementia?
clinical
single photon emission computed tomography -SPECT . - DaTscan.
123-I-FP-CIT - radioisotope.
sensitivity: 90%
specificity : 100%
Management of Lewy Body Dementia
both acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine) and memantine.
What drugs should be avoided in lewy body dementia and why?
neuroleptics
lewy body dementia patients extremely sensitive and could develop irreversible parkinsonism.
if they say pt with antipsycotic agent deteriorated = LBD
What is vascular dementia?
2nd mc cause of dementia after AD
group of syndrome of cognitive impairment caused by either ischaemic or haemorrhage secondary to cerebrovascular disease.
vascular cognitive impairement
epidemiology of vascular dementia
prevalence of it following a stroke depends on location and size of infarct, definition of dementia, interval after stroke and age. stroke double risk of dementia.
subtypes of Vascular dementia
stroke related - multi infarct or single infarct dementia
subcortical - caused by small vessel disease
mixed : both VD and alzheimers
risk factors of vascular dementia
hx of stroke/tia
af
htn
dm
smoking
obesity
coronary heart disease
hyperlipidemia
fhx of stroke/cv
RARELY GENETIC - CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)
typical presentation of VD -vascular dementia
several months/years of hx of a sudden or stepwise deterioration of cognitive function
symptoms of Vascular dementia
focal neurological abnormalities eg visual disturbance, sensory or motor symptoms
difficult with attention and concentration
seizures
memory disturbance
gait disturbance
speech disturbance
emotional disturbance
How can I make a diagnosis of Vascular Dementia?
comprehensive history and physical examination.
formal screen for cognitive impairment
medical review to exclude medication cause of cognitive decline
MRI - infarcts and extensive white matter changes
which criteria does nice recommend for vascular dementia diagnosis?
NINS-AIREN for probable vascular dementia
presence of cognitive decline that inferes with ADL, not due to secondary effects of cerebrovascular event - clinical exam and neuropsychological testing.
cerebrovascular disease - neuroloigcal signs and/or brain imaging
relationship between above 2 disorders shown by :
- fluctuating stepwise progression of cognitive deficits
- abrupt deterioration in cognitive functions
- onset of dementia within 3 months following recognised stroke
what is the management for vascular dementia?
detect cv rf and control.
non pharm:
cognitive stimulation programme, multisensory stimulation,music/art therapy, animal assisted therapy.
pain relief, avoid overcrowding, clear communication
pharm:
none specifically
consider AchE inhibitor/memantine for ppl with VD if comorbid AD, Parkinsons dementia or LBD.
no evidence aspirin is effective in treating pts with VD.
Causes of parkinsonisms
Parkinsons
dementia pugilistica - secondary to chronic head trauma like boxing.
multiple system atrophy
progressive supranuclear palsy
Wilsons
post-encephalitis
drug induced - antipsychotics, metoclopramide
toxins - carbon monoxide, MPTP
Why does domperidone (anti-sickness) not cause (dystonia) extra-pyramidal side effects?
doesnt cross blood brain barrier.
What is Parkinsons disease?
progressive neurodegenerative condition caused by degeneration of dopaminergic neurones in the substantia nigra.
reduction in dopaminergic output causes the classic triad of symptoms.
Classic Triad of Symptoms - PARKINSONS
bradykinesia
tremor
rigidity
SYMPTOMS CLASSICALLY ASYMMETRICAL
are the symptoms for Parkinsons symmetrical or asymmetrical?
asymmetrical
epidemiology of parkinsons
twice as common in men
average age 65 yrs
explain bradykinesia - PD
poverty of movement - hypokinesia
short shuffling steps with reduced arm swinging
difficulty in initiating movement
explain tremor - PD
most marked at rest 3-5hz
worse when stressed or tired - improves with voluntary movement !
typically pill-rolling - in the thumb and index finger
explain rigidity - PD
lead pipe
cogwheel: due to superimposed tremor
other characteristic features of PD
mask-like facies
flexed posture
micrographia - small handwriting
drooling of saliva
psychiatric features: depression mc common feature (40%), dementia, psychosis and sleep disturbances may also occur.
impaired olfaction
REM sleep behaviour disorder
fatigue
autonomic dysfunction: postural hypotension
how is drug-induced parkinsonism different in presenting features to parkinson’s disease?
motor symptoms - rapid onset and bilateral
rigidity and rest tremor uncommon
How to diagnose PD?
clinical
hard to differentiate between essential tremor and PD.
DO SPECT - 123i-fp-cit.
Management of Parkinsons
1st line: if motor symptoms affecting QoL - levodopa
if not : dopamine agonist (non-ergot derived so ropinirole, rotigotine, apomorphine), levodopa or monoamine oxidase B inhibitor
colour stain for lewy body?:
brown alpha synuclein
Of the parkinsons drugs what arte best for improvement in motor symptoms and ADL’s?
improvement in symptoms and ADL’s and has more motor complications :
levodopa
less improvement in motor and adl but less motor complications : dopamine agonists and MAO-B inhibitors
which class of drug has more specified adverse events associated to it for PD tx?
dopamine agonist
excessive sleepiness
hallucinations
impulse control disorder
what to do if pt continues to have symptoms despite optimal levodopa tx or develop dyskinesia?
add dopamine agonist, MAO-B inhibitor or COMT inhibitor. as adjunct.
which PD tx drugs should improvement in motor symptoms and ADLS?
dopamine agonist
MAO-B inhibitor
COMT inhibitor
Amantadine - no evidence showing improvement
which drugs for PD tx show off time reduction?
adverse events of them too
hallucinations too
dopamine agonist - more off-time reduction (intermediate risk of adverse events) more risk of hallucinations
MAO-B inhibitor
Comt inhibitor - these both show off time reduction and fewer adverse events. fewer hallucination risk
Amantadine - no off time reduction and no adverse events . no hallucination
What could happen in PD patients where there medication isnt absorbed and why?
due to gastroenteritis for example.
DONT GIVE DRUG HOLIDAY
risk of acute akinesia or neuroleptic malignant syndrome.
Causes of impulse control disorders?
dopamine agonist therapy
hx of previous impulse control disorder (inhibition disordeR)
hx of alcohol consumption and/or smoking
what is modafinil?
for excessive daytime sleepiness in PD patients.
what is Midodrine and what is it used for?
for orthostatic hypotension in PD patients.
acts on peripheral alpha-adrenergic receptors to increased arterial resistance.
How would you control drooling of saliva in PD patients?
glycopyrronium bromide
Why is levodopa prescribed with a decarboxylase inhibitor and give examples of decarboxylase inhibitors?
carbidopa and benserazide
prevents peripheral metabolism of levodopa to dopamine outside of brain and hence reduces side effects.
reduced effectiveness after 2 yrs
no use in neuroleptic induced parkinsonism
common adverse effects of levodopa
dry mouth
anorexia
palpitations
postural hypotension
psychosis
dyskinesia
on-off effect
cardiac arrhythmia
n+v
reddish discolouration of urine upon standing
What potential effects of levodopa tx may occur to the pt due to achieving a steady dose of it in PD patients?
end-of dose wearing off : sx worsen towards end of dosage interval. decline in motor activity.
on-off phenomenon - independent of medication timing. large variation in motor perforemance. normal function - on . weakness/restricted mobility in “off” period.
dyskinesias at peak dose: dystonia, chorea, athetosis (involuntary writhing movement)
effects could worsen over time.
why cant you acutely stop levodopa?
acute dystonia
give dopamine agonist patch as rescue medication if you have to
give me examples of dopamine receptor agonists?
ergot derived
non ergot derived
ergot: bromocriptine , cabergoline
non ergot: ropinirole, rotigotine, apomorphine,
side effects of dopamine receptor agonists
ergot derived : pulmonary, retroperitoneal, cardiac fibrosis. do echocardiogram esr creatinine and cxr before tx and closely monitor pts.
impulse control disroder
excessive daytime somnolence
more likely than levodopa to cause hallucinations in older pts.
potentially:
nasal congestion
postural hypotension
give an example of a monoamine oxidase-B inhibitor (MAO-B) and in mechanism of action?
selegiline
inhibits the breakdown of dopamine secreted by the dopaminergic neurons
What is amantadine?
drug not fully understood - probs increase dopamine release and inhibits its uptake at dopaminergic synapses.
side effects:
ataxia
slurred speech
confusion
dizziness
livedo reticularis - net like red skin condition
What is catechol-o-methyl transferase inhibitors (COMT)?
give examples
eg’s: entacapone, tolcapone
enzyme involved in dopamine breakdown.
could use as adjunct in levodopa therapy. esp in pts with established PD.
What are antimuscarinics?
give examples
use?
block cholinergic receptors
treat drug-induced parkinsonisms rather than idiopathic PD
help tremor and rigidity
procyclidine
benzotropine
trihexyphenidyl (benzhexol)
What is osteoporosis?
disorder affecting skeletal system characterised by loss of bone mass.
BMD decreases with age but if bmd is less than 2.5 standard deviations below young adult mean its osteoporosis.
increases risk of fragility.
fractured neck of femur associated with morbidity and mortality
major risk factors of osteoporosis
hx of glucocorticosteroid use
advancing age and female - 50% post menopausal women get osteoporotic fracture at some point.
RHEUMATOID ARTHRITIS
current smoking
alcohol excess
parental hip fracture hx.
low bmi
fhx
other:
sedentary lifestyle
premature menopause
white and asian
CKD
osteogenesis imperfecta, homocystinuria
gi: ibd, malabsorption, coeliac, gastrectomy, liver disease, chronic pancreatitis
multiple myeloma , lymphoma
endocrine: hyperthryoid, hypogonadism (turners, testosterone deficiency), GH def, hyperparathyroidism, DM
what screening tools are there for osteoporosis?
frax
qfracture
assess 10 yr risk of pt developing fragility fracture.
how would you assess actual BMD ?
dexa scan
dual energy x ray absorptiometry.
looks at hip and lumbar spine.
if t score is less than -2.5 then tx is recommended.
what is the 1st line tx for osteoporosis?
oral bisphosphonates - alendronate.
explain scoring for dexa scan?
t score = based on bmd of young adult population
z score = adjusted for age gender and ethnicity
t score of -1.0 = bmd 1 SD below young adult pop
t score :
more than -1.0 = normal
-1.0 - -2.5 = osteopenia
-.25 or less = osteoporosis
what medications can worsen osteoporosis
GLUCOCORTICOIDS
SSRI
antiepileptics
proton pump inhibitor
glitazone
long term heparin therapy
aromatase inhibitors - anastrozole
investigations for osteoporotic pt?
history and physical exam
blood cell count, sedimentation rate , crp, serum calcium, albumin, creatinine, phosphate, alkaline phosphatase and liver transaminase.
TFT
bone densitometry - DEXA
at min : fbc, u+e,, lft, bone profile, crp , tft
other potentials:
PTH
serum testosterone, sex hormone binding globulin (shbg) , fhs, LH
serum prolactin
24 hr urinary cortisol/dex supression test (Cushings)
isotope bone scan
urinary calcium excretion
markers of bone turnover
25OHD (vitd bone health)
endomysial/tissue transglutaminase antibodies (Coeliac)
protein immunoelectrophoretic and urinary bence-jones proteins (multiple myeloma screen)
how can cushings cause osteporosis?
excess cortisol can lead to osteoporosis.
who should be assessed for osteoporosis according to nice?
all women over 65 and all men over 75.
younger if :
smoke
previous fragility fracture
low bmi - less than 18.5
alcohol over 14 units a week
fhx hip fracture
hx of falls
glucocorticoid use
in what situations should a dexa scan be offered without calculating the fragility risk score?
over 50 with hx of fragility fracture
under 40 with major risk factor for fragility fracture - refer to specialist depending on the t score.
before starting tx that might have rapid adverse effect on bone density eg : sex hormone deprivation for tx for breast/prostate cancer
if a patient has had a recent fragility fracture what should you look for?
non-osteoporotic causes like bone metastases, myeloma and pagets disease
if the QFracture 10 yr fracture risk is over 10% , what should you do?
if over 10% then a dexa scan should be arranged.
how to interpret the frax score and what to do? next steps?
colour risk is given by calculator - green , orange, red
pts in orange zone should have a dexa scan to further refine 10 yr risk.
pts in red zone should have dexa scan to act as a baseline and guide drug tx.
if a patient over 75 has had a fragility fracture what to do?
if under 75 then?
assume underlying osteoporosis
give alendronate
no need for dexa
if under: DEXA then enter them into FRAX.. to get risk.
what to do in women over 50 with fragility fracture?
give alendronate
although benefits possible in checking bmd especially in younger postmenopausal women.
if a patient has just been diagnosed with a condition like polymyalgia rheumatica and you know they are going to have corticosteroid ie: prednisolone what to do?
if they take equivalent of prednisolone 7.5mg a day for 3+ months.
give anticipatory bone protection straight away. dont wait to 3 months.
if over 65: give it if previous had fragility fracture.
if under 65: offer bone density scan.
if t score greater than 0 reassure.
between 0 and -1.5 - repeat bone density scan in 1-3 yrs
if less than -1.5 then give bone protection
alendronate - make sure pt is calcium and vit d replete.
clinical scenarios where youd treat a pt for osteoporosis?
pt identified at high risk of fragility fracture based on screening
pt about to start tx with corticosteroids.
pt just had fragility fracture - symptomatic osteoporotic vertebral fracture
Lifestyle advice for osteoporosis pt
healthy diet - moderate alcohol and stop smoking
calcium+vit d 0 supplment for women.
regular weight bearing and muscle strengthening exercise
how would i treat hypogonadism (secondary cause of osteoporosis)
hormone replacement therapy for premature menopause
pharm tx of osteoporosis
1st line: alendronate and risedronate - oral bisphosphonate. take weekly. have to take in a particular way to avoid oesophageal side effects
if hip fracture, give iv zolendronate as 1st line tx. given yearly
2nd line: denosumab
other tx:
strontium ranelate
raloxifene
teriparatide
romosozumab
what is the follow up for osteoporosis pt given tx?
prescribe bisphosphonates for 5 years at lkeast,
or iv bisphosphonates for at least 3 years and then reassess fracture risk.
how do bisphosphonates work?
how should they be given?
bind to hydroxyapatite in bone, inhibiting osteoclast-mediated bone resorption
give with full glass of water
on empty stomach
remain upright for at least 30 mins after
common side effects of bisphosphonates
GI discomfort
oesophagitis
hypocalcaemia
rare risks:
atypical femoral fractures
osteonecrosis of jaw
What is denosumab?
MoA
Use
Administration
human monoclonal antibody inhibits RANK ligand - inhibits maturation of osteoclasts
also used in cancer pts with bone mets to reduce skeletal related events.
single subcut injection every 6 months
What is raloxifene?
class
positives
negatives
selective oestrogen receptor modulator (SERM)
prevents bone loss
reduce risk of vertebral fracture
not shown to reduce risk of non-vertebral fractures.
increases bone density in spine and proximal femur
decrease breast cancer risk
increase thromboembolic event risk and may worsen menopausal symptoms.
what is strontium renelate?
side effects - negatives
dual action bone agent - increases deposition of new bone by osteoblasts (promotes differentiation from pre-osteoblast to osteoblast) and reduces resorption of bone by inhibiting osteoclasts.
only give if this is the only remaining option.
increased risk of cv event : CI if cv disease hx or risk.
increased risk of thromboembolic event: if hx of VTE CI’d.
possible stevens johnson sydrome as side effect - serious skin reactions
what is teriparatide?
recombinant form of parathyroid hormone
very effective at increasing BMD but role in management of osteoporosis is yet to be defined
what is romosozumab?
monoclonal antibody that inhibits sclerostin - increasing bone formation and decreasing bone resorption.
dual action improves bone density and reduced fracture risk
what is a stroke?
cerebrovascular accident
sudden interruption in vascular supply of the brain.
neural tissue is completely dependent on aerobic metabolism so any issue with oxygen supply will quickly lead to irreversible damage.
what are the 2 main types of stroke?
ischaemic - another subtype of ischaemic is TIA (*check neuro)
haemorrhagic
explain ischaemic stroke
essential problem
proportion of strokes
subtypes
risk factors
blockage in blood vessel stops blood flow
85%
thrombotic stroke : thrombosis from large vessels like carotid
embolic: blood clot fat, air or clumps of bacteria act as embolus. AF important cause of emboli forming in the heart.
rf:
age
htn
smoking
hyperlipidemia
dm
rf for cardioembolism: AF
MAJOR RISK FACTOR FOR CARDIOEMBOLISM
AF
explain haemorrhagic stroke
essential problem
proportion of strokes
subtypes
risk factors
blood vessel bursts leading to reduction in blood flow.
15%
intracerebral haemorrhage: bleeding within brain
subarachnoid haemorrhage: bleeding on surface of brain
rf:
age
htn
arteriovenous malformation
anticoagulation therapy
features of stroke
motor weakness
speech problems - dysphasia
swallowing problems
visual field defects - homonymous hemianopia
balance problems
stroke : cerebral hemisphere infarct symptoms
contralateral hemiplegia: initial flaccid then spastic
contralateral sensory loss
homonymous hemianopia
dysphasia
stroke: brainstem infarction symptoms
possibly more severe symptoms including quadriplegia and lock-in syndrome
stroke: lacunar infarcts
what is it and symptoms?
small infarcts around the basal ganglia, internal capsulse, thalamus and pons
STRONG ASSOCIATION WITH HTN
present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
classification of stroke and what criteria:
oxford stroke - bamford
assess:
1. unilateral hemiparesis and/or hemisensory loss of face, arm and leg
2. homonymous hemianopia
3. higher cognitive dysfunction eg dysphasia
types of stroke
total anterior circulation infarct 15%
partial anterior circulation infarct 25%
lacunar infarcts 25%
posterior circulation infarcts - 25%
strokes: total anterior circulatory infarcts
involves middle and anterior cerebral arteries
all 3 of bamford criteria
strokes: partial anterior circulation infarcts
involves smaller arteries of anterior circulation eg: upper and lower division of middle cerebral artery
2 of bamford criteria
strokes: lacunar infarcts
involves perforating arteries around internal capsule, thalamus, and basal ganglia
presents with 1 of :
1. ataxic hemiparesis (weakness and difficulty coordinating movement on same side of body)
2. pure sensory stroke
3. unilateral weakness (and/or sensory deficit) of face and arm, and leg or all 3.
strokes: posterior circulation infarcts
involves vertebrobasilar artieres
presents with 1 of:
1. loss of conciousness
2. isolated homonymous hemianopia
3. cerebellar or brainstem syndromes
pt presents with ataxia and widespread cerebellar signs, what does he have?
stroke: posterior circulation infarct
what symptoms are more likely in haemorrhagic stroke than ischaemic?
decrease in conciousness level - 50% pts
headache
nausea vomiting
seziures - 25% pts
FAST - STROKE PNEUMONIC
face - face fallen on 1 side? can they smile?
arms - can they raise both and keep them there?
speech - slurred?
time - call 999 if any of signs
investigations for stroke
imaging: ct and mri
urgency
to see whether pt is suitable for thrombolytic therapy to treat early ischaemic strokes.
1st line radiological : NON-CONTRAST CT HEAD - ischaemic or haemorhagic. rarely tumour?
who would i offer thrombolysis to?
criteria is pt presents within 4.5 hrs of onset
pt hasnt had previous intracranial haemorrhage, uncontrolled htn, pregnant
how to figure out whether its ischaemic or haemorrhagic stroke?
then if its ischaemic what do u give?
neuroimaging - ct/mri
aspirin 300mg asap
continue antiplatelet therapy.
what do you call it when you have more than 1 tia and what should you do in this case?
crescendo tia
discuss admission or observe urgent with stroke specialist
what to do in the case of a haemorrhagic stroke?
imaging
most not suitable for surgery.
supportive: stop anticoagulant like warfarin and antithrombotic meds (clopidogrel) - prevent further bleeding
if pt anticoagulated - reverse asap.
trials prove pts that have bp lowered acutely have better outcomes.
stroke: effect if lesion is anterior cerebral artery
contralateral hemiparesis and sensory loss,
lower extremity > upper extremity
stroke: effect if lesion is middle cerebral artery
contralateral hemiparesis and sensory loss,
upper extremity > lower extremity
contralateral homonymous hemianopia
aphasia
stroke: effect if lesion is posterior cerebral artery
contralateral homonymous hemianopia with macular sparing
visual agnosia
stroke if lesion : webers syndrome - branches of posterior cerebral artery that supply midbrain
ipsilateral CN III palsy (oculomotor palsy)
contralateral weakness of upper and lower extremity.
stroke if lesion site : posterior inferior cerebellar artery (lateral medullary syndrome, wallenberg syndrome)
sudden onset vertigo, vomiting, dysphagia
ipsilateral : facial pain and temp loss
contralateral: limb/torso pain and temp loss
ataxia, nystagmus
stroke if lesion site: anterior inferior cerebellar artery (lateral pontine syndrome)
symptoms similar to wallenberg’s. sudden onset vertigo and vomiting,
but
ipsilateral : facial paralysis and deafness
stroke if lesion site: retinal/opthalmic artery
transient unilateral visual loss like curtain descending
amaurosis fugax
stroke if lesion site: basilar artery
locked-in syndrome
screening for public
screening for medics for stroke
FAST
ROSIER
loss of conciousness or syncope - -1 point
seizure activity - -1 point
+1 point:
assymetric facial weakness
asymmetric arm weaknes
asymmetric leg weakness
speech disurbance
visual field defect
stroke likely if score >0
what would the non-contrast ct head show for ischaemic stroke ? (acute)
low density in the grey and white matter of the territory. these changes may take time to develop.
HYPERDENSE ARTERY CORRESPONDING WITH THE RESPONSIBLE ARTERIAL CLOT - in contrast to changes in parenchyma - visible immediately
what would the non-contrast ct head show for haemorrhagic acute stroke?
areas of hyperdense material (blood) surrounded by low density - oedema
Which obs should be maintained during the management of acute stroke?
blood glucose
hydration
oxygen sats
temperature
bp - dont lower in acute phase of stroke unless hypertensive encephalopathy/thrombolysis
in what case should bp control be considered in acute ischaemic stroke?
if present within 6 hrs and have systolic bp over 150.
if giving thrombolysis should be lowered to 185/110.
what should you give as tx for acute ischaemic stroke when haemorrhagic stroke is excluded?
aspirin 300mg orally/rectally ASAP.
if cholestrol over 3.5 give statin. delay until 48 hrs after stroke, reduce risk of haemorrhagic transformation.
anticoagulants not start until brain imagine exclude haemorrhage and not until 14 days passed after ischaemic stroke.
Standard Criteria for thrombolysis for acute ischaemic stroke tx
ALTEPLASE/TENECTEPLASE
administer within 4.5 hrs of onset of stroke symptoms and haemorrhage excluded. (imaging)
new guidlines 2023 - if acute ischaemic stroke, regardless of age, 4.5-9 hrs after symptoms/wake-up stroke
if ischaemic stroke acute has come to your attention 4.5-9 hours after symptom onset what to do?
if 4.5-9 hours after known onset or within 9 hours of midpoint of lseep then:
have evidence from CT/MR perfusion (core perfusion mismatch) or MRI (DWI-FLAIR mismatch) of the potential to salvage brain tissue
Alteplase/Tenecteplase
regardless whether its a large artery occlusion and require mechanical thrombectomy.
Name some relative contraindications to thrombolysis (acute ischaemic stroke tx)
pregnancy
concurrent anticoagulation (INR>1.7)
Haemorrhagic diathesis (predisposition)
Active Diabetic Haemorrhagic Retinopathy
Suspected Intracardiac Thrombus
Major Surgery/Trauma in Preceding 2 weeks
What are the absolute contraindications to thrombolysis (Acute Ischaemic Stroke)
previous intracranial haemorrhage
active bleed
oesphageal varices
uncontrolled htn over 200/120
gi haemorrhage in preceding 3 weeks
seizure at stroke onset
intracranial neoplasm
suspected subarachnoid haemorrhage
stroke/traumatic brain injury in preceding 3 months.
lumbar puncture in preceding 7 days
Surgical procedure for acute ischaemic stroke - who to give and when to give?
mechanical thrombectomy
u need :
pre-stroke functional status - less than 3 (MODIFIED RANKIN SCALE)
National Institutes of Health Stroke Scla e(NIHSS) - more than 5
ASAP - within 6 hrs of symptoms together with IV thrombolysis (if within 4.5 hrs) to ppl with acute ischaemic stroke + confirmed occlusion of PROXIMAL ANTERIOR CIRCULATION proven by CTA or MRA
when would you do mechanical thrombectomy for stroke?
when symptoms within 6 hrs of onset with thromblysis (can be extended to 6-24 hours if there is potential to salvage brain tissue shown by ct perfusion or diffusion weighted MRI showing LIMITED INFARCT CORE VOLUME
including wake up if : PROXIMAL POSTERIOR CIRCULATION (BASILAR/POSTERIOR CEREBRAL ARTERY)
and occlusion in POSTERIOR ANTERIOR CIRCULATION
confirmed by computer tomography angiography - CTA and magnetic resonance angiography MRA
Name the secondary prevention for stroke
clopidogrel - now better to use vs aspirin+dipyridamole - in ppl whove already had ischaemic stroke
aspirin after ischaemic stroke only if clopidogrel contraindicated
what to do if pt suffered stroke/TIA in carotid territory and isnt severely disabled?
carotid endarterectomy
only if stenosis is over 50%. (some say 70%)
do within 7 days.
Importance of fluid management in stroke patients
over 80% pts that cant swallow post stroke will recover within 2-4 weeks.
hypovolemia can worsen ischaemic penumbra, infection,dvt,constipation and delirium risk increase too.
overhydration can lead to cerebral oedema, cardiac failure, hyponatraemia.
nice guidline recommended blood glucose maintined level for acute stroke patients
between 4 and 11 mmol/L
if diabetic, post acute stroke give intensive management, optimise insulin treatment iv insulin and glucose infusion.
in post acute stroke diabetic patient what why does hypoglycaemia need to be managed?
cause neuronal injury
mimic stroke-related neurological deficit.
how would you manage blood pressure in acute stroke pts?
only use antihypertensives in post ischaemic stroke if emergency:
- hypertensive encephalopathy/nephropathy/cardiac failure/MI
- aortic dissection
-pre-eclampsia
lowering bp - compromise collateral blood flow to region - hasten complete and irreversible tissue infarction.
if you are to lower bp in ischaemic stroke (post) pt , how would you do it?
15% in first 24 hrs after stroke onset.
iv labetalol, nicardipine and clevidipine as 1st line - rapid and safe titration to control bp.
what score is used to assess disability is post stroke pts?
barthel index
10 tasks
0-100 - 0 is dependent 100 is independent.
assess functional status of pt
What is BnP and where is it produced?
B-type natriuretic peptide - hormone
produced by left ventricular myocardium in response to strain.
causes of elevated bnp?
anything that causes left ventricular dysfunction
heart failure
MI
valvular disease
CKD - reduced excretion.
what can reduce bnp levels?
ace inhibitor
angiotensin - 2 receptor blockers
diuretics
effects of bnp
vasodilator
diuretic and natriuretic
suppresses both sympathetic tone and RAAS (renin angiotensin-aldosterone system)
what is considered a low conc of bnp?
less than 100 pg/ml - makes heart failure diagnosis unlikely
effective tx will lower bnp level
