Passmed geriatrics Flashcards
acute confusional state predisposing fx
age > 65 years
background of dementia
significant injury e.g. hip fracture
frailty or multimorbidity
polypharmacy
acute confusional state precipitating fx
infection: particularly urinary tract infections
metabolic: e.g. hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration
change of environment
any significant cardiovascular, respiratory, neurological or endocrine condition
severe pain
alcohol withdrawal
constipation
clinical fx acute confusional state
memory disturbances (loss of short term > long term)
may be very agitated or withdrawn
disorientation
mood change
visual hallucinations
disturbed sleep cycle
poor attention
how to manage acute confusional state
- non medical
- medical
tx underlying cause - ie, constipation
modify environment - side room
1st line for delirium - haloperidol or olanzapine, except in parkison’s - reduction of parkinson meds and if require urgent tx then atypical antipsychotics (quetiapine, clozapine)
non pharmacological mx of alzheimer’s
activities to promote wellbeing
cognitive stimulation therapy
group reminiscence therapy and cognitive rehab
pharmacological mx of alzheimer’s
acetylcholinesterase inhibitors - donepezil, galantamine, rivastigmine
2nd line - memantine (NMDA receptor antagonist) - used when intolerant of 1st line, as an add on in severe, or monotherapy in severe
mx non cognitive sx of alzheimer’s
NO ANTIDEPRESSANTS
antipsychotics used if risk of harming themselves, agitation, hallucination, delusions
other tx options of alzheimer’s
donepezil
donepezil c/i and adverse effect
in pts with bradycardia
s/e - insomnia
alzheimer’s risk fx
increasing age
family history of Alzheimer’s disease
5% of cases are inherited as an autosomal dominant trait
mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form
apoprotein E allele E4 - encodes a cholesterol transport protein
Caucasian ethnicity
Down’s syndrome
macroscopic changes in alzheimer’s
widespread cerebral atrophy, particularly involving the cortex and hippocampus
microscopic change alzheimer’s
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 the tau protein
biochemical changes alzheimer’s
a deficit of acetylcholine from damage to an ascending forebrain projection
define neurofibrillary tangles and how affect in AD
paired helical filaments are partly made from a protein called tau
tau is a protein that interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules
in AD are tau proteins are excessively phosphorylated, impairing its function
factors favouring delirium over dementia
acute onset
impairment of consciousness
fluctuation of symptoms: worse at night, periods of normality
abnormal perception (e.g. illusions and hallucinations)
agitation, fear
delusions
order of prev in dementia types
1.alzheimers
2. vascular
3. lewy body
assessment tools for dementia
10-point cognitive screener (10-CS), 6-Item cognitive impairment test (6CIT)
other ways to assess dementia but not NICE recommended
abbreviated mental test score (AMTS), General practitioner assessment of cognition (GPCOG) and the mini-mental state examination (MMSE)
MMSE score indicated dementia
24 or less /30
dementia ix
blood screen to exclude reversible causes - FBC, UE, LFT, calcium, ESR/CRP, TFT, vit B12, folate
neuroimaging - subdural haematoma, normal pressure hydrocephalus
rare causes of dementia
Huntington’s
CJD
Pick’s disease (atrophy of frontal and temporal lobes)
HIV (50% of AIDS patients)
ddx dementia
hypothyroidism, Addison’s
B12/folate/thiamine deficiency
syphilis
brain tumour
normal pressure hydrocephalus
subdural haematoma
depression
chronic drug use e.g. Alcohol, barbiturates
what parts of body involve normal gait
The neurological system - basal ganglia and cortical basal ganglia loop.
The musculoskeletal system (which must have appropriate tone and strength).
Effective processing of the senses such as sight, sound, and sensation (fine touch and proprioception).
risk fx for falling
Lower limb muscle weakness
Vision problems
Balance/gait disturbances (diabetes, rheumatoid arthritis and parkinson’s disease etc)
Polypharmacy (4+ medications)
Incontinence
>65
Have a fear of falling
Depression
Postural hypotension
Arthritis in lower limbs
Psychoactive drugs
Cognitive impairment
what establish from falls hx
Where was the patient when they fell?
When did they fall?
Did anyone else see the patient fall? (collateral history)
What happened? Were there any associated features before/during/after
Why do they think they fell?
Have they fallen before?
Systems review
Past medical history (especially issues related to balance/sight/gait)
Social history
meds that cause postural hypotension
nitrates
diuretics
anticholinergics
antidepressants
beta blockers
L-Dopa
ACEi
meds that cause falls due to other mechanisms
benzo
antipsychotics
opiates
anticonvulsants
codeine
digoxin
other sedatives
ix when someone falls
Bedside tests - Basic observations, blood pressure, blood glucose, urine dip and ECG
Bloods - Full Blood Count, Urea and Electrolytes, Liver function tests and bone profile
Imaging- X-ray of chest/injured limbs, CT head and cardiac echo
nice cks mx of falls to assess risk
Identify all individuals who have fallen in the last 12 months.
As per above identify why they are at risk.
For those with a falls history or at risk complete the ‘Turn 180° test’ or the ‘Timed up and Go test’.
pts >65 when require MDT assessment
> 2 falls in the last 12 months
A fall that requires medical treatment
Poor performance or failure to complete the ‘Turn 180° test’ or the ‘Timed up and Go test’
3 types of frontotemporal lobar degeneration
Frontotemporal dementia (Pick’s disease)
Progressive non fluent aphasia (chronic progressive aphasia, CPA)
Semantic dementia
common fx of frontotemporal lobar dementia
Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change and social conduct problems
pick’s disease clinical fx
personality change
impaired social conduct
hyperorality
disinhibition
increased appetite
perseveration
pick’s disease macroscopic changes
Focal gyral atrophy with a knife-blade appearance
Atrophy of the frontal and temporal lobes
microscopic changes pick’s disease
Pick bodies - spherical aggregations of tau protein (silver-staining)
Gliosis
Neurofibrillary tangles
Senile plaques
avoid in pick’s disease
AChE inhibitors or memantine
CPA clinical fx
non fluent speech. They make short utterances that are agrammatic. Comprehension is relatively preserved.
semantic dementia clinical fx
fluent progressive aphasia. The speech is fluent but empty and conveys little meaning. Unlike in Alzheimer’s memory is better for recent rather than remote events.
pathological fx in lewy body dementia
alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.
clinical fx lewy body dementia
progressive cognitive impairment
typically occurs before parkinsonism, but usually both features occur within a year of each other. This is in contrast to Parkinson’s disease, where the motor symptoms typically present at least one year before cognitive symptoms
cognition may be fluctuating, in contrast to other forms of dementia
in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
parkinsonism
visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
how lewy body dementia diagnosed
clinical
SPECT - single proton emission computed tomography
lewy body dementia mx
acetylcholinesterase inhibitors - donepezil, rivastigmine
memantine
neuroleptics avoided - can develop irreversible parkinsonism
definition of multimorbidity
The presence of two or more long-term health conditions, including: Defined physical or mental health conditions, learning disabilities, symptom complexes such as chronic pain, sensory impairments and alcohol or substance misuse
prevalence of comorbidity
higher in females
combined mental and physical is more common in younger adults
socioeconomic deprivation
most common comorbid conditions
HTN
pain
DM
hearling loss
depression
anxiety
IBS
chronic pain
prostate disorders
thyroid disorders
CAD
risk fx comorbid conditions
Increasing age
Female sex
Low socioeconomic status
Tobacco and alcohol usage
Lack of physical activity
Poor nutrition and obesity
complications comorbid conditions
decreased QoL
increased treatment burden
mental health issues
polypharmacy
carers welfare
how frailty assesed
evaluation of gait speed, self-reported health status, or the PRISMA-7 questionnaire: The PRISMA-7 involves questions considering the age, sex, health problems, assistance required and walking aid use of the patient
mx of comorbid conditions
optimising care
offer alternative f/u
reduce no of high risk meds
Consider a ‘bisphosphonate holiday’ in those taking bisphosphonates for longer than three years as there is no consistent evidence of continued benefits after this point. Discuss stopping bisphosphonates after 3 years and include patient choice, fracture risk and life expectancy in the discussion.
STOPP/START tool
individualised management plan
education
Use the action plan to follow up with the patient at agreed points: NHS England recommends a yearly review of all medications for people aged over 65, however, medications should be reviewed periodically to ensure that patients are being informed, given adequate laboratory tests and that treatments are optimised
define pressure ulcers
develop in patients who are unable to move parts of their body due to illness, paralysis or advancing age. They typically develop over bony prominences such as the sacrum or heel
risk fx of pressure ulcers
malnourishment
incontinence
lack of mobility
pain (leads to a reduction in mobility)
risk of pressure score how assessed
The Waterlow score is widely used to screen for patients who are at risk of developing pressure areas. It includes a number of factors including body mass index, nutritional status, skin type, mobility and continence.
grading of pressure ulcers
Grade 1 Non-blanchable erythema of intact skin. Discolouration of the skin, warmth, oedema, induration or hardness may also be used as indicators, particularly on individuals with darker skin
Grade 2 Partial thickness skin loss involving epidermis or dermis, or both. The
ulcer is superficial and presents clinically as an abrasion or blister
Grade 3 Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.
Grade 4 Extensive destruction, tissue necrosis, or damage to muscle, bone or
supporting structures with or without full thickness skin loss
mx of pressure ulcers
moist wound environment - hydrocolloid dressings and hydrogels
avoid soap
only swab wound and give abx if evidence of surrounding infection
consider referral to tissue viability nurses
may require surgical debridement
vascular dementia define
a group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease
epidemiology vascular dementia
Prevalence of dementia following a first stroke varies depending on location and size of the infarct, definition of dementia, interval after stroke and age among other variables. Overall, stroke doubles the risk of developing dementia.
Incidence increases with age
main subtypes of vascular dementia
Stroke-related VD – multi-infarct or single-infarct dementia
Subcortical VD – caused by small vessel disease
Mixed dementia – the presence of both VD and Alzheimer’s disease
risk fx of vascular dementia
History of stroke or transient ischaemic attack (TIA)
Atrial fibrillation
Hypertension
Diabetes mellitus
Hyperlipidaemia
Smoking
Obesity
Coronary heart disease
A family history of stroke or cardiovascular
how can VD be inherited in rare cases
CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
clinical fx of vascular dementia
Several months or several years of a history of a sudden or stepwise deterioration of cognitive function
Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
The difficulty with attention and concentration
Seizures
Memory disturbance
Gait disturbance
Speech disturbance
Emotional disturbance
how diagnosed vascular dementia
clinical fx
formal screen for cog impairment
medical review to exclude medication cause
MRI scan - infarcts and white matter changes
criteria for vascular dementia
NINDS-AIREN criteria:
Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event
established using clinical examination and neuropsychological testing
Cerebrovascular disease
defined by neurological signs and/or brain imaging
A relationship between the above two disorders inferred by:
the onset of dementia within three months following a recognised stroke
an abrupt deterioration in cognitive functions
fluctuating, stepwise progression of cognitive deficits
general mx of vascular dementia
address cardiovascular risk fx
non pharmacological tx of vascular dementia
cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication
pharmacological tx of vascular dementia
no specific tx
AChE inhibitors or memantine for people with vascular dementia if they have suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia or dementia with Lewy bodies.
There is no evidence that aspirin or statins are effective
Reflex syncope definition
loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery
Types of reflex syncope
Vasovagal
Situational - cough, micturition, GI
Carotid sinus syncope
Vasovagal syncope clinical fx
Triggered by emotion, pain, stress
Warm prior to loss of consciousness
Brief myoclonus jerks can occur during uncomplicated
1-2 mins duration
Prolonged fatigue in post octal is suggestive of other cause
Orthostatic syncope causes
primary autonomic failure: Parkinson’s disease, Lewy body dementia
secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia
drug-induced: diuretics, alcohol, vasodilators
volume depletion: haemorrhage, diarrhoea
Cardiac syncope causes
arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular)
structural: valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy
others: pulmonary embolism
Syncope ix
cardiovascular examination
postural blood pressure readings: a symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic
ECG for all patients
other tests depend on clinical features
patients with typical features, no postural drop and a normal ECG do not require further investigations
Malnutrition how common
10% in more than 65 yr olds
Malnutrition mx
dietician support if the patient is at high-risk
a ‘food-first’ approach with clear instructions (e.g. ‘add full-fat cream to mashed potato’), rather than just prescribing oral nutritional supplements (ONS) such as Ensure
if ONS are used they should be taken between meals, rather than instead of meals
1st line ix for stroke
NON CONTRAST CT
Stroke
See neuro flash cards
First line laxatives for constipation
bulk-forming laxative first-line, such as ispaghula
2nd line mx for constipation
Osmotic - macrogol
Causes of hypercalcaemia
Primary hyperparathyoidism
Malignancy - s.c.c lung cancer, bone mets, myeloma, sarcoidosis, vitamin D intoxication
acromegaly
thyrotoxicosis
Milk-alkali syndrome
drugs:
thiazides
calcium-containing antacids
dehydration
Addison’s disease
Paget’s disease of the bone
usually normal in this condition but hypercalcaemia may occur with prolonged immobilisation
Clinical fx of hypercalcaemia
bones, stones, groans and psychic moans’
corneal calcification
shortened QT interval on ECG
hypertension
ECG changes in hyperkalaemia
tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern and asystole
Causes of hyperkalaemia
acute kidney injury
drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
metabolic acidosis
Addison’s disease
rhabdomyolysis
massive blood transfusion
Food
Beta blockers if renal impairment
LMWH
Mx of severe hyperkalaemia
IV calcium gluconate: to stabilise the myocardium
insulin/dextrose infusion: short-term shift in potassium from ECF to ICF
other treatments such as nebulised salbutamol may be given to temporarily lower the serum potassium
Ways to reduce hyperkalaemia including medications
stop exacerbating drugs e.g. ACE inhibitors
treat any underlying cause
lower total body potassium
calcium resonium
loop diuretics
dialysis
Causes of hypernatraemia
dehydration
osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
diabetes insipidus
excess IV saline
Hypocalcaemia causes
vitamin D deficiency (osteomalacia)
chronic kidney disease
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
pseudohypoparathyroidism (target cells insensitive to PTH)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis
Mx of hypocalcaemia
severe hypocalcaemia (e.g. carpopedal spasm, tetany, seizures or prolonged QT interval) requires IV calcium replacement
the preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
intravenous calcium chloride is more likely to cause local irritation
ECG monitoring is recommended
further management depends on the underlying cause
Hypocalcameia clinical fx
tetany: muscle twitching, cramping and spasm
perioral paraesthesia
if chronic: depression, cataracts
ECG: prolonged QT interval
Trousseau’s sign
carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
Hypokalamia with alkalosis causes
vomiting
thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
Hypokalaemia wirh acidosis causes
diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis
Hypomagnesaemia causes
drugs
diuretics
proton pump inhibitors
total parenteral nutrition
diarrhoea
may occur with acute or chronic diarrhoea
alcohol
hypokalaemia
hypercalcaemia
e.g. secondary to hyperparathyroidism
calcium and magnesium functionally compete for transport in the thick ascending limb of the loop of Henle
metabolic disorders
Gitleman’s and Bartter’s
Clinical fx of hypomagnesia
paraesthesia
tetany
seizures
arrhythmias
decreased PTH secretion → hypocalcaemia
ECG features similar to those of hypokalaemia
exacerbates digoxin toxicity
Tx of hypomagneasamia
<0.4 mmol/L or tetany, arrhythmias, or seizures
intravenous magnesium replacement is commonly given.
an example regime would be 40 mmol of magnesium sulphate over 24 hours
> 0.4 mmol/l
oral magnesium salts (10-20 mmol orally per day in divided doses)
diarrhoea can occur with oral magnesium salts
Low sodium blood, high urinary sodium causes
Sodium depletion, renal loss (patient often hypovolaemic)
diuretics: thiazides, loop diuretics
Addison’s disease
diuretic stage of renal failure
Patient often euvolaemic
SIADH (urine osmolality > 500 mmol/kg)
hypothyroidism
Low serum and urine sodium causes
Sodium depletion, extra-renal loss
diarrhoea, vomiting, sweating
burns, adenoma of rectum
Water excess (patient often hypervolaemic and oedematous)
secondary hyperaldosteronism: heart failure, liver cirrhosis
nephrotic syndrome
IV dextrose
psychogenic polydipsia
Acute hyponatraemia wirh severe sx tx
Patients with acute, severe (<120 mmol/L) or symptomatic hyponatraemia require close monitoring, preferably in an HDU or above setting.
Hypertonic saline (typically 3% NaCl) is used to correct the sodium level more quickly than would be done in patients with chronic hyponatraemia.
Complication of tx of hyponatrameia
Osmotic demyelination syndrome (central pontine myelinolysis)
can occur due to over-correction of severe hyponatremia
pathophysiology:
thought to develop secondary to astrocyte (and possibly oligodendrocyte) apoptosis
astrocytes and oligodendrocytes (cells of the glial syncytium) are crucial for normal myelination
chronic hyponatraemia → loss of osmotically active organic osmolytes (such as myoinositol, glutamate, glutamine) from astrocytes. These provide protection against cerebral oedema
What considered in ‘best interests’
- Whether the person is likely to regain capacity and can the decision wait.
- How to encourage and optimise the participation of the person in the decision.
- The past and present wishes, feelings, beliefs, values of the person and any other relevant factors
- Views of other relevant people
LPA what
The Act allows a person to appoint an attorney to act on their behalf if they should lose capacity in the future, replacing the current Enduring Power of Attorney (EPA)
LPA what decisions make
life-sustaining treatment if the LPA specifies that
Advance decision define
can be drawn up by anybody with capacity to specify treatments they would not want if they lost capacity. They may be made verbally unless they specify refusing life-sustaining treatment (e.g. Ventilation) in which case they need to be written, signed and witnessed to be valid. Advance decisions cannot demand treatment
1st line for osteoposis
Alendronate
drugs to be aware of in older persons
NSAIDS – not use systemically in older pts, with kidneys and sodium levels. Can be used in short term, PPI cover. Topical better
Oral hypoglycaemics – gliclazide – risk of hypoglycaemia
Antidepressants – SSRI carry risk of hyponatraemia and postural hypotension. Adjust dose, eg: half dose of citalopram
Benzodiazepines and z drugs – confusion, cog impairment, falls. Can used short term and regular reviews
Anticoagulation – dose appropriate, check indication
Opioids – can cause CNS depression, confusion, falls, constipation. Short term use and regular reviews
older age affects in terms of drug
creatinine clearance reduced
must be adjust for bmi
prescription cascade
treat side effects from each new drug introduced rather than consider new sx is a side effect and change medication
comprehensive geriatric assesment
see PP
anticholinergic burden
risk of falls and cognitive impairment
dry mouth
blurred vision
contipation
urinary retention
lots of meds
dosette box
blister pack
carousel tablet dispenser - audible reminder
cant see med box
speaking labels or large print
eye drops
opticare to assist
dementia hx
progression of sx
home safety and accidents
further ix for dementia
mention cognitive tests
osteoporosis mx
alendronate
vid d and calcium - combo
bppv dix hallpike positive findings
a positive test recreates the symptoms of benign paroxysmal positional vertigo
rotatory nystagmus
latency, torsional geotropic nystagmus, fatigue, habituation
meniere’s patho
endolymph
bppv patho
caused by crystals of calcium carbonate called otoconia that become displaced into the semicircular canals. This occurs most often in the posterior semicircular canal. They may be displaced by a viral infection, head trauma, ageing or without a clear cause.
The crystals disrupt the normal flow of endolymph through the canals, confusing the vestibular system. Head movement creates the flow of endolymph in the canals, triggering episodes of vertigo.
