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OPIC > Passmed geriatrics > Flashcards

Passmed geriatrics Flashcards

1
Q

acute confusional state predisposing fx

A

age > 65 years
background of dementia
significant injury e.g. hip fracture
frailty or multimorbidity
polypharmacy

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2
Q

acute confusional state precipitating fx

A

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

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3
Q

clinical fx acute confusional state

A

memory disturbances (loss of short term > long term)
may be very agitated or withdrawn
disorientation
mood change
visual hallucinations
disturbed sleep cycle
poor attention

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4
Q

how to manage acute confusional state
- non medical
- medical

A

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)

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5
Q

non pharmacological mx of alzheimer’s

A

activities to promote wellbeing
cognitive stimulation therapy
group reminiscence therapy and cognitive rehab

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6
Q

pharmacological mx of alzheimer’s

A

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

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7
Q

mx non cognitive sx of alzheimer’s

A

NO ANTIDEPRESSANTS
antipsychotics used if risk of harming themselves, agitation, hallucination, delusions

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8
Q

other tx options of alzheimer’s

A

donepezil

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9
Q

donepezil c/i and adverse effect

A

in pts with bradycardia
s/e - insomnia

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10
Q

alzheimer’s risk fx

A

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

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11
Q

macroscopic changes in alzheimer’s

A

widespread cerebral atrophy, particularly involving the cortex and hippocampus

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12
Q

microscopic change alzheimer’s

A

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

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13
Q

biochemical changes alzheimer’s

A

a deficit of acetylcholine from damage to an ascending forebrain projection

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14
Q

define neurofibrillary tangles and how affect in AD

A

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

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15
Q

factors favouring delirium over dementia

A

acute onset
impairment of consciousness
fluctuation of symptoms: worse at night, periods of normality
abnormal perception (e.g. illusions and hallucinations)
agitation, fear
delusions

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16
Q

order of prev in dementia types

A

1.alzheimers
2. vascular
3. lewy body

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17
Q

assessment tools for dementia

A

10-point cognitive screener (10-CS), 6-Item cognitive impairment test (6CIT)

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18
Q

other ways to assess dementia but not NICE recommended

A

abbreviated mental test score (AMTS), General practitioner assessment of cognition (GPCOG) and the mini-mental state examination (MMSE)

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19
Q

MMSE score indicated dementia

A

24 or less /30

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20
Q

dementia ix

A

blood screen to exclude reversible causes - FBC, UE, LFT, calcium, ESR/CRP, TFT, vit B12, folate
neuroimaging - subdural haematoma, normal pressure hydrocephalus

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21
Q

rare causes of dementia

A

Huntington’s
CJD
Pick’s disease (atrophy of frontal and temporal lobes)
HIV (50% of AIDS patients)

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22
Q

ddx dementia

A

hypothyroidism, Addison’s
B12/folate/thiamine deficiency
syphilis
brain tumour
normal pressure hydrocephalus
subdural haematoma
depression
chronic drug use e.g. Alcohol, barbiturates

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23
Q

what parts of body involve normal gait

A

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).

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24
Q

risk fx for falling

A

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

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25
Q

what establish from falls hx

A

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

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26
Q

meds that cause postural hypotension

A

nitrates
diuretics
anticholinergics
antidepressants
beta blockers
L-Dopa
ACEi

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27
Q

meds that cause falls due to other mechanisms

A

benzo
antipsychotics
opiates
anticonvulsants
codeine
digoxin
other sedatives

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28
Q

ix when someone falls

A

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

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29
Q

nice cks mx of falls to assess risk

A

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’.

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30
Q

pts >65 when require MDT assessment

A

> 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’

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31
Q

3 types of frontotemporal lobar degeneration

A

Frontotemporal dementia (Pick’s disease)
Progressive non fluent aphasia (chronic progressive aphasia, CPA)
Semantic dementia

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32
Q

common fx of frontotemporal lobar dementia

A

Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change and social conduct problems

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33
Q

pick’s disease clinical fx

A

personality change
impaired social conduct
hyperorality
disinhibition
increased appetite
perseveration

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34
Q

pick’s disease macroscopic changes

A

Focal gyral atrophy with a knife-blade appearance
Atrophy of the frontal and temporal lobes

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35
Q

microscopic changes pick’s disease

A

Pick bodies - spherical aggregations of tau protein (silver-staining)
Gliosis
Neurofibrillary tangles
Senile plaques

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36
Q

avoid in pick’s disease

A

AChE inhibitors or memantine

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37
Q

CPA clinical fx

A

non fluent speech. They make short utterances that are agrammatic. Comprehension is relatively preserved.

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38
Q

semantic dementia clinical fx

A

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.

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39
Q

pathological fx in lewy body dementia

A

alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.

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40
Q

clinical fx lewy body dementia

A

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)

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41
Q

how lewy body dementia diagnosed

A

clinical
SPECT - single proton emission computed tomography

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42
Q

lewy body dementia mx

A

acetylcholinesterase inhibitors - donepezil, rivastigmine
memantine
neuroleptics avoided - can develop irreversible parkinsonism

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43
Q

definition of multimorbidity

A

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

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44
Q

prevalence of comorbidity

A

higher in females
combined mental and physical is more common in younger adults
socioeconomic deprivation

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45
Q

most common comorbid conditions

A

HTN
pain
DM
hearling loss
depression
anxiety
IBS
chronic pain
prostate disorders
thyroid disorders
CAD

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46
Q

risk fx comorbid conditions

A

Increasing age
Female sex
Low socioeconomic status
Tobacco and alcohol usage
Lack of physical activity
Poor nutrition and obesity

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47
Q

complications comorbid conditions

A

decreased QoL
increased treatment burden
mental health issues
polypharmacy
carers welfare

48
Q

how frailty assesed

A

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

49
Q

mx of comorbid conditions

A

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

50
Q

define pressure ulcers

A

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

51
Q

risk fx of pressure ulcers

A

malnourishment
incontinence
lack of mobility
pain (leads to a reduction in mobility)

52
Q

risk of pressure score how assessed

A

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.

53
Q

grading of pressure ulcers

A

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

54
Q

mx of pressure ulcers

A

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

55
Q

vascular dementia define

A

a group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease

56
Q

epidemiology vascular dementia

A

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

57
Q

main subtypes of vascular dementia

A

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

58
Q

risk fx of vascular dementia

A

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

59
Q

how can VD be inherited in rare cases

A

CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

60
Q

clinical fx of vascular dementia

A

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

61
Q

how diagnosed vascular dementia

A

clinical fx
formal screen for cog impairment
medical review to exclude medication cause
MRI scan - infarcts and white matter changes

62
Q

criteria for vascular dementia

A

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

63
Q

general mx of vascular dementia

A

address cardiovascular risk fx

64
Q

non pharmacological tx of vascular dementia

A

cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication

65
Q

pharmacological tx of vascular dementia

A

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

66
Q

Reflex syncope definition

A

loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery

67
Q

Types of reflex syncope

A

Vasovagal
Situational - cough, micturition, GI
Carotid sinus syncope

68
Q

Vasovagal syncope clinical fx

A

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

69
Q

Orthostatic syncope causes

A

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

70
Q

Cardiac syncope causes

A

arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular)
structural: valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy
others: pulmonary embolism

71
Q

Syncope ix

A

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

72
Q

Malnutrition how common

A

10% in more than 65 yr olds

73
Q

Malnutrition mx

A

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

74
Q

1st line ix for stroke

A

NON CONTRAST CT

75
Q

Stroke

A

See neuro flash cards

76
Q

First line laxatives for constipation

A

bulk-forming laxative first-line, such as ispaghula

77
Q

2nd line mx for constipation

A

Osmotic - macrogol

78
Q

Causes of hypercalcaemia

A

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

79
Q

Clinical fx of hypercalcaemia

A

bones, stones, groans and psychic moans’
corneal calcification
shortened QT interval on ECG
hypertension

80
Q

ECG changes in hyperkalaemia

A

tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern and asystole

81
Q

Causes of hyperkalaemia

A

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

82
Q

Mx of severe hyperkalaemia

A

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

83
Q

Ways to reduce hyperkalaemia including medications

A

stop exacerbating drugs e.g. ACE inhibitors
treat any underlying cause
lower total body potassium
calcium resonium
loop diuretics
dialysis

84
Q

Causes of hypernatraemia

A

dehydration
osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
diabetes insipidus
excess IV saline

85
Q

Hypocalcaemia causes

A

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

86
Q

Mx of hypocalcaemia

A

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

87
Q

Hypocalcameia clinical fx

A

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

88
Q

Hypokalamia with alkalosis causes

A

vomiting
thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)

89
Q

Hypokalaemia wirh acidosis causes

A

diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis

90
Q

Hypomagnesaemia causes

A

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

91
Q

Clinical fx of hypomagnesia

A

paraesthesia
tetany
seizures
arrhythmias
decreased PTH secretion → hypocalcaemia
ECG features similar to those of hypokalaemia
exacerbates digoxin toxicity

92
Q

Tx of hypomagneasamia

A

<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

93
Q

Low sodium blood, high urinary sodium causes

A

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

94
Q

Low serum and urine sodium causes

A

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

95
Q

Acute hyponatraemia wirh severe sx tx

A

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.

96
Q

Complication of tx of hyponatrameia

A

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

97
Q

What considered in ‘best interests’

A
  1. Whether the person is likely to regain capacity and can the decision wait.
  2. How to encourage and optimise the participation of the person in the decision.
  3. The past and present wishes, feelings, beliefs, values of the person and any other relevant factors
  4. Views of other relevant people
98
Q

LPA what

A

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)

99
Q

LPA what decisions make

A

life-sustaining treatment if the LPA specifies that

100
Q

Advance decision define

A

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

101
Q

1st line for osteoposis

A

Alendronate

102
Q

drugs to be aware of in older persons

A

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

103
Q

older age affects in terms of drug

A

creatinine clearance reduced
must be adjust for bmi

104
Q

prescription cascade

A

treat side effects from each new drug introduced rather than consider new sx is a side effect and change medication

105
Q

comprehensive geriatric assesment

A

see PP

106
Q

anticholinergic burden

A

risk of falls and cognitive impairment
dry mouth
blurred vision
contipation
urinary retention

107
Q

lots of meds

A

dosette box
blister pack
carousel tablet dispenser - audible reminder

108
Q

cant see med box

A

speaking labels or large print

109
Q

eye drops

A

opticare to assist

110
Q

dementia hx

A

progression of sx
home safety and accidents

111
Q

further ix for dementia

A

mention cognitive tests

112
Q

osteoporosis mx

A

alendronate
vid d and calcium - combo

113
Q

bppv dix hallpike positive findings

A

a positive test recreates the symptoms of benign paroxysmal positional vertigo
rotatory nystagmus

latency, torsional geotropic nystagmus, fatigue, habituation

114
Q

meniere’s patho

A

endolymph

115
Q

bppv patho

A

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.

116
Q
A

OPIC (2 decks)

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