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Delta Med - Geriatrics > Delta Med - Geriatrics > Flashcards

Delta Med - Geriatrics Flashcards

1
Q

What are changes in the structure of the urinary tract with ageing?

A 
Decreased renal mass, cortex > medullla
decrease in # glomeruli prop to mass
glomeruli increasingly sclerosed
intrarenal vascular changes seen in all - larger vessels
decrease in bladder size
increase in detrusor activity
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2
Q

What are changes in renal physiology with ageing?

A

decreased renal blood flow 10% per decade
GFR decreases 8mls/min/decade
reduction in maximum and minimum urine osmolality
reduction in sodium conservation (prone to hypovolemia with volume depletion)

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3
Q

What are changes in the lower urinary tract with ageing?

A

variable reduction in bladder capacity and contractility
increased detrusor hyperactivity (URGE incontinence most common in elderly)
decreased urethral ouflow resistance in women, increased in men
increased nocturnal polyuria (reduced nocturnal ADH - drugs CCF, decreased bladder capacity also contribute

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4
Q

What are adrenal changes with ageing?

A

basal renin decreased by 30-50% (normal substrate)
reduction in aldosterone (reduced clearance also) - ratio remains constant
decreased aldosterone increases risk of hyperkalaemia
stimulus response preserved, magnitude decreased

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5
Q

What are liver changes with ageing?

A

37% reduction in volume, 50% reduction in wt, 35% reduction in renal blood flow (10% reduction per unit volume) - interferes with drug clearance

Functional changes are minimal - no significant change in LFTs, albumin does not decline in well elderly

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6
Q

What are cardiac changes in the elderly?

A

cardiac output at rest largely unchanged
decreased maximal heart rate (MHR = 220-age)
myocardial atrophy, increased LV wall thickness and L atrial size occurs with age
alterations in elastin/collagen and calcium deposition result in decreased arterial compliance and valve motility
reduced HR response to stress and respiration

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7
Q

What are age related changes in lung physiology?

A

20% reduction in size, secondary to elastic recoil loss
larger terminal air spaces and thinner alveolar walls
20% reduction in surface area
FEV1 and FVC fall (FEV1 faster as you age)
residual volume increased as terminal bronchioles close in dependent parts of lung w tidal breathing
V/Q mistmatching increases with increased dead space
vent resp to low PaO2 and inc PaCO2 blunted
diminished mucocilliary clearance

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8
Q

What are changes in the humoral immune system with ageing?

A

total Ig remains same, increase IgG, IgA
diminished antibody response (increased risk of autoantibodies)
monoclonal immunoglobulins increase >70y

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9
Q

What are changes in cell mediated immunity with age?

A

thymus involutes (

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10
Q

What are changes in the endocrine system with ageing?

A

increased insulin in response to insulin resistance
increase rate of AI thyroiditis
increased PTH with consequence increase in bone resorption
increased vasopressin and hence hyponatraemia risk, ANP rises in response to IV volume, leading to nocturia
rise in FSH/LH
uterine and vulval atrophy
decreased peroxide sec by lactobaciili - UTIs
decline in male testosterone - decreasing male sexual drive and effect on muscle mass
reduced GH

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11
Q

What are pharmacokinetic changes with ageing?

A

absorption is essentially unaltered - despite reduced H+
reduced 1st pass metabolism
reduction in lean body mass with increased fat = increased Vd for lipid soluble drugs = increased t1/2
water soluble drugs have a reduced Vd and higher concentration
reduced protein binding in unwell elderly can possibly increase free drug (e.g. warfarin)

reduced hepatic clearance (10% blood flow per unit volume) - minor decrease in metabolism

renal excretion reduced in parallel with GFR and tubular secretion (MTX, cyclophosphamide, platins, digoxin, gentamicin, penicillins, trimethoprim, doxy, Li, atenolol, sotalol)

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12
Q

What are features of delirium?

A

attention deficit
changes in alertness
diffuse cognitive changes
acute, fluctuating course
psychotic features
language disturbance
disrupted sleep-wake cycle
alterations in psychomotor behaviour (hyper/hypo-alert forms)
single/multifactorial precipitant
duration may be longer than initial insult
hypoalert often missed - poorer prognosis, less likely to fully recover
no relationship between form at aetiology
recover is often incomplete (4% resolved at D/C, 31% still present at 6/12)

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13
Q

In what situations is prevalence of delirium highest?

A

up to 80% inpatients medical
up to 83% ICU inpatients
Up to 70% RACP

Incidence same in medical and surgical inpatients

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14
Q

What are features of the CAM?

A

1) evidence of acute change, fluctuation
2) inattention
3) disorganised thinking
4) altered level of consciousness

1+2 and either 3 or 4 = diagnosis

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15
Q

What are epidemiological features of delirium?

A

30% have partial syndrome
1/3-2/3 missed by treating physician
incidence increasing with aged population
increased post dischage costs
2 x risk of hospital acquired complications
3-7x risk of admission to RACF
2.2 x increased LoS

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16
Q

what is the mortality of delirium?

A

15-30%
predicted by severity of medical illness - 12 month mortality 35-40%
5 year mortality 50%
patients with partial syndromes still at risk
5 year mortality 50%

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17
Q

What are features of the pathophysiology of delirum?

A 
reduced reserve
28% reduction in cerebral blood flow
neruonal loss (neocortex, hippocamp, Subst nig)
reduced GABA, serotonin, ACh
inflammatory CKs implicated
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18
Q

What premorbid RFs for delirium?

A 
Cognitive impairment RR 2.8 - 7.3
visual impairment RR 3.5
severe illness RR = 3.5
dehydration RR = 2.0
hearing impairment
psychoactive drug use
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19
Q

What are in-hospital risk factors for delirium?

A 
use of restrains RR = 4.4
malnutrition RR = 4.0
addition of >3 medications in 24 hrs RR = 2.9
IDC insertion RR = 2.4
iatrogenic event (any) = 1.9
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20
Q

What are first line Ix in delirium?

A

FBE, UEC, LFTs, Ca, troponin, CRP, TFT
MSU, other cultures
CXR
check drug chart repeatedly

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21
Q

What are 2nd line therapy in delirium?

A

CTB, EEG, LP

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22
Q

What are general management principles in delirium Mx?

A 
Manage underlying cause
provide familiarity
optimise sensory input
avoid complications - dehydration, malnutrition, pressure areas, constipation
no good evidence for efficacy
NO role for restraints
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23
Q

What are pharmacological measures in Delirium?

A

can give haloperidol PO at low doses (0.25-0.5mg) - titrate (1 RCT)
some small trial ssupport risperidone, olanzepine
BDZ may worsen prognosis, only use in withdrawal

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24
Q

What non-pharma interventions reduce rates of delirum?

A

multicomponent intervention targeting risk factors reduces rates of delirium

early geriatrics consultation reduces delirium in surgical inpatients (32 vs 50%)

no pharmacological interventions prevent delirium

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25
Q

What is the prevalence of dementia?

A

rate doubles every 5.1 years

1.2% in 65-74, 25%>85, 47% 90s

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26
Q

What is the Dx criteria for major neurocognitive disorder?

A

A) Evidence of significant cognitive decline in cog domains
B) interference in IADLs
C) not in context of delirium
D) not better explained by other disorder

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27
Q

What are features of the MMSE test?

A

not effective for frontal/executive fucntion

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28
Q

What are Dx features of probable AD?

A

insidious, gradual progression
cognitive loss documented by neuropsychological tests (rapid forgetting) + other cortex problem (praxis, speech, executive, visuospatial)
no physical signs/lab evidence of other causes of dementia

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29
Q

What are risk factors for Dementia?

A 
AGE (strongest)
family
female
head injury
MCI
vascular disease
decrease folate, b12
apolipoprotein E e4 allele
Downs syndrome
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30
Q

What are current preventative factors in AD?

A

only with increasing evidence is physical activity in preventing cognitive and ADL impairment

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31
Q

What are features of Autosomal Dominant AD?

A

early onset

32
Q

What are features of apolipoprotein in dementia?

A

E4 stron risk factor
50% homozygous E4 cog intact at 80
>50% late sporadic AD have E4
20% have at least one E4 mutation

33
Q

What is the definition of vascular dementia?

A

cognitive loss
cerebrovascular lesions on imaging (focal neurological signs which correlate to lesions)
onset of dementia within 3m of a symptomatic stroke
link between stroke and cognitive change

34
Q

What are clinical features of vascular dementia?

A

early attention, executive function and self monitoring change
memory often mildly affected
early gait disturbance
lesions on neuroimaging do not exclude AD
MMSE = poor screening tool

35
Q

What are features of LBD?

A

usually AD pathology
criteria have high Sp but low Sn
rapid onset with progressive decline (1-4yrs vs 5-9yrs)
AChEI may be more effective (catastrophic withdrawal)
neuroleptics should be avoided - quetiapine if needed

36
Q

What are the Dx criteria for DLB?

A

progressive cognitive impairment
- impaired memory, deficits in attention, exec function, visuospatial ability
core features (2 = probable, 1 = possible)
- fluctuating cognition, attention, alertness
- recurrent visual hallucinations (typically people in room)
- spontaneous motor parkinsonism

37
Q

What are supporting features of DLB?

A 
recurrent falls
syncope
transient LoC
neuroleptic sensitivity
systematised delusions
sleep disturbance (REM sleep disorder)
depression

PET can be useful to differentiate
over lap clinically with PDD

38
Q

What are features of FTD?

A 
diverse group
 - behavioural
 - semantic dementia (fluent)
 - primary progressive aphasia (non-fluent)
 - motor subtypes (MND, PSP, CBD)
6th, 7th decased
1/2 have FHx
assoc with MND, chromosome 17 (FTDP-17)
TPD-43 also found
39
Q

What are general clinical features in FTD?

A

personality and social conduct impaired
disinhibition, apathy, perseveration, sterotypy, hyperorality
impairment of drive, motivation, attention and planning
memory often relatively preserved
DDx is frontal variant AD

40
Q

What are pathology features of dementia subtypes?

A

AD - plaques (amyloid), tangles (tau), lewy bodies (alpha synuclien)
PD/DLB - lewy bodies and AD pathology
FTD - 50% tau, 50% TDP 43
VaD - ischaemic changes +/- amyloid

41
Q

What are appropriate first line Ix in dementia w/u?

A

FBC, UEC, TSH, Ca, B12, glucose, syphilis serology
CT/MRI - useful in detecting causes and other path
PET increasing used to RULE IN AD
ApoE4 not recommended
CSF biomarkers research only (AB42 decreased, p-tau increased)
neuropsychology assessment

42
Q

What are imaging findings in AD?

A

generalised atrophy, hippocampal volume decreased on MRI
FDG-PET -hypometabolism of precuneus, and lat parietotemoral cortex
PIB scan (amyloid)

43
Q

What are imaging findings in DLB?

A 
generalised atrophy (not sensitive) on cortex MRI
FDG-PET - hypometabolism, occipial cortex, dopamine transporter scan
44
Q

What are imaging findings in FTLD?

A

regional trophy on MRI

hypometabolism frontal/temporal areas

45
Q

What is the principle of cholinergic medications in AD?

A

atrophy of nucleus basalis leads to deficiency in acetyl choline tranferase, with reduced synthesis of ACh
impaired cholinergic transmission with intact cholineric receptors

46
Q

What are examples of cholinesterase inhibitors?

A

Donepezil
rivastigmine
galantamine

47
Q

What are SEs of cholinesterase inhibitors?

A 
increased GIT motility - nausea, diarrhoea, anorexia
sleep disturbance and vivid dream
sagitations and derlirium
vagotonic bradycardia
risk of asthma exacerbation
1/12 have serious AEs
48
Q

What are the results of cholinesterase inhibitors in AD?

A

modest mean bnefits, 10-33% will have discernable benefit
no way of predicting benefit
failure to decline - response
peak efficacy at 3 months
max difference between drug and placebo at 6 months
cognitive decline continues later in treated patients >1year
all equal in effectiveness
improvement in ADL retention at 1 year

49
Q

What is the role of cholinesterase inhibitors in other dementia subtypes?

A 
VaD - unclear - modest benefit
MCI - not genrally recommended, ? increased vasc deaths
DLB - good quality data lacking
PDD - modest ben in rivastigmine
FTD - no role
50
Q

What is the role of memantine in AD?

A

neuroprotective NDMA antagonist (blocks glutamate mediated cytotoxicity)
may be used with cholinesterase inhibitors
well tolerated
rare lazarus effects
studies in mod-severe AD and Vascular Dementia

51
Q

What are non-pharmacological measures in dementia?

A

care giver training leads to sustained benefit OR of staying at home 5
cognitive training also useful

52
Q

What are Mx options for behavioural disturbance?

A

risperidone in NH patients (0.5-2mg)

olanzapine also has evidence

53
Q

What are features of MCI?

A

condition intermediary between normal cog and dementia
normal function with subjective or objective memory impairment
0-34% annual conversion rates
some rremain stable, and others revert to non-MCI
no intervention works other than exercise
PET shows extensive amyloid in those who subsequently convert to AD

54
Q

What are predictors of progression in MCI?

A 
increasing Age
strong FHx of AD
typical AD findings on imaging
CSF biomarkers
amnestic findings on neuropsych testing (rapid forgetting)
55
Q

What are epidemiological features of falls?

A 
35-40% of comm dwellers have falls >65yo
6-40% cause fractures or serious injury
fear of falling greatest fear in elderly
8% of total direct healthcare cost in australia
decline in ADLS and social function
56
Q

What are features of fall in RACF?

A 
30-50% fall per year
10x higher risk of hip fracture
RFs:
previous falls
cognitive impairment
lower limb neuro impairment/gait abn
gait aid
>4 medications
very poor vision/poor contrast sensitivity
57
Q

What are causes of syncope/falls?

A 
neurocardiovascular:
- carotid sinus hypersensitivity
- vasovagal
- orthostatic hypotension
arrhythmias
- SSS
- AV block
- brady-tachyarrhythmias
58
Q

What risk factors for falls have the strongest evidence?

A

History of falls
Advancing age
ADL limitations

then female, living alone, inactivity

NO evidence for alcohol

59
Q

What balance and mobility factors have the strongest evidence for falls?

A

impaired gait/mobility
impaired STS
impaired transfers

then impaired stability in standing/leaning stab, slow voluntery stepping and least indaequate resp to ext pertumbation

60
Q

What sensory/neuromuscular features have the strongest evidence for falls?

A

visual contrast sensitivity
reduced peripheral sensation
muscle weakness
poor reaction time

then visual field dependence, VA
no evidence for vestibular function

61
Q

What medical risk factors have the strongest evidence for falls?

A

impaired congition
stroke
parkinson’s disease

then depression, neuro signs, incontinence, acute illness, arthritis, foot problems, lowest dizziness

no evidence for vestibular dz or orthostatic hypotension

62
Q

What medication factors have the strongest association with falls?

A

psychotropic medication use
>4 medications

then antihypertenstive use
no evidence for NSAIDs

63
Q

What environmental factors have evidence for contribution to falls?

A

poor footwear

inappropriate spectacles

64
Q

What interventions have evidence in reducing the risk of falls in community and RACF patients?

A

MDT - education, PT, OT
medication review - incl psychoactives
Vit D at daily doses
exercise - balance component important (tai chi)

65
Q

What interventions have evidence in reducing falls in community dwellers?

A

footwear/podiatry
cataract repair
need to fall 300 times/year to prevent 1 serious bleed on warfarin

66
Q

What interventions have evidence in reducing falls in NH residents?

A

alarm mats
scheduled toileting
?hip protectors

67
Q

What are risk factors for hip fracture?

A 
Age, female
Hx of falls (esp prev adult #)
cognitive impairment
poor functional status
psychoactive drug use (sedatives/hypnotics, TCA, anticonvulants, l-dopa)
visual impairment
osteopenia/osteoporosis
68
Q

What is the outcome of hip fracture?

A

15-30% operative mortality at 1 year
risk doubled if op delayed 2 days
>20% never get home
use of op therapies not universal on DC

69
Q

What types of incontinence?

A 
urge - common to have detrusor overactivity (most common)
stress - esp in owmen
mixed urge-stress (common)
overflow
functional
faecal
70
Q

What medications impair CNS control of voiding?

A

sedatives, hypnotics, antipsychotics, antidepressants, antiemetics, analgesics, alcohol

can only cause incontinence in patients already susceptible

71
Q

What medications impair bladder function?

A

anticholinergics - reduced flow rate and increased residual
cholinergics - may precipitate or worsen urge symptoms or incontinence
bladder irritants - cyclophosphamide, BCG, raditaion, caffeine

72
Q

What are features of outflow resistance in incontinence?

A

decreased outflow resistance - alpha adrenergic blockers (Smooth muscle) - prazosin, labetalol
drugs which induce striated muscle contraction - baclofen BDZ

increased outflow resistance - TCAs, occ iproduce retention, alpha agonists (pseudoephedrine)

73
Q

What are other drugs which worsen continence?

A
  • constipators - anticholinergics (red peristalsis), ca antagonists (smooth muscle), diuretics (dehydration)
  • drugs that promote diuresis - diuretics, lithium
74
Q

What are non-pharmacological methods of treating incontinence?

A

pelvic muscle exercises for geniuine stress incont (1st line, always)
bladder retraining
timing of oral fluids, reduce caffeine, rationalise meds
treat constipation
weight loss in obese

75
Q

What are drug treatment options in incontinence?

A

urge incontinence in cognitively intact - antimuscarinic agent - oxybutynin, solifenacin, tolteridone, darifenacin (can have peripheral anticholinergic effects, delirium)

Stress incontinence - topical oestrogens, not HRT
little evidence for duloxetine

surgery is last line!

76
Q

What are interventions in polypharmacy?

A

Medication reviews - reduce inappropriate medications, changes sustained at 12 months, required fewer medical interventions, patients percieved outcomes unchanged.

Delta Med - Geriatrics (1 decks)

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