geriatrics Flashcards

1
Q

changes in ADME in older people

A

drug stays in body longer so can be toxic (S/E) at lower doses

  • reduced first pass metabolism
  • reduced hepatic metabolism
  • reduced renal excretion
  • increased distribution of lipophilic drugs (due to increased body fat concentraion and decreased body water concentration) –> stays in body longer
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2
Q

propanolol in older people

A

first pass metabolism declines
so more in system/ toxic at lower doses

Fatigue
Hypotension
Dizziness

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3
Q

hepatic metabolism decreased by

A

HF
smoking
ageing

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4
Q

digoxin in older people

A

reduced renal excretion so more in system/toxic at lower doses

nausea and vomiting
abdominal pain
Arrhythmias
Yellow discoloration of vision
Hyperkalemia 
ECG reverse kick sign
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5
Q

lipophilic drugs in older people

A
  • increased distribution of lipophilic drugs
  • due to increased body fat concentraion and decreased body water concentration
  • diazepam
  • Chlordiazepoxide
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6
Q

diazepam in older people

A

Increased distribution of lipophilic drugs due to increased body fat concentraion and decreased

Drowsy
Confused

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7
Q

when cutting down polypharmacy, which are often booted out (8)

A
  • secondary prevention drugs (bisphosphonates, statins)
  • antihypertensives if patient experiencing postural hypotension
  • quinine (Prescribed for night leg cramps but doesn’t work)
  • Tricyclics, amitriptyline, anti-constipation (bad for cognition)
  • st johns wart
  • weak painkillers when on stronger ones
  • dual antiplatlet therapy if MI over 1y ago
  • high risk of toxic effects (diazepam, propanolol, warfarin, nitrates, digoxin,…)
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8
Q

define fragility fracture

A

fall from standing height or less that results in broken bone

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9
Q

things that improve orthogeriatric outcomes

A
Prompt orthogeriatric assessment -- 72h
Prompt surgery -- 36h
Pre-surgical cognitive testing
Prompt mobilisation after surgery -- day on / after surgery
Not delirious in post-surgery assessment
Returned to original residence by 120 days
Nutrition assessment
Fracture prevention assessment
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10
Q

frailty =

A

Related to age but not essential with ageing
Multiple body systems
Less ability to withstand an insult
- More at risk of adverse outcomes - hospital admission, reduced mobility, loss of independance, reduced ADL function, death

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11
Q

frailty prevention

A

Good nutrition
Physical activity
Avoid social isolation
Limited alcohol intake

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12
Q

frailty assessment

A

Clinical frailty scale (CFS) aka Rockwood

  • 1-9
  • quick and easy
  • not valid for measuring improvement after acute illness or if patient younger than 65
Fried criteria (phenotype)
3 or more of:
- Unintentional weight loss
- Self-reported exhaustion
- Weakness - grip strength
- Slow walking speed
- Low physical activity
2 = “pre-frail”

e-FI electronic frailty index
36 possible deficits
- Comorbidities - DM, HTN, Renal disease
- Polypharmacy / multimorbidity
- Sensory impairment
- Self-reported symptoms (Dizziness, Sleep disturbance)
- Social factors (Social isolation, Living alone)
presence/ absence of deficits as a proportion of the 36

Walking speed

Grip strength

Up and go time

  • Time to stand up walk 6m (or 3m, turn and back) and sit again
  • Should be 10s or less

PRISMA 7

  • 7 item questionnaire
  • 3 or more is :/

Groningen questionnaire

  • 15 items
  • 4 or more is :/
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13
Q

first line bisphosphonate

A

alendronic acid

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14
Q

difficulty with taking alendronic acid

alternative

A

need to take 1st thing in morning and remain upright for 30 mins
this is hard when cognitive impairment is involved

zolendronic acid IV - sometimes just one dose for a few months-years

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15
Q

end of life indicators

A
Weight loss
Recurrent unplanned admissions
Delirium
Frailty rising
Frailty plus dementia
Comorbidities 
Recurrent and persistent infections
Not responding to medication
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16
Q

when is there increased nutrition requirements

A

injury

sepsis

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17
Q

consequences of malnutrition

A
Weakened immune system
- Prone to infection
Muscle wasting
- Arms and legs especially visible
- Falls, mobility problems
- Increased chest infections
Impaired wound healing
- Longer hospital stay
Micronutrient deficiency
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18
Q

MUST tool =

A

malnutrition universal screening tool

  • BMI (weight, height)
  • weight loss
  • acute disease effect (Yes/no) = Patient nil by mouth or likely not to eat at all for 5 days or more (past or future)
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19
Q

malnutrition treatment

A
  1. food - snacks, nourishing drinks, food fortification
  2. oral nutrional supplements (ONS) - improve micro/macro intake: juice/ milkshake/ soup/ powder/ semisolid
  3. enteral feeding
  4. parentral feeding
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20
Q

enteral feeding types

A

straight into gut:

NG nasogastric tube
nasojejunal tube
PEG tube (percutaneous endoscopic gastrostomy )
PEJ percutaneous endoscopic jejunostomy

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21
Q

parental feeding =

A

fed via IV- PICC / central line

when gut is inaccessible or unable to absorb sufficiently

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22
Q

TPN =

A

TPN = total parenteral nutrition

IV feeding via central/PICC line

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23
Q

parental feeding pros and cons

A
Advantages
- Meet nutritional requirements
- Easily tolerated
Disadvantages
- More costly
- Risk of line infection
---- Unlikely but serious risk if occurs
- More invasive
- Gut atrophy - villi flatten 
---Reduced absorption when go back to gut feeding
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24
Q

indications for parental feeding

A
Inadequate absorption
-- Short - bowel syndrome 
-- Due to surgery
Gastrointestinal fistulae
Bowel obstruction
Prolonged bowel rest
-- Severe IBS sometimes want to rest the gut
 Severe malnutrition, significant weight loss and/or hypoproteinemia when enteral feeding isnt an option
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25
Q

enteral feeding pros and cons

A
Advantages
- Preserves gut mucosa and integrity
- Improves nutritional status
- Inexpensive (compared to parenteral nutrition)
Disadvantages
- Tolerance issues
--- Nausea
--- Satiety
--- Bowels
--- But may be something else so need to check first eg Medication esp if changed recently
- Discomfort of tube placement
- Quality of life, dignity, confidence (aesthetic displeasing appearance for patients)
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26
Q

NG tube

  • how is it inserted
  • check its position how
  • maximum duration of tube presence
A

inserted on ward - slide tube in with lube, swallowing helps

Check it is in the right place using aspirate pH (gold standard) – <5.5
X Ray confirmation is second line position check

<30days (consider PEG after)

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27
Q

nasojejunal feeding

  • how is it inserted
  • maximum duration of tube presence
A

Needs to X Ray guided, not on ward
Unable to use aspirate to check if it is in the right place

<60days

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28
Q

PEG tube indications

A
  • Consider if NG tube in for 30days
  • Dysphagia (stroke, head injury, neck surgery) Not improving
  • Cystic fibrosis – High nutritional requirements
  • Oral intake inadequate and this is likely to be the case long term
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29
Q

PEJ indications

A

Not tolerating PEG feeding
Delayed gastric emptying
Upper GI/ pancreatic surgery (bypass pancreas)
High risk of aspiration
Severe acute pancreatitis (bypass pancreas)

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30
Q

refeeding syndrome

  • what is this
  • risks
  • actions
A

When malnutrition/ starved patient when reintroducing nutrition - Due to energy stores shift from fat metabolism to carbohydrate metabolism. This promotes insulin secretion and therefore cellular uptake of potassium, phosphate and magnesium

  • electrolytes drop
  • Fluid retention
  • Cardiac arrhythmias
  • Respiratory insufficiency
  • Death (Rarely)
  • refeeding bloods monitoring to check for electrolytes
  • Slow introduction of nutrition - esp carbs
  • in high risk patients : IV (if unable to take tablets) pabrinex or thiamine + vitamin B co-strong PRIOR to feeding and 10 days into feeding
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31
Q

falls risk factors (12)

A
  • previous fall
  • fear of falling
  • balance problems (ataxia, vertigo, cerebellar stroke, inner ear infection)
  • gait problems (PD, OA)
  • pain
  • drugs
  • CVD (heart block, syncope (AF), stroke, antihypertensive medication)
  • cognitive impairment
  • urinary incontinence (catheter connections tripped over, urge - rushes , UTI - confusion)
  • stroke
  • DM (hyper, hypo, diabetic retinopathy- vision, diabetic neuropathy - sensation)
  • sensory impairment
32
Q

how can drugs increase risk of falls

A

antihypertensives (b blockers, diuretics) and tamsulosin (alpha blocker) - postural hypotension

amitriptyline and tricyclics - bad for cognition

benzodiazepines - confusion

33
Q

possible causes of falls

A
  • syncope
  • postural hypotension
  • delirium (can be caused by electrolyte imbalance)
  • hypo/hyperglycemia
  • reduced mobility, frail
  • medications
  • mechanical
  • sensory impairment eg glasses not currently being worn
  • UTI
  • osteoarthritis
34
Q

postural hypotension =

A

systolic drops 20, diastolic drops 10

35
Q

lifestyle changes for syncope/ postural hypotension

A

get up slowly
pedal feet before standing
compression stockings
recognise symptoms and sit down or whatever

36
Q

deconditioning

A

unable to do things previously done due to immobility

improved with rehab

37
Q

time up and go test should be less than how many seconds

A

10

38
Q

frailty measured by Phenotype (observable characteristics)– Fried criteria

  • what are the markers
  • how many for frail/prefrail
A

3 or more = frail:
2 = “pre-frail”

  • Unintentional weight loss
  • Self-reported exhaustion
  • Weakness - grip strength
  • Slow walking speed
  • Low physical activity
39
Q

Cumulative deficit
e-FI electronic frailty index

  • how many defecits possible
  • some examples
A
36
Comorbidities
- DM
- HTN
- Renal disease
Polypharmacy / multimorbidity
Sensory impairment 
Self-reported symptoms
- Dizziness 
- Sleep disturbance
Social factors
- Social isolation
- Living alone

presence/ absence of deficits as a proportion of the 36

40
Q

when is end of life care considered

A

definite or at risk of dying in next 12 months

41
Q

which is more common hyper or hypoactive delerium

A

hyper

42
Q

hyperactive delerium characteristics

A
Agitation
Delusions
Hallucinations
Wandering
Aggressions
43
Q

delerium definition

A

an acute confusional state that fluctuates in severity and is usually reversible. It is usually the result of another organic process

44
Q

confusion = ??? until proven otherwise

A

delerium

45
Q

hyperactive delerium management

A

Non pharmacological first line

  • Calm and defuse, cup of tea
  • Orientation
  • Reassurance
  • Continuity of staff and environment
  • Quiet environment
  • Provide hearing aids / glasses (if they have impairment)
  • Potential for 1:1 supervision
  • Family members come and help settle them down
  • Check obs and reexamined
  • Review of drugs
  • Control pain
  • Avoid catheters and drips unless necessary

Pharmacological

  • Sedation
    • If risk to patient or other people
    • Use lowest dose possible
    • haloperidol best
    • (lorazepam included in geriatrics, but advised to avoid in psych as can increase confusion and sedation)
46
Q

delerium investigations

A

check obs and reexamined
review of drugs
Order confusion bloods (set of bloods that look for common reversible causes of delirium: B12 deficiency, folate deficiency, hypercalcaemia, ferritin, TSH etc)

47
Q

hypoactive delerium characteristics

A
Easier to miss
May be mistaken for depression
Lethargy
Slowness with tasks
Excessive sleeping
Inattention
Confused, unable to follow conversation
Less willing to engage
48
Q

delerium risk factors

A
Old age
Dementia
Past hospital admission, 
past delirium 
Significant comorbidities
Sensory impairment
Change of environment
Polypharmacy
Sleep deprivation
Pain 

lower threshold for delerium

49
Q

delerium causes

A
Infections (eg pneumonia)
Drugs
- Staring, stopping
Metabolic (Eg constipation)
Neurological (eg SAH)
50
Q

delerium precipitating factors

A
Change of environments
Sleep deprivation
Pain
Attachments - drips, catheters
Lack of mobilising
51
Q

dementia definition and charachteristics

A

a syndrome of acquired, chronic, global impairment of higher brain function, in an alert patient, which interferes with the ability to cope with daily living.

decline in memory and at least 1 funtion:

  • Skilled movements
  • Language
  • Executive function
  • – Working memory
  • – Monitoring and regulating behaviours, actions, alertness and emotions
  • – Cognitive flexibility
  • – Attention
  • – Organizing
  • – Sustained effort
  • Impair social or occupational functioning

progressive

52
Q

dementia assessment

A

MOCA screens then assessed by a doctor

53
Q

BPSD=

A

BPSD = behavioural and psychological symptoms of dementia. This is a heterogenous group of non-cognitive symptoms and behaviours

Agitation
Irritability
Depression, apathy
Disinhibition- sexual, social
Hallucinations, delusions
Aggression
Anxiety

occur in most dementia patients

(treatment? = pain relief and non-pharmalogical intervantions 1st line)

54
Q

alzheimers symptoms

A
Memory and language affected first
- Short term memory
- Disorientation
Then personality changes
Visual spatial disorientation
Dysphasia
Dyscalculia 
Dyspraxia 
- Motor problems 
Lack of physical motor signs
- Few UMN signs initially
- End stage - rigidity / spasticity , And myoclonus and visual hallucinations, language
55
Q

where in brain most affected in alzheimers

A

Posterior cortical affected most

Atrophy

56
Q

vascular dementia symptoms

A

stepwise presentation- sudden/ abrupt presentation
Mental slowing
Poor attention and retrieval
Reduced mental manipulation
Mood disturbance
Apathy
Physical signs - apraxic gait, urinary incontience, pyramidal signs
Lack of cortical signs (if pure)
Good on multiple choice prompt for memory withdrawal

57
Q

vascular dementia risk factors

A

alcohol

smoking

58
Q

lewy body dementia pathophysiology as in where

A

cortical

59
Q

vascular dementia pathophysiology inc as in where

A

subcortical

multi-infarct
cerebreal small vessel disease
post stroke/ tia - usually within 3m

60
Q

lewy body dementia symptoms

A
Visual hallucinations 
- Earlier than in alzheimers
delusions 
Parkinsonism (usually before PD)
Cognition may be fluctuating even though it is progressive
Perceptual-spatial deficits
Myoclonus
- Earlier than in alzheimers
transient loss of concsiousness
61
Q

frontotemporal dementia pathophysiology as in where

A

fronto cortical

frontal and temporal neocortical

62
Q

semantic dementia

A

type of frontotemporal dementia

Fluent speech but lose picture meaning

63
Q

Primary progressive aphasia dementia

A

type of frontotemporal dementia

non-fluent aphasia

64
Q

frontotemporal symptoms

A

Change in behaviour - social breakdown
- Withdrawal and lost interest in hobbies
- Disinhibition
— Eg urinating in living room, naked
— Unhygienic
- Altered eating patterns
—- Eg Now like sweet food more
- Behaviour stereotypes - repeated behaviours
—- eg singing a certain melody
—- Eg want to take certain chains of buses regularly (But able to pay and plan and get on bus etc)
- Apathetic
- Frontal cognitive function - in executive function = dysexecutive syndrome (if tested)
No motor signs initially (some none)
Long disease course

65
Q

pseudodementia

  • what is affected
  • what is the cause
A

Memory loss, attention impairment - so harder to retain

Often secondary to mental health
- Most commonly depression

66
Q

Paraphasic errors

A

mispronounce words

67
Q

primitive reflexes (dementia)

A

Pout reflex
– After stroking upper lip / tapping lips
Palmomental reflex
– Scratch palm, chin crinkles

68
Q

dementia treatment

- including egs and s/e and when to use what

A

Acetylcholinesterase inhibitors (for mild/moderate)

  • Rivastigmine
  • Donepazil
  • Galantamine
  • S/E - bradycardia, diarrhea, vomiting, headache

NMDA (N-methyl-D-aspartate) antagonist (if above is contraindicated/ SEs)

  • Memantine
  • alzheimers or agressive
  • If severe impairment of AChE i not working (can be switched or can be used together)
  • S/E - dizzy, confusion, hallucinations, seizure

cognitive social and physical stimulation

  • Cognitive reorientation
  • – Life stories and reminiscence work (Talk about memories, create photo album, listen to old music etc)
  • Reassure
  • Psychoeducation
  • Cognitive stimulation therapy
  • – Group activities
  • –Exercise
  • –Socialising
  • –Improves memory, language, problem solving skills - benefits mild and moderate dementia
  • Cognitive rehabilitation
  • —Learn a skill eg mobile phone
69
Q

which dementia is most common

A

alzheimers

70
Q

“normal” score on adenbrookes cognitive exam (ACE).

why is normal in “””””

A

Scores out of 100. “Normal” - 82-88. (one specific one sensitive)

Normal doesn’t exclude dementia (premorbid IQ (judged by profession- so high IQ person getting 85 may be bad whereas may be normal for someone else)

71
Q

adenbrooks domains and what is affected in dementia

A
Attention
Memory
Fluency 
Language
Visuospatial 

Dementia - 2 or more demain deficits normally

72
Q

mild cognitive impairment

  • charachterisitcs
  • diagnosis
A

Cognitive impairment with no functional impairment

Diagnosis from cognitive testing (like dementia)

73
Q

additional treatment for vascular dementia

A

vascular risk factors - prevent on stroke

74
Q

dementia vs delerium

A
  • dementia : progressive, slow long onset, delerium: acute, sudden, short lasting
  • delerium: variation in intensity - worse in evenings
  • delerium: attention affected, dementia : memory
  • delerium: often reversible, dementia: irreversible mainly
  • hallucinations (Esp visual and tactile) are more common in delerium than dementia (although lewy body experiences these)
75
Q

“worried well” = ?

A

memory loss without pathology, due to stress

76
Q

amnesia

A

Attention good

Prompting memory recall does not help poor memory