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3a > Geriatrics > Flashcards

Geriatrics Flashcards

1
Q

What is dementia ?

A

disorders characterised by loss of memory + other cognitive abilities affecting IADLs + ADLs
- group of disease (like cancer)

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2
Q

what acronym can be sued for overall presentation of dementias ?

A

DIRE
- Decline in cognition (language, attention)
- Impairment (not keeping up with IADL + ADLs)
- Rule out delirium (acute state of confusion)
- Exclude mental disorders (depression, schizophrenia)

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3
Q

what are IADLS ? acronym

A

SHAFT
- Shopping
- Houskeeping
- Accounting
- Food prep
- Transportation

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4
Q

what are ADLs ? acronym >

A

DEATH
- Dressing
- Eating
- AMbulating
- Toilet
- Hygiene

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5
Q

what are the different types of dementia ? (5) most common ?

A
  • Alzheimers disease (most common)
  • Vascular
  • Lewy body
  • Frontotemporal
  • Mixed (multiple types)
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6
Q

Describe the presenfiaotn of Alzheimers disease ? onset ? symptoms ?

A

gradual onset
- amnesia + neurocognitive deficits (amnesia, aphasia, apraxia, agnosia)
- Psychiatric symptoms: mood changes (depressed, anxious, irritability), psychotic symptoms (delusional misidentification
- activity; sundown activity
- lack of insight (don’t usually have knowledge of illness)

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7
Q

Alzheimers disease pathophysiology ?

A

caused by plaques made of beta amyloids
- tends to misgold => becomes sticky => clumping => large insoluble fibril s=> plaques => weaken communication + plasticity at synapses => neurodegeneration + neural death

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8
Q

How Is Alzheimers investigation ? diagnosed ?

A
  • diagnosis made clinically
  • bedside cognitive test
  • FBC (rule out delirium)
  • CSF testing (amyloid + tau biomarkers)
  • Structural MRI (atrophy => shrinkage)
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9
Q

what found in css in alzeihmers disease ?

A

amyloid plaques + neurofibirially tau tangles

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10
Q

alzheimers epi ?

A

less than 1%
(20% >80, 50% >90)
F>M

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11
Q

Alzheimers disease management ?

A

can’t halt or reverse progression (so symptom reduction and slow progression)
- cholinesterase inhibitors (=> increase Ach in brain)
- Antidepressants and antipsychotics

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12
Q

What is vascular dementia ? pathophys

A

infarction, haemorrhage + small vessel changes cause damage to white + grey matter (loss of brain parenchyma)
- multiple infarcts exhaust the brains compensatory mechanisms

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13
Q

vascular dementia présentation ?

A

due to the vascular pathology, doesn’t present with specific sign or symptoms but series of stepwise decreases in cognition

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14
Q

what will be seen on imaging in vascular dementia ?

A

imagine of brain will show multiple areas of ischaemic damage to varying ages

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15
Q

vascular dementia mangment ? (2)

A
  • Cholinesterase inhibitors
  • Reduce stroke RF: atiplatelt therapy, BP control, statins, control DM
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16
Q

what causes dementia with leeway bodies ?

A

accumulation of leeway bodies in CNS: protein alpha-synuclein accumulations that affects synaptic communication + plasciticy

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17
Q

dementia will Lewy bodies presentation ? age of onset ?

A

earlier onset (staring around 50) + worse decline than Alzheimers
- visual hallucinations (distinctive features - visual Hal-lewy-cinations, often have insight that not real)
- cognitive defects (memory not affected as much, more attention + concentration)
- neuroleptic sensitivity
- sleep
- Parkinsonism

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18
Q

describe how sleep is affected in dementia with Lewy bodies ?

A

REM sleep behaviour disorder => thrashing + flailing while asleep
(often one of the first signs)

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19
Q

why should you be careful prescribing antipsychotics to a px with Lewy body dementia ?

A

greater risk of neuroleptic malignant syndrome
- don’t give em (easily mistaken with psychosis)
- AP => extrapyramidal SE, confusion, catatonia, neuroleptic malignant syndrome)

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20
Q

Lewy body dementia epi ?prognosis ?

A

M=F
4 yrs life expectancy form diagnosis (alzheiemrs is 5-10)

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21
Q

Lewy body dementia management ? avoid what ?

A
  • cholonetsrase inhibitors
  • antiparkinsonsims (levodopa)
  • Avoid AP
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22
Q

what is frontotemporal dementia ? (2)

A

degeneration of the frontal + temporal lobes of brain => decline in cognition + inappropriate/impulseive behaviour

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23
Q

fronttemporal dementia pathophysiology ?

A

caused by focal neurodegeneration of the frontal or temporal lobes of the brain
- neuronal loss, gloss, microvascular changes

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24
Q

frontotemporal dementia presentation ?

A
  • obliviousness (saying hurtful things, not respecting pals personal space)
  • hyperorality (even inedible objects)
  • disinihibition (hypersexual)
  • apathy (indifference to self care)
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25
Q

frontotemporal dementia epi ?

A

quite rare
- earlier onset (45-65)
- M=F
- Familial link ?

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26
Q

frontotempora dementia mangmet ?

A

behavioural interventions, social wokr
- SSRIs

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27
Q

What is delirium ?

A

fast developing type of confusion that affects ability to focus of attention

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28
Q

What are the consequences of delirium (3) ?

A
  • Can increase mortality
  • Can increase number of patient that end up in care home
  • increase length of hospital stay and risk of acquired infections
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29
Q

What is delirium generally caused by ?

A

results form underlying organic illness

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30
Q

What is the triad of delirium ?

A
  • Acute confusion
  • Disturbed consciousness
  • Altered behaviour (hyper/hypoactivity)
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31
Q

Causes of delirium ? pneumonic

A

DELIRIUM
- Drugs (poly pharmacy, withdrawal from drugs)
- Eyes or ears (sensory defects - hearing aid, glasses)
- Low oxygen (MI, Stroke, PE)
- Infection: most common is chest or urinary infection
- Retention: urianry retention or constipation
- Ictal states
- Undernutrition: not eating or drinking properly
- Metabolic causes: diabetes, post op state

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32
Q

How common is delirium on post op ward ?

A

10-15% develop delirium

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33
Q

In what groups of people is delirium most common (4) ?

A
  • ICU
  • stroke
  • hip fracture
  • terminal illness
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34
Q

What investigations might you do for delirium ?

A

try to investigate for the cause
- Bloods: FBC (inflam marksers, U+E (metabolic problems), CROP, Calcium, glucose
- TFT
- Urinalysis
- Blood culture
- Sputum culture

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35
Q

Delirium Mx ?

A
  • Recognise and investigate cuases
  • Orientate the patient: hearing aids/glasses on, clock + calendar visible, display familiar personal items, encourage visits form family, consistent staffing
  • Medication review
  • If severe: medical sedation
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36
Q

name some potentially treatable causes of cognitive impairment ? (6)

A
  • Depression
  • Delirium
  • Vitmin deficiecny
  • Stroke
  • Tumour
  • Intoxication
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37
Q

What is BPPV ? what Stan for ?

A

Peign paroxysmal positional vertigo
- common cause of recurrent eps of vertigo, triggered by head movement
- common in older adults

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38
Q

is BPPV peripheral or central cause of vertigo ?

A

peripheral cause of vertigo

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39
Q

BPPV presentation ? triggered by ?

A

20-60s eps => asymptomatic inbetween
- triggered by turning head (running in bed)
- no hearing loss or tints

40
Q

BPPV pahtophsyiolgy ?

A

calcium carbonate crystals (otoconia) become displaced in to the semicircular canals => disrupt endolymph flow => confuse vestibular system

41
Q

what could displace otoconia in BPPV ? (aetiology)

A

displaced due to viral infection, head trauma, aging
(BPPV)

42
Q

how is BPPH diagnosed ?

A

(Dix => Dx)
- Dix Hallpike manœuvre

43
Q

what is dix hall pike manoeuvre for ? what does it aim to do ?

A

do diagnose BPPV
- move patients head to move endolymph through semi circular canal => trigger vertigo

44
Q

How is BPPH treated ?

A

reply manoeuvre

45
Q

what is employ manoeuvre for ? what does it aim to do ?

A

move crystals in semicircular canal to position that doesn’t disrupt endolymph

46
Q

Nam some RF for falls ? (7)

A
  • fear of falling
  • vision changes (changing glasses)
  • medications (which act on CNS)
  • under/malnourishment: contributes to frailty + loss of muscle mass + strength)
  • Diabetes: peripheral neuropathy
  • Dementia: cognitive impairment
  • Incontinence: rushed movement to bathroom
47
Q

Name some RF for poor bone health ? (6)

A
  • Low dietary calcium => low BMD + early bone loss
  • Physical inactivity
  • Tobacco + alcohol use
  • Sex: female
  • Hormones: high thyroid hormone, menopause (low oestrogen)
  • Medications: steroids, SSRIs, PPIs
48
Q

what is chronic Heart Failure ? specifically affects which bit fo the heart ?

A

clinical features of impaired heart function specifically function of LV

49
Q

describe the pathophys of chronic HF and what this leads to ?

A

chronic back flow of blood to LA, pul veins, lungs => increase vol and pressure of blood => start to leak fluid => pulmonary oedema

50
Q

what is normal ejection fraction ?

A

normal >50 %

51
Q

what is heart failure with presence EF ?

A

clinical HF features with EF > 50% due to diastolic dysfunction

52
Q

causes of chronic heart failure ?

A
  • IHD
  • vascular heart disease (aortic stenosis)
  • hypertension
  • arrthymias (AF)
  • cardiomyopathy
53
Q

HF presentation ?

A
  • breathlessness 9worse on exertion)
  • cough (frothy white/pink sputum)
  • orthopnea
  • paroxysmal nocturnal dyspnoea
  • oedema
  • fatigue
54
Q

what is paroxysmal nocturnal dyspnoea ? associated with what ? pathophsycioloyg (3)

A

waking up in the night with sever attack of Sob, cough + wheeze (associated with HF)
- life flat => fluid settles
- resp centre less responsive during sleep (reduced RR despite hypoxia)
- low Ad during sleep so myocardium more relaxed

55
Q

signs of HF ?

A
  • tachycardia
  • tachypnoea
  • hypertension
  • murmur (valvular heart disease)
  • bilateral basal crackers
  • raised JVP
  • peripheral oedeem
56
Q

what do bilateral basal crackles in person with HF indicate ?

A

pros pulmonary oedema

57
Q

what investigations for HF ? (4)

A
  • clinical assessment
  • NT-proBNP
  • ECG
  • Echo
58
Q

HF mangement ? overall Mx ?

A
  • refer to cardiology
  • medical
  • procedural
59
Q

what determines how quick the referral to cardiology must be for patient presenting with HF ?

A

depend on the NT-proBNP result
- 400-2000: within 6 weeks
- >2000: within 2 weeks

60
Q

Medical management of HF ? (4)

A

ABAL
- ACEI
- BB
- Aldosterone antoagnosit
- Loop dieretic

61
Q

What changes would be seen on XR in HF ?

A

ABCDE
- Alveolar oedema (bat wing opacification)
- Kerley B lines (interstitial oedema)
- Cardiomegaley
- Dilated upper lobe vessels
- Effusions (with blunted costophrenic angles)

62
Q

Where and when is BNP produced ?

A

hormone produced mainly by the left ventricular myocardium in response to strain

63
Q

What is reduced LVEF typically defined as ? what measures this ?

A

echocardiograph <35 to 40 %
(this is around half of the patients with HF)

64
Q

What classification system can classify the severity of heart failure ? how many categories ?

A

New York Heart Association (NYHA) classification
class I - IV (worst)

65
Q

what is is NYHA Class II ?

A

HF severity scale
- mild symptoms
- slight limitation of physical activity, comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

66
Q

What is NYHA Class III ?

A

HF severity scale
- moderate symptoms
- marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

67
Q

What blood test is first line in HF diagnosis ?

A

N-terminal pro_b-type natriuretic peptide (NT-proBNP)

68
Q

What are some clinical sings of right sided heart failure ? (3)

A
  • raised JVP
  • Ankle oedema
  • Hepatomegaly
69
Q

Patient is on second line therapy for chronic heart failure. what drug types are they on ? and what electrolyte do they need to be cautious about/ monitored ?

A

ACEI, BB, aldosterone antagnost
- risk of hyperkalaemia (due to ACEI and AA)

70
Q

What is osteoporosis ? osteopenia ?

A

condition here there is reduced density of bones ? osteopenia is a less reduced version
- low BMD => less strain => more prone to fractures

71
Q

osteoporosis RF ? (6) which drugs associated with increased risk? (5)

A
  • increasing age
  • female (especially PM)
  • reduced mobility
  • low BMI
  • alcohol and smoking
  • low vit D and Ca diet
  • long termcorticosteroids
  • SSRI
  • PPI
  • Antiepileptics
  • Antioestrogens (used in breast cancer)
72
Q

what tool is used related to osteoporosis ? what does this calculate risk of ?

A

FRAX tool
- risk of fragility fracture in next 10 yrs

73
Q

what assess BMD ? interpret the results ?

A

DEXA scan (reading at the hip)
- Z score (compared to someone their age)
- T Score (compared to healthy person): normal>-1, osteopenia -1 to -2.5, osteoporosis <-2.5

74
Q

osteoporosis Mx ? first line ?

A

depend on FRAX score
- lifestyle changes
- calcium + vit D supplements
- Bishphosiphoantes (first lien treatment)
- HRT in PM women

75
Q

modifiable RF for osteoporosis ? lifestyle changes ?

A
  • increase activity
  • maintain healthy weight
  • increase dietary Ca and vit D
  • avoid falling
  • smoking cessation
  • reduce alcohol
76
Q

How do bisphosphanates work ? SE (3) how must they be taken ?

A

interfere with osteoclasts
- take on empty stomach + sit up for next 30 mins to prevent reflux
- SE: reflux, oesophageal erosions, atypical fractures

77
Q

What scale used to assess frailty ? how many categories ?

A

Rockwood frailty scale
- 1 (very fit)
- 9 (Terminally ill)

78
Q

What is multimorbidity ?

A

presence of 2 or more long term health conditions

79
Q

Underlying medical conditions causing constipation ? (3)

A
  • hypothyroidism
  • multiple sclerosis
  • structural abnormalities (haemorrhoids, anal fissure)
80
Q

Medications causing constipation ? (4)

A

(iatrogenic)
- Opiods
- iron supplements
- tricyclic antidepressants
- Antipsychotics

81
Q

name the different types of laxatives (4)

A
  • Bulk forming
  • osmotic
  • stimulant
  • stool softening
82
Q

give example of bulk forming laxative ? how does it work ?

A

ispghula husk, methycellulose
- bulks out the stool with soluble fibre => increase faecal mass and stimulate peristalsis
(patients should increase fluid intake when taking this laxative type)

83
Q

give example of somatic laxative ? how do they work ?

A

lactulose
- draw water via osmosis into stool => softer and easier to pass

84
Q
A
85
Q

give an example of stimulant laxative ? how do they work ?

A

Senna, sodium picosulfate
- stimulate the nerves of the digestive tract to cause peristalsis

86
Q

where do pressure ulcers typically develop ?

A

bony prominences (sacrum or heel)

87
Q

what scale is used to screen for patients at risk of developing pressure areas ?

A

Waterlow score

88
Q

how many grades are there to pressure sores ? which is worse ? describe a bit

A

grades 1-4 (worse)
- 1: non-blanch able erythema, discolouration of skin
- 4: tissue encores, damage to muscle or bone

89
Q

pressure sores management ? (3)

A
  • moist wound environment encourage healing
  • wound swabs (as often colonised with bacteria)
  • surgical debridement
90
Q

What is squamous cell carcinoma of the skin ?

A

common variant of skin cancer
- metastases may occur in 2-5% of patients

91
Q

SCC of skin RF ?

A
  • excessive exposure to sunlight
  • immunosuppression
  • smoking
92
Q

SCC of skin Mx ?

A

surgical excision

93
Q

definition of malnutrition ?

A
  • BMI < 18.5
  • unintentional weight loss greater than 10% within last 3-6 months
  • BMI <20 plus unintentional weight loss greater than 5%
94
Q

what screening tool is there for malnutrition ?

A

MUST (malnutrition universal screen tool)
- categorises into low, medium and high risk

95
Q

what temperature counts as hypothermia ?

A

milk: 32-35
moderate or severe: <32

96
Q

why avoid rapid re-warming in hypothermic patient ?

A

can lead to peripheral vasodilation and shock

3a (43 decks)

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