Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 3a Revision > COTE > Flashcards

COTE Flashcards

1
Q

COTE ASSESSMENT
What is frailty?
Is it inevitable?

A
  • State of increased vulnerability resulting from ageing-associated decline in reserve + function across multiple physiological systems resulting in compromised ability to cope with everyday or acute stressors
  • Not inevitable, not irreversible + not simply due to chronic conditions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

COTE ASSESSMENT

What is the impact of frailty?

A
  • Poor functional reserve (trivial insult to young person = large impact in elderly)
  • Vulnerable to decompensation when faced with illness, drug SEs + metabolic disturbance
  • Different type of doctor (geriatricians)
  • Failure to integrate responses in the face of stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

COTE ASSESSMENT

What is acopia?

A
  • Social admission – non-specific presentation, not a Dx just describes a patient unable to cope with ADLs
  • High mortality rate, vast majority have medical pathology.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

COTE ASSESSMENT
What are the geriatric giants?
What do they represent?

A 
4Is –
- Instability (falls)
- Immobility
- Intellectual impairment (confusion)
- Incontinence
They are not diagnoses but more general things that COTE pts present with, often indicator of underlying problem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

COTE ASSESSMENT

What are the geriatric 5Ms?

A
  • Mind = dementia, delirium, depression
  • Mobility = impaired gait + balance, falls
  • Medications = polypharmacy, medication burden, adverse effects, de-prescribing/optimal prescribing
  • Multi-complexity = multi-morbidity, biopsychosocial
  • Matters most = individual meaningful health outcomes + preferences
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

COTE ASSESSMENT
What is a comprehensive geriatric assessment?
What does it focus on?
Who is part of the geriatric MDT?

A
  • Multidimensional, MDT diagnostic process in geriatrics.
  • Determining a frail older person’s medical, psychological + functional capability
  • Geriatrician, social worker, physio, OT, SALT, nurse etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

COTE ASSESSMENT
What is the role of the comprehensive geriatric assessment?
What is the process?

A
  • Development of a coordinated, integrated plan for treatment + long-term support
  • Assessment > problem list > personalised care plan > intervention > regular planned review > assessment etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

COTE ASSESSMENT

What are the components of the comprehensive geriatric assessment and who might be involved?

A
  • Medical assessment = Dr, nurse, pharmacist, dietician, SALT
  • Functional assessment (OT, physio, SALT)
  • Psychological assessment (Dr, nurse, OT, psychologist)
  • Social + environmental assessment (OT, social worker)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

COTE ASSESSMENT
What is involved in…

i) medical assessment?
ii) functional assessment?
iii) psychological assessment?
iv) social + environmental assessment?

A

i) Problem list, co-morbid conditions + disease severity, med review, nutritional status
ii) ADLs, activity/exercise status, gait + balance
iii) Cognitive status testing, mood testing (PHQ-9)
iv) Informal support needs + assets, eligibility or need for carers, home safety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

COTE ASSESSMENT

What is rehabilitation?

A
  • Process of restoring a patient to maximum function (need to know pre-morbid function), can happen in variety of settings, involves MDT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

COTE ASSESSMENT
What is pharmacodynamics?
How does this change for the elderly?

A
  • What the DRUG does to the BODY

- In elderly, effects of similar drug conc. may be different to younger so prone to adverse drug reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

COTE ASSESSMENT
What is pharmacokinetics?
How does this change for the elderly?

A
  • What the BODY does to the DRUG
  • Changes in absorption, distribution, metabolism + excretion of drugs
  • May mean drugs hang around longer or elderly pts may experience more toxicity from smaller dose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

COTE ASSESSMENT

Give some specific pharmacokinetic issues in geriatrics.

A
  • Hepatic first pass metabolism declines
  • Reduced absorption as gastric pH increases due to atrophy
  • Vascular system less responsive due to calcification of vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

COTE ASSESSMENT

Why might inappropriate drug use occur in geriatrics?

A
  • May not understand instructions
  • May be unable to read instructions
  • May make own interpretation of instructions
  • Could be due to lack of treatment supervision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

COTE ASSESSMENT
What is polypharmacy?
Why are geriatric patients at increased risk?

A
  • Concurrent use of multiple medications by one person (some studies label >5)
  • Higher rates of chronic illness so more likely to have multiple meds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

COTE ASSESSMENT
What is multimorbidity?
What is the impact of multimorbidity?

A
  • ≥2 chronic conditions, often long-term requiring ongoing care.
  • Complexity + restrictions with cross-over of Sx
  • Medication burden (SEs, drug interactions, monitoring, compliance)
  • Appt burden
  • Mental health impact
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

COTE ASSESSMENT

What are some potential problems with polypharmacy?

A
  • Drug interactions + increased SEs
  • Can affect compliance + lead to decreased pt satisfaction
  • Pill burden
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

COTE ASSESSMENT
What is appropriate polypharmacy?
What can this lead to?

A
  • Prescribing multiple medications for either a complex condition or multiple conditions where medicine has been optimised
  • Can extend life expectancy + improve QOL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

COTE ASSESSMENT
What is problematic polypharmacy?
How can this be prevented?

A
  • Multiple medications prescribed inappropriately, increasing the risk of SEs
  • MDT case conferences, computerised support systems, pharmacists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

COTE ASSESSMENT

What are the reasons for problematic polypharmacy?

A
  • Multimorbidity (increased prevalence with increasing age)
  • Incremental prescribing (prescribing cascade) = prescribers may not recognise Sx iatrogenic so prescribe more meds to counter SEs of other drugs
  • End-of-life considerations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

COTE ASSESSMENT
What is the impact of adverse drug reactions?
What specific issue can this impose in geriatrics?

A
  • Increasing fragility means reduced ability to cope with ADRs
  • May go unnoticed as Sx mimic problems associated with elderly (forgetfulness, weakness, tremor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

COTE ASSESSMENT

What are some common ADRs in geriatrics?

A
  • Falls (postural hypotension with ACEi, beta-blockers)
  • Confusion (sedation with anticholinergics)
  • Bowel problems (opioids, PPIs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

MEDICO-LEGAL ASPECTS

What is the purpose of the Mental Capacity Act, 2005?

A
  • Empower + protect people >16y who lack capacity to make their own decisions about their care + treatment since 1/10/07
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

MEDICO-LEGAL ASPECTS

What is the two-step test in MCA?

A
  • Does the person have an impairment of their mind or brain? E.g. dementia, severe LD, brain injury, coma
  • Is this impairment significant enough to deem them unable of making a particular decision?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

MEDICO-LEGAL ASPECTS

What are the 4 aspects of assessing capacity?

A
  • Does the pt UNDERSTAND the information?
  • Can the pt RETAIN that information?
  • Can the pt use the information to WEIGH UP the pros + cons?
  • Can the pt COMMUNICATE their decision back (ensure different methods explored)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

MEDICO-LEGAL ASPECTS

What are the 5 principles underpinning the MCA?

A
  • Assume capacity until proven otherwise
  • Maximise decision-making capacity (all practical support to help them make decision given)
  • Freedom to make seemingly unwise choice (unwise decision ≠ incapacity)
  • All decisions on behalf of patient in best interests
  • Least restrictive option should be chosen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

MEDICO-LEGAL ASPECTS

What are some important considerations about a person’s capacity status?

A
  • Can fluctuate with time (temporary cognitive impairment like delirium)
  • Decision specific so may have capacity for some decisions, do not just completely write off
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

MEDICO-LEGAL ASPECTS

What is an independent mental capacity advocate (IMCA)?

A
  • Commissioned from independent organisations by the NHS + local authorities to ensure MCA followed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MEDICO-LEGAL ASPECTS

What is the role of an IMCA?

A
  • Support + represent people who lack capacity + do not have anyone else to represent them in major decision (serious Tx)
  • Have authority to make enquiries about pt + contribute to decision by representing the patient’s interests but cannot make a decision on their behalf
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

MEDICO-LEGAL ASPECTS

What are some important considerations when making best interest decisions?

A
  • Encourage participation of the patient wherever possible
  • Find out person’s views (past + present wishes, feelings, beliefs + values)
  • Avoid discrimination (don’t make assumptions on any personal features)
  • Regaining capacity (can the decision wait?)
  • Identify all relevant circumstances to identify what they would have taken into account if they were making this decision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

MEDICO-LEGAL ASPECTS

Who would you consult when making best interest decisions?

A
  • Anyone previously named by the individual
  • Anyone engaged in caring for them
  • Close relatives + friends
  • Any appointed attorney or deputy appointed by Court of Protection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

MEDICO-LEGAL ASPECTS

What is a deprivation of liberty safeguard, DoLS (new name Liberty Protection Safeguards)?

A
  • Amendment of MCA with aim to protect people in care homes + hospitals from being inappropriately deprived of their liberty, meaning safeguards have been put in place to make sure someone’s liberty is only restricted safely + correctly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

MEDICO-LEGAL ASPECTS

When is a DoLS required?

A
  • When a person does not or cannot consent to care or treatment but are having it anyway (dementia pt not free to leave ward + lacks capacity to consent to this)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

MEDICO-LEGAL ASPECTS

What is the acid test for DoLS?

A

Must meet 3 criteria –

  • Lack of capacity to consent to the arrangements or their care
  • Subject to continuous supervision + control
  • Not free to leave their care setting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

MEDICO-LEGAL ASPECTS
How should a DoLS be attained?
What are the limitations of an urgent DoLS?

A
  • Officially verified by local DoLS team apart from an urgent DoLS which can be executed without prior formal authorisation
  • Only if in best interests, up to 7d + must be least restrictive alternative to preventing harm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

MEDICO-LEGAL ASPECTS

What is an advanced directive?

A
  • Written statement that sets down a person’s preferences, wishes, beliefs + values regarding their future care
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

MEDICO-LEGAL ASPECTS

What are the roles of an advanced directive?

A
  • Aims to provide guide for anyone who might make decisions in their best interests when they lose capacity
  • Allows people who understand implications of their choices to state wishes in advance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

MEDICO-LEGAL ASPECTS

What can an advanced directive include?

A
  • Where they would like to be cared for (home, nursing home), concerns about practical issues (who will look after pet if ill)
  • Can authorise or request specific procedures (Where suitable)
  • Can refuse treatment in a predefined future situation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

MEDICO-LEGAL ASPECTS
What is an advanced refusal of treatments?
Is it legally binding?

A
  • A living will
  • Yes if:
    – Adult ≥18y
    – Was competent + fully informed when made decision
    – Decision is clearly applicable to current circumstances
    – No reason to believe changed mind
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

MEDICO-LEGAL ASPECTS
What is an advanced requests for treatment?
Is it legally binding?

A
  • Patient’s wish for treatment
  • Less legal binding but if it’s patient’s known wish to be kept alive then reasonable efforts (nutrition, hydration) should be considered
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

MEDICO-LEGAL ASPECTS

What is a Lasting Power of Attorney (LPA)?

A
  • Document which a person can use to nominate someone else to make certain decisions on their behalf when they are unable to do so themselves whilst they still have capacity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

MEDICO-LEGAL ASPECTS
What are the 2 types of LPA?
What is needed for it to be valid?

A
  • Health/welfare LPA = make decisions relating to treatment, discharge destination
  • Financial LPA = make decisions relating to finances (bank accounts) + property
  • Must be registered with the Office of the Public Guardian
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

MEDICO-LEGAL ASPECTS
What is…

i) court appointed deputy?
ii) enduring power of attorney (EPA)?

A

i) Alternative from Court of Protection once the person lacks capacity
ii) Under previous law + was restricted to decisions over property + affairs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

MEDICO-LEGAL ASPECTS
What is abuse?
What are some types?
Who may the perpetrator be?

A
  • Single or repeated act or lack of appropriate action that occurs in a relationship where there is an expectation of trust which causes harm or distress
  • Physical, neglect, psychological, financial, sexual, discriminatory
  • Family, partner, friends, neighbours, carers, strangers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

MEDICO-LEGAL ASPECTS

How should abuse be managed?

A
  • Avoid asking too many questions – LISTEN
  • Don’t agree to keep secret –duty to report to safeguarding
  • Do NOT confront abuser
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

DELIRIUM

What is delirium?

A
  • Transient, acute syndrome characterised by disturbance of consciousness, perception, sleep-wake cycle, emotion + cognition
  • Acute confusional state, fluctuates in severity, usually reversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

DELIRIUM

What is the aetiology of delirium?

A

PINCH ME –

  • Pain
  • Infection (UTI, pneumonia, septicaemia)
  • Nutrition (thiamine, B12 + folate deficiency)
  • Constipation (faecal impaction)
  • Hydration (dehydrated)
  • Metabolic/medication
  • Environment/electrolytes (changes in environment, hyper/hypo Ca2+, Na+, K+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

DELIRIUM

What are some metabolic/medication causes of delirium?

A
  • Hyper/hypo thyroid + glycaemia
  • Hypercortisolaemia
  • Substance misuse
  • Withdrawal (incl. delirium tremens)
  • Opioids, anticholinergics, Parkinson’s meds, steroids, BDZs, interactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

DELIRIUM

What are some other causes of delirium?

A
  • Urinary retention, vascular events (CVA, MI)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

DELIRIUM

Who are high risk patients that require screening on admission?

A
  • > 65y, men, previous delirium
  • Pre-existing cognitive deficit (dementia, PD, stroke)
  • Sensory impairment (hearing/visual)
  • Significant illness (hip #, cancer)
  • Poor nutrition
  • Hx of alcohol excess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

DELIRIUM
What are the 2 sub-types of delirium?
Which is more dangerous?

A
  • Hyperactive = agitated/aggressive, hallucinations, delusions, wandering + restless
  • Hypoactive = withdrawn, quiet, lethargic, lacks concentration, slow
  • Hypoactive as less likely to be recognised
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

DELIRIUM

What is the ICD-10 diagnostic criteria for delirium?

A
  • Impaired consciousness + inattention (poor conc, memory deficit, “clouding of consciousness”)
  • Perceptual OR cognitive disturbance (agitation, hallucinations > Lilliputian)
  • Acute onset + fluctuating course (often worse at night = sundowning)
  • Evidence it may be related to a physical cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

DELIRIUM

What are some other/non-specific features of delirium?

A
  • Disinhibition
  • Falls
  • Loss of appetite
  • Labile mood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

DELIRIUM

What is a suitable screening tool for delirium?

A

4AT (≥4 = likely) –

  • Alertness
  • AMT4 (age, DOB, hospital name, year)
  • Attention (list months backwards)
  • Acute change or fluctuating course
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

DELIRIUM

What other cognitive tools can be used in the assessment of delirium/dementia?

A
  • GP-COG (GP assessment of cognition)
  • 6-CIT (6-item cognitive impairment test)
  • AMT (abbreviated mental test)
  • MOCA (Montreal Cognitive Assessment, <26/30)
  • MMSE
  • ACE-III
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

DELIRIUM

What general investigations would you do/enquiry about in a patient with delirium?

A
  • Full physical exam
  • Vitals (?sepsis), ECG
  • Check if passed stools
  • Check nutritional + hydration status
  • Confusion screen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

DELIRIUM

What is a confusion screen?

A
  • FBC, B12 + folate, U+Es, Ca2+, ?phosphate, TFTs, LFTs, glucose, INR + clotting, blood + urine cultures, ?CRP/ESR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

DELIRIUM

What other investigations or referral could you consider?

A
  • CXR or CT head if indicated

- Referral to memory clinic or old age psychiatrist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

DELIRIUM

What is the mainstay of delirium management?

A
  • Identify + treat cause with sufficient nutrition, hydration + mobilisation
  • Maximise orientation + make environment safe + comforting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

DELIRIUM

How should a patient be managed in the first instance?

A

Conservative de-escalation

  • Talk to pt + listen to them
  • Quiet bay or side room
  • Big clocks, calendars, same staff members for orientation
  • Family visits + personal belongings (pictures)
  • Tx sensory impairments (glasses, hearing aids)
  • Prevent ward changes
  • Sleep hygiene (promote night sleep, not daytime)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

DELIRIUM

Sometimes conservative de-escalation is inadequate and medications may be required. What are some options?

A
  • Short-term antipsychotics – haloperidol 0.5mg or olanzapine
  • Short-acting BDZ like lorazepam 0.5mg (caution may exacerbate confusion + over sedate)
  • Long-acting BDZ if withdrawing (chlordiazepoxide, diazepam)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

DEMENTIA
What is dementia?
What time frame is used?

A
  • Syndrome of acquired, chronic, global impairment of higher brain function in an alert patient, which interferes with ability to cope with daily living
  • Deterioration present for ≥6m for diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

DEMENTIA

What are the 2 types of dementia and where is affected?

A
  • Cortical dementias affect the cerebral cortex

- Subcortical dementia affect the basal ganglia + thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

DEMENTIA
How does cortical dementia present?
Give some examples.

A
  • Memory impairment, dysphasia, visuospatial impairment (apraxia), problem solving + reasoning deficit
  • AD, lewy-body, frontotemporal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

DEMENTIA
How does subcortical dementia present?
Give some examples

A
  • Psychomotor slowing, impaired memory retrieval, depression/apathy, executive dysfunction, personality change, language preserved
  • PD, Huntington’s, alcohol-related + AIDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

DEMENTIA
How does delirium differ from dementia for…

i) deterioration?
ii) course?
iii) consciousness?
iv) thought content?
v) hallucinations?

A

i) Rapid (hours-days) + usually reversible vs. slow (months-years) + not reversible
ii) Acute + fluctuating vs. insidious + progressive
iii) Clouded vs. alert
iv) Vivid, complex + muddled vs impoverished
v) V common, visual vs. in 1/3rd, auditory/visual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

DEMENTIA

What are some diagnostic features of dementia?

A
  • Multiple cognitive deficits (memory, orientation, language, reasoning)
  • Resulting impairment in ADLs (washing, dressing)
  • Clear consciousness
  • Other common Sx include behavioural + psychological Sx of dementia (BPSD), sleep issues (insomnia, daytime drowsiness, nocturnal restlessness)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

DEMENTIA
What are behavioural + psychological symptoms of dementia (BPSD)?
What causes them?

A
  • Heterogenous group of non-cognitive symptoms + behaviours seen in dementia
  • Same aetiology as delirium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

DEMENTIA
How does BPSD present?
What is the management?

A
  • Anxiety/depression, agitation, psychosis (may think nurses out to get them), disinhibition
  • Exclude/Tx underlying cause, similar Mx to delirium (supportive environment, meds last line), educate family/carer about Sx + causes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

DEMENTIA

What are some general investigations for dementia?

A
  • Full Hx + collateral with full physical exam + MSE

- Check for reversible causes with confusion screen ± CXR ± CT head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

DEMENTIA

What might a MMSE + Addenbrooke’s cognitive examination III (ACE-III) score indicate in dementia?

A

MMSE (/30) –
- 21–26 = mild, 14–20 = mod, 10–14 mod-severe, <10 = severe cognitive impairment
ACE-III (/100) –
- <82 likely dementia + need abnormal scores in ≥2 domains (attention/orientation, memory, language, visuospatial, fluency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

DEMENTIA

What type of imaging may be used in dementia?

A
  • SPECT to differentiate between Alzheimer’s + frontotemporal
  • DaTscan shows ‘comma’ in normal but 2 dots in Lewy body + Parkinson’s dementia at the basal ganglia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

DEMENTIA

What biological and psychological treatment can be used in dementia?

A
  • Bio = risperidone for agitation (apart in Lewy-Body)
  • Psycho = CBT for depression, counselling, reminiscence therapy + reality orientation, keep stimulated with puzzles, word searches, activities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

DEMENTIA

What social treatment can be used in dementia?

A
  • OT assessment to remain independent (pendent, labels on cupboards, key safe, carers, handrails)
  • Physio assessment
  • Encourage family visits + photos
  • Animal/pet therapy, music, arts + crafts
  • Care plans + advanced directives before worsens
  • Services – Dementia UK, Alzheimer’s society, Age UK, admiral nurses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

ALZHEIMER’S DISEASE

What is the pathophysiology of Alzheimer’s disease?

A
  • Accumulation of beta-amyloid peptide plaques which result in degeneration of cerebral cortex with cortical atrophy + loss of acetylcholine.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

ALZHEIMER’S DISEASE
What is the onset of Alzheimer’s disease like and why?
What neurotransmitters are affected?

A
  • Insidious onset dementia due to generalised deterioration of the brain
  • ACh, noradrenaline, serotonin, somatostatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

ALZHEIMER’S DISEASE
What are the causes of Alzheimer’s disease?
What is the epidemiology?
What condition has increased rates of Alzheimer’s?

A
  • Unknown but most common type of dementia
  • > 65y, if <65 then early onset + associated with more rapid decline + FHx
  • Down’s syndrome (most develop by 50)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

ALZHEIMER’S DISEASE
What genes have been implicated to…

i) familial early-onset Alzheimer’s?
ii) late onset Alzheimer’s?

A

i) APP gene, presenilin 1 + 2 (autosomal dominant)

ii) Apolipoprotein E (ApoE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

ALZHEIMER’S DISEASE

What are some risk factors for Alzheimer’s?

A
  • CVD = HTN, DM, hypercholesterolaemia, smoking

- FHx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

ALZHEIMER’S DISEASE

What is the clinical presentation of Alzheimer’s

A

4As of Alzheimer’s –
- Amnesia (recent memories poor, disorientation about time)
- Apraxia (unable to button clothes, use cutlery)
- Agnosia (unable to recognise body parts, objects, people)
- Aphasia (later feature, mixed receptive/expressive)
Insidious + progressive course of short-term memory loss Sx in early disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

ALZHEIMER’S DISEASE
On CT/MRI head in Alzheimer’s disease, what are the…

i) macroscopic pathological changes?
ii) microscopic or histological pathological changes?

A

i) Diffuse cerebral atrophy (shrunken brain), increased sulcal widening, enlarged ventricles
ii) Neuronal loss, neurofibrillary tangles, beta-amyloid plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

ALZHEIMER’S DISEASE

What is the management of Alzheimer’s?

A
  • No cure, does not improve life expectancy but thought to slow rate of decline + allow functioning at higher level
  • AChEi (donepezil, rivastigmine) for mild–mod
  • NMDA antagonist (memantine) for mod–severe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

VASCULAR DEMENTIA
What causes vascular dementia?
What are the risk factors?

A
  • Any type of vascular disease affecting blood vessels of brain
  • CVA/TIA = 9x increased risk of dementia
  • CV = HTN, DM, hypercholesterolaemia, smoking
  • Hx of peripheral vascular disease, IHD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

VASCULAR DEMENTIA

What is the clinical presentation of vascular dementia?

A
  • Stepwise deterioration with short periods of stability then suddenly decline
  • Patchier cognitive impairment than Alzheimer’s
  • Focal neuro signs if caused by stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

VASCULAR DEMENTIA

What would a CT head show in vascular dementia?

A
  • ≥1 areas of cortical infarction (white on CT), may show micro-infarcts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

VASCULAR DEMENTIA

What is the management of vascular dementia?

A

Not reversible but prevent further decline –

  • Lifestyle (lose weight, healthy diet, stop smoking + alcohol)
  • Atorvastatin 80mg if high cholesterol
  • Optimise co-morbidities (HTN, DM)
  • Aspirin or clopidogrel (75mg OD)
87
Q

LEWY-BODY DEMENTIA
What is the pathophysiology of Lewy-Body dementia?
What might it be confused with?

A
  • Presence of Lewy bodies (protein deposits) in the basal ganglia + cerebral cortex, typically presents between 50–80y
  • Delirium due to fluctuating consciousness + hallucinations
88
Q

LEWY-BODY DEMENTIA
What condition is Lewy-Body dementia closely associated to?
How can you differentiate?

A
  • Parkinson’s disease (25% of PD patients will develop)
  • Dementia before movement signs = Lewy-body dementia
  • Movement before dementia signs = Parkinson’s dementia
89
Q

LEWY-BODY DEMENTIA

What is the clinical presentation of Lewy-Body dementia?

A
  • Fluctuating onset, progression, cognition + consciousness
  • Vivid visual hallucinations (small children, animals)
  • Parkinsonism (tremor, stooped + shuffling gait, hypomimia)
  • Frequent falls
  • REM sleep behaviour disorder (sleep walking, aggression) commonly precedes other Sx
  • Rapid decline more so than other types
90
Q

LEWY-BODY DEMENTIA

What is the management of Lewy-Body dementia?

A
  • Conservative management
  • AChEi used in mild–mod (rivastigmine 1st line), memantine last resort
  • SENSITIVE to antipsychotics, can make worse + lead to neuroleptic malignant syndrome
91
Q

FT DEMENTIA
What are 2 common features in frontotemporal (FT) dementia?
What are some pathological features?

A
  • Early personality changes + relative intellectual sparing.

- Microscopic = ubiquitin + tau deposits

92
Q

FT DEMENTIA

What causes FT dementia?

A
  • Unknown, younger mean age of onset
  • Can be due to neurosyphilis (typically causes frontal lobe Sx such as aggression + personality change), associated with MND
93
Q

FT DEMENTIA
What are the

i) frontal lobe symptoms
ii) temporal lobe symptoms
iii) generic features

of FT dementia?

A

i) Euphoria, disinhibition, personality changes + emotional blunting
ii) Speech disturbances (progressive non-fluent aphasia, may end up mute), expressive dysphasia
iii) Insidious onset with poor insight, amnesia not as severe as Alzheimer’s

94
Q

FT DEMENTIA

What is the management of FT dementia?

A
  • No specific treatment

- SSRIs may help behavioural symptoms

95
Q

CJD

What is Creutzfeldt-Jacob Disease (CJD)?

A
  • Prion infection which infects the brain causing spongiform encephalopathy
96
Q

CJD

What is the aetiology of CJD?

A
  • Sporadic (Dx by LP)
  • Contamination (infected hospital equipment)
  • Familial
  • Variant (vCJD) aka Mad Cow’s disease from eating meat in cattle with bovine spongiform encephalopathy
97
Q

CJD

What is the clinical presentation of CJD?

A
  • Rapidly progressive cognitive decline (rapidly fatal dementia usually within 1y)
  • Myoclonic jerks
  • Personality changes
  • Memory loss
  • Extra-pyramidal signs (stiff limbs)
98
Q

CJD

What is the management of CJD?

A
  • No cure but clonazepam may help with stiff limbs + seizures
99
Q

HIV DEMENTIA
Why has HIV dementia rates decreased?
How may it present now?
How does it progress?

A
  • Antiretroviral treatment
  • Some patients may experience milder cognitive impairment with issues with concentration, memory, planning, organisation or decisiveness
  • Sx often stable over time rather than progressing to dementia
100
Q

NEUROSYPHILIS
What is neurosyphilis?
How does it present?
How is it managed?

A
  • Infection of CNS with treponema pallidum (serological testing)
  • Tabes dorsalis (locomotor ataxia), paralysis, dementia, Argyll-Robertson (prostitute’s) pupil (accommodates but does not react), paranoia
  • Penicillin
101
Q

WILSON’S DISEASE
What is Wilson’s disease?
How is it managed?

A
  • Copper excess leading to neuro + psych signs, liver disease, Kayser-Fleischer rings in cornea (brown circles surrounding iris)
  • Copper chelation with penicillamine
102
Q

HYDROCEPHALUS
What is normal pressure hydrocephalus?
What is the triad of symptoms?

A
  • Accumulation of CSF that causes ventricles in brain to become enlarged
  • ‘Wet, wacky, wobbly’ = urinary incontinence, dementia (can be controlled or reversed with treatment), ataxia
103
Q

HYDROCEPHALUS

What is the management of normal pressure hydrocephalus?

A
  • CT/MRI head showing enlarged ventricles

- Ventriculoperitoneal shunt to drain excess fluid

104
Q

ALCOHOL DEMENTIA
What is alcohol-related dementia?
How common is it?
How is it managed?

A
  • Generalised brain damage > cognitive decline in cortical function (caused by excessive alcohol consumption
  • Accounts for 10%
  • Prevent further damage + stop drinking alcohol
105
Q

PSEUDODEMENTIA
What is pseudodementia?
How does it present?

A
  • Cognitive impairment secondary to mental illness (often depression)
  • “Don’t know” answers, no confabulation, may present with depression Sx, recent loss, impairment in executive functioning + attention
106
Q

PSEUDODEMENTIA
What might MRI head show in pseudodementia?
What is the management?

A
  • Frontal lobe changes, white matter hyperintensities

- CBT + interpersonal therapy

107
Q

MILD COG IMPAIRMENT
What is mild cognitive impairment?
How does it present?
How does it progress?

A
  • Cognitive impairment without functional impairment (ADLs minimally affected)
  • Reduced fluency + some short-term memory difficulties
  • 1/3rd improve, 1/3rd stable, 1/3rd progress to dementia
108
Q

FALLS

What is a fall?

A
  • Event that results in unintentionally coming to rest at a lower level, usually the floor
109
Q

FALLS

What are some neurological causes of falls?

A
  • Stroke
  • PD or other movement disorders (Huntington’s)
  • Visual impairment
  • Peripheral neuropathy or myopathy
110
Q

FALLS

What are some cardiovascular causes of falls?

A
  • Vasovagal or situational syncope
  • Postural hypotension
  • MI, arrhythmias
  • Dehydration or shock
111
Q

FALLS

What are some iatrogenic causes of falls?

A
  • BDZs (sedative so impairs coordination)
  • Polypharmacy (combination of drugs + interactions)
  • Anti-hypertensives (ACEi, CCB, beta-blockers, diuretics)
  • Anti-depressants + anti-psychotics
112
Q

FALLS

What are some power causes of falls?

A
  • Inactivity > muscle weakness
  • Dizziness/loss of balance or proprioception (vertigo)
  • Pain/MS > osteoarthritis
113
Q

FALLS

What are some environmental causes of falls?

A
  • Loose rugs
  • Pets
  • Furniture
  • Unstable footwear
  • Poor lighting
114
Q

FALLS

What are some other causes of falls?

A
  • Infection or sepsis
  • Delirium
  • Incontinence
  • Hypoglycaemia
  • Alcohol (intoxication, neuropathy, Korsakoff’s or Wernicke’s)
115
Q

FALLS

What parts of the history are important when assessing falls?

A
  • Collateral Hx
  • Circumstances (timing, physical environment)
  • Sx before + after fall
  • Previous falls, #, syncope or near misses
  • PMH for co-morbidities
  • Functional performance (assess ADLs)
116
Q

FALLS
What clinical scale can be used to assess frailty?
What clinical examinations would you perform?

A
  • Rockwood clinical frailty scale (from very fit, vulnerable, moderately frail to terminally ill)
  • CVS (LSBP, HR + rhythm, murmurs esp. AS)
  • MSK (assess footwear, joints for deformity + stiffness)
  • Neuro (identify stroke, peripheral neuropathy, ?Parkinson’s)
117
Q

FALLS

What investigations would you do for someone presenting with a fall?

A
  • FBC, B12 + folate, U+Es, Ca2+, phosphate, glucose, TFTs, vitamin D
  • 24h ECG, ECHO if ?cardiac cause
  • Head-up tilt table testing if unexplained syncope with normal ECG + no structural heart disease
118
Q

FALLS

What are some complications of a long-lie following a fall?

A
  • Pressure ulcers
  • Dehydration
  • Rhabdomyolysis
  • Hypothermia
119
Q

FALLS

What is rhabdomyolysis?

A
  • Skeletal muscle breakdown due to traumatic, chemical or metabolic injury
120
Q

FALLS

What can cause rhabdomyolysis?

A
  • Crush injuries
  • Prolonged immobilisation following a fall
  • Prolonged seizures
  • Hyperthermia
  • Neuroleptic malignant syndrome
121
Q

FALLS
How may rhabdomyolysis present?
What markers are elevated in rhabdomyolysis?
Is that an issue?

A
  • Urine may be dark (‘Coca-Cola urine) + urinalysis +ve to Hb but without RBCs
  • K+, phosphate, myoglobin + creatinine kinase
  • Myoglobin is nephrotoxic as causes acute tubular necrosis
122
Q

FALLS

What is the management of rhabdomyolysis?

A
  • Measure U+Es, creatinine, CK levels + monitor urine output

- Supportive with IV fluids, correct electrolytes, ?temporary dialysis

123
Q

FALLS

How can falls be prevented in a hospital setting?

A
  • Treat infection, dehydration + delirium actively
  • Stop incriminating drugs or avoid staring them
  • Provide good quality footwear + access to walking aid
  • Keep a call bell close to hand
  • Good lighting
124
Q

FALLS

How can fall frequency be reduced?

A
  • Drug review to reduce meds that can increase risk
  • Strength + balance training with physio (Tai Chi)
  • Walking aids
  • Environmental assessment + mods by OT
  • Ensure vision optimised with glasses
125
Q

FALLS

How can adverse consequences from falls be reduced?

A
  • Osteoporosis detection + treatment
  • Alarms such as pullcord or pendant alarms to summon help
  • Supervision via visits from carers, family, neighbours
126
Q

POSTURAL HYPOTENSION

What is the pathophysiology of postural hypotension?

A
  • When standing, gravity causes blood to pool in legs + abdo which decreases BP as less blood circulating back to heart
  • Normally, baroreceptors near heart + carotid arteries sense this lower BP + send signals to brain to signal heart to beat faster, pump more blood, cause vasoconstriction + stabilise BP
  • In postural hypotension, something interrupts this mechanism
127
Q

POSTURAL HYPOTENSION
What are some…

i) iatrogenic
ii) cardiac
iii) endocrine
iv) neuro

causes of postural hypotension?

A

i) Diuretics, anti-hypertensives, antidepressants, polypharmacy
ii) Aortic stenosis, arrhythmias, MI, cardiomyopathy, anaemia, CHF
iii) DM, hypoadrenalism, hypothyroidism
iv) PD + PD+ syndromes

128
Q

POSTURAL HYPOTENSION
What are some other causes of postural hypotension?
How common is it?

A
  • Blood loss, dehydration + shock

- Occurs in 30% of patients >70y

129
Q

POSTURAL HYPOTENSION
How may postural hypotension present?
What are these patients at risk of?

A
  • Postural light-headedness, dizziness, blurred vision
  • Weakness, fatigue, palpitations + headache may be present
  • Risk of falls + syncope, CV disease or stroke
130
Q

POSTURAL HYPOTENSION

What investigations would you do to diagnose postural hypotension?

A

Lying + standing blood pressure
- Abnormal drop in BP of ≥20/10mmHg within 3 minutes of standing (<20/10 is physiological)
Investigate medical causes (FBC, U+Es, B12 + folate, TFTs, LFTs, CRP/ESR, ECG)

131
Q

POSTURAL HYPOTENSION

What is the conservative management of postural hypotension?

A
  • Drinks lots of water
  • Avoid alcohol
  • Compression garments (stockings)
  • Stand slowly, elevating head of the person’s bed
132
Q

POSTURAL HYPOTENSION

What is the pharmacological management of postural hypotension?

A
  • Med review + stop causative agent
  • Fludrocortisone (raises BP by raised Na+ levels + affecting blood volume) but can cause uncomfortable oedema
  • Midodrine (when cause if autonomic dysfunction) but can cause retention, itchy scalp + paraesthesia
133
Q

PRESSURE ULCERS
What is an ulcer?
What is a pressure ulcer?
Where would you commonly find them?

A
  • Open sore caused by a break in the skin or mucous membrane which fails to heal
  • Areas of skin necrosis due to pressure-induced ischaemia
  • Sacrum, heels, greater trochanters, shoulders
134
Q

PRESSURE ULCERS
How rapidly can a new pressure ulcer develop?
When do they typically occur?
How rapidly can an existing pressure ulcer develop?

A
  • 2h of tissue ischaemia sufficient for subsequent development of ulcer + there’s a considerable lag between ischaemic insult + resting ulcer
  • Just prior to or at time of admission
  • Grade I can progress to deep ulcers over days-weeks without further insult
135
Q

PRESSURE ULCERS

What are 4 contributing factors to pressure ulcer development?

A
  • Pressure
  • Shear
  • Friction
  • Moisture
136
Q

PRESSURE ULCERS
Explain how…

i) pressure
ii) shear

cause pressure ulcers.

A

i) Capillary pressures >35mmHg compress capillaries + cause ischaemia
ii) Skin pulled away from fixed axial skeleton so blood vessels can be kinked or torn (may occur during lifts or transfers)

137
Q

PRESSURE ULCERS
Explain how…

i) friction
ii) moisture

cause pressure ulcers.

A

i) Rubbing skin decreases integrity

ii) Sweat, urine + faeces cause maceration + decrease integrity

138
Q

PRESSURE ULCERS
What score is used to screen for risk of pressure ulcer development?
What are some risk factors for pressure ulcers?

A

Waterlow score

  • Peripheral vascular disease (poor healing, reduced tissue perfusion)
  • Immobility (#, pain)
  • Dehydration + malnourishment
  • Obesity
  • Incontinence
139
Q

PRESSURE ULCERS

What are the different grades for pressure ulcers?

A
  • 0 = skin hyperaemia
  • I = non-blanching erythema with intact skin
  • II = broken skin or blistering (epidermis ± dermis only)
  • III = full-thickness skin loss involving damage/necrosis of subcutaneous tissue
  • IV = extensive loss, destruction/necrosis of muscle, bone, joint or tendon
  • Unstageable = depth unknown, base of ulcer covered by debris
140
Q

PRESSURE ULCERS

What are some investigations for pressure ulcers?

A
  • FBC (WCC), cultures
  • CRP/ESR
  • Swabs for MC&S if infected
  • XR for bone involvement (?osteomyelitis)
141
Q

PRESSURE ULCERS

How can pressure ulcers be prevented?

A
  • Keep pt as mobile as possible
  • Repositioning (6h or 4h in high risk)
  • Pressure redistributing mattress + chair and friction reduction (heel support, cushions)
  • Barrier creams as moist environment promotes healing
  • Regular skin assessment
142
Q

PRESSURE ULCERS

What is involved in a skin assessment?

A
  • Check for areas of pain + discomfort, skin integrity at pressure areas
  • Colour changes
  • Variations in heat, firmness + moisture (incontinence, oedema, dry/inflamed skin)
143
Q

PRESSURE ULCERS

What is the management of pressure ulcers?

A
  • Pain relief
  • Refer to tissue viability nurse
  • Empirical Abx then matched with sensitivities if signs of infection
  • Wound dressing (gels to soften, hydrogels often seaweed based for cavities)
  • Debridement with scalpel, maggots or topical streptokinase for grade 3/4
144
Q

MALNUTRITION

What is malnutrition?

A
  • State in which a deficiency of energy, protein ± other nutrients causes measurable adverse effects on the body’s form, composition, function + clinical outcome
145
Q

MALNUTRITION

What patients are at risk of malnutrition?

A
  • Eaten little/nothing for >5d (or likely to do so)
  • Poor absorptive capacity
  • High nutrient losses
  • Increased nutritional needs from causes such as catabolism
146
Q

MALNUTRITION

What are the 3 broad categories of causes of malnutrition?

A
  • Inadequate nutritional intake
  • Increased nutrient requirements
  • Inability to utilise ingested nutrients (malabsorption)
    (Or a combination)
147
Q

MALNUTRITION
What can cause…

i) inadequate nutrient intake?
ii) increased nutrient requirements?
iii) malabsorption?

A

i) Reduced appetite, pain, dysphagia, starvation, unfamiliar foods, mood
ii) Infection/wound healing, cancer, sepsis, surgery, trauma, liver disease
iii) Poor gut absorption (IBD, coeliac), increased losses from drains + wounds, D+V, pancreatic insufficiency

148
Q

MALNUTRITION

How is malnutrition defined?

A
  • BMI <18.5kg/m^2
  • Unintentional weight loss >10% in last 3–6m
  • BMI <20kg/m^2 AND unintentional weight loss >5% in last 3–6m
149
Q

MALNUTRITION
What investigations would you do in someone with malnutrition?
What tool should you use on those at risk?

A
  • U+Es, LFTs + ECG prior to commencing feedings
  • Serum albumin often marker of nutrition (can be inaccurate)
  • Malnutrition Universal Screening Tool (MUST) on admission
150
Q

MALNUTRITION
What are the components of MUST?
What do the scores mean?

A
  • BMI = 18.5-20 (1), <18.5 (2)
  • Hx of weight loss = 5-10% (1) ≥10% (2)
  • Acutely unwell or likely to have no intake >5d (2)
  • 1 = medium risk (observe, if inadequate set goals to improve intake)
  • ≥2 = high risk (refer to dietician, set goals to improve intake)
151
Q

MALNUTRITION

What are some consequences of malnutrition?

A
  • Impaired immunity, wound healing + recovery from illness
  • More hospital admissions, prolonged stays + refeeding syndrome
  • Loss of muscle mass (falls, more chest infections, decreased mobility)
  • Micronutrient deficiencies (selenium, zinc, Fe anaemia, vitamin D = osteomalacia)
152
Q

MALNUTRITION

What is the impact of the consequences from malnutrition?

A
  • Lead to poorer prognosis
  • Reduced QOL
  • Greater healthcare needs
153
Q

MALNUTRITION

What is the overall principle for the management of malnutrition?

A
  • Food first – if the gut works, use it

- Snacks, nourishing drinks, food fortification (add full-fat cream to mashed potato)

154
Q

MALNUTRITION
What is the second line management of malnutrition?
What are they?
Who overviews this care and what is their role?

A
  • Oral nutritional supplements (ONS)
  • Liquid/powder/semi-solid with macro + micronutrients (milkshake, semi-solid, soup)
  • Registered dietician Ax to take into account nutritional requirements, taste + texture preferences, suitability (vegan, halal), volume consideration (fluid restriction), cost into account > tailored prescription
155
Q

MALNUTRITION

What is the role of a dietician?

A
  • Only qualified HCP that assesses, Dx + Tx nutritional + dietary issues
  • Advice on therapeutic diets, appropriate feeding methods, identifies + advises on managing refeeding syndrome
156
Q

MALNUTRITION

If ONS fails, what two options for feeding are there and what is the difference?

A
  • Enteral feeding = direct feeding into gut via tube in the stomach, duodenum or jejunum
  • Parenteral feeding = IV access (often peripheral inserted central catheter, PICC line or central line) where gut feeding is inaccesible or unable to absorb sufficient nutrients
157
Q

MALNUTRITION

What are the 4 different types of enteral feeding?

A
  • Nasogastric tube = feeds into the stomach, can be inserted at ward level, short-term use (<30d)
  • Nasojejunal tube = feeds into jejunum, radiologically guided, short-term (<60d)
  • Percutaneous endoscopic gastrostomy = long-term enteral nutrition
  • Post-pyloric/percutaneous endoscopic jejunostomy = long-term enteral nutrition
158
Q

MALNUTRITION
How do you confirm NG tube position on insertion?
How do you confirm NJ tube position on insertion?

A
  • Check pH aspirate to (<5.5), XR confirmation second line

- Can’t check using pH requires XR

159
Q

MALNUTRITION

What are the indications for PEG?

A
  • Dysphagia (stroke, head + neck surgery, neuro conditions)
  • Cystic fibrosis (high nutritional requirements)
  • Oral nutrition intake inadequate + likely long-term
160
Q

MALNUTRITION

What are the indications for PEJ/surgical JEJ?

A
  • Delayed gastric emptying
  • Upper GI/pancreatic surgery
  • High risk of aspiration or severe acute pancreatitis
161
Q

MALNUTRITION
What are the advantages of enteral feeding?
What are the disadvantages of enteral feeding?

A
  • Preserves gut mucosa + integrity (NG/NJ), improves nutritional status, inexpensive compared to parenteral nutrition
  • Tolerance (nausea, satiety, bowels both constipation + diarrhoea), tube can be uncomfortable to place, reduced QOL + appearance issues
162
Q

MALNUTRITION

What are the indications for parenteral feeding?

A
  • Inadequate absorption (short bowel syndrome)
  • GI fistula
  • Bowel obstruction
  • Prolonged bowel rest
  • Severe malnutrition
  • Significant weight loss ± hypoproteinaemia when enteral therapy not possible
163
Q

MALNUTRITION
What are the advantages of parenteral feeding?
What are the disadvantages of parenteral feeding?

A
  • Easily tolerated

- Risk of line infection, expensive + invasive procedure

164
Q

OSTEOPOROSIS

What is osteoporosis?

A
  • Systemic skeletal disease characterised by low bone mass + micro-architectural deterioration of bone tissue with consequent increase in bone fragility + susceptibility to #
165
Q

OSTEOPOROSIS

What are 2 factors that are important in determining likelihood of an osteoporotic fracture?

A
  • Propensity to fall leading to trauma

- Bone strength

166
Q

OSTEOPOROSIS

What makes up bone strength?

A
  • Bone mineral density
  • Bone size
  • Bone micro-architecture
  • Bone mineralisation
167
Q

OSTEOPOROSIS

What happens to the bone micro-architecture in osteoporosis?

A
  • Trabecular thickness decreases, especially in the horizontal plane, meaning fewer connections between trabecular + so overall decrease in trabecular strength
168
Q

OSTEOPOROSIS

What is the pathophysiology of osteoporosis?

A
  • Imbalance between modelling + resorption
  • Inadequate formation of new bone during remodelling occurs
  • Excessive bone resorption (PTH can trigger this as RANK-ligand binds to RANK activating osteoclasts)
169
Q

OSTEOPOROSIS

What are 2 important components in calcium homeostasis?

A
  • Vitamin D

- Parathyroid hormone (PTH)

170
Q

OSTEOPOROSIS

What is the role of vitamin D?

A
  • Increased Ca2+ absorption in gut + released from bone
171
Q

OSTEOPOROSIS

What is the role of PTH?

A
  • Released from chief cells of parathyroid gland in response to low serum Ca2+ detected by Ca2+ sensor cells
  • Increased osteoclast activity, increased intestinal Ca2+ absorption, vitamin D activation + renal tubule reabsorption of Ca2+
172
Q

OSTEOPOROSIS

What are 2 important factors in osteoporosis development/primary causes?

A
  • Increasing age

- Post-menopause as oestrogen is protective

173
Q

OSTEOPOROSIS

What are the secondary causes/risk factors for osteoporosis?

A

SHATTERED

  • Steroids
  • Hyper/hypothyroid
  • Alcohol/smoking
  • Thin (low BMI)
  • Testosterone low (F)
  • Early menopause
  • Renal/liver failure
  • Relatives (FHx)
  • Erosive bone disease (RA)
  • Dietary Ca2+ low
174
Q

OSTEOPOROSIS

What is the clinical presentation of osteoporosis?

A
  • Develops asymptomatic where # often first sign at common sites
  • Distal radius = Colles’ # (fall on outstretched arms)
  • Proximal femur (neck of femur)
  • Vertebrae leading to shorter + stooped posture (lumbar, thoracic > kyphosis aka widow’s stoop)
  • Hip
175
Q

OSTEOPOROSIS

What investigations would you do in someone suspected of osteoporosis?

A
  • FBC, U+Es, TFTs, LFTs, biochemistry (Ca2+, phosphate, ALP + PTH all normal)
  • XR will show # (spinal = vertebral crush #)
  • Dual-energy x-ray absorptiometry (DEXA) scan gold standard to look at bone mineral density
176
Q

OSTEOPOROSIS
What does a DEXA scan look at?
What 2 scores are generated?

A
  • Lumbar spine + hip as commonly affected areas
  • T-score = standard deviation comparing how much higher/lower the patient’s bone density is to bone density of healthy 30y/o
  • Z-score compares bone condition to others of their demographics
177
Q

OSTEOPOROSIS

What DEXA T-scores are significant?

A

≤ -2.5 = osteoporosis (+ current fragility # = severe)

  • 2.5 < T-score ≤ -1 = osteopenia (low bone mass)
  • 1 < T-score < 1 = healthy
178
Q

OSTEOPOROSIS
What risk score can be calculated?
What does it tell you?

A
  • FRAX

- 10-year probability of fragility # (hip, major osteoporotic) for patients aged 40–90

179
Q

OSTEOPOROSIS

What factors are assessed in the FRAX score?

A
  • Personal = age, sex, weight, height
  • PMH = RA, previous #, secondary osteoporosis (renal/liver disease, coeliac, thyroid issues)
  • DH = glucocorticoids, lithium
  • FHx = parental hip #
  • Social = smoking, alcohol (≥3 drinks/day)
  • Other = femoral neck BMD
180
Q

OSTEOPOROSIS

What is the management of the various FRAX score outcomes?

A
  • Low risk = reassure, lifestyle, follow up in 5y
  • Intermediate = offer DEXA scan + Rx if appropriate
  • High risk = Rx
181
Q

OSTEOPOROSIS

What is the overall management of fragility fractures?

A
  • Any patient should have calcium + vitamin D supplementation as well as bisphosphonate regardless of biochemistry as usually normal anyway
182
Q

OSTEOPOROSIS

What is the lifestyle advice for osteoporosis management?

A
  • Quit smoking + alcohol
  • Weight-bearing exercise may increase BMD (walk)
  • Calcium + vitamin D rich diet + supplements (AdCal-D3)
  • Balance exercises to reduce risk of falls (tai chi)
183
Q

OSTEOPOROSIS

What pharmacological management is there for osteoporosis?

A
  • Bisphosphonates first line (alendronate)
  • Denosumab (s/c 6/12) human monoclonal antibody to RANK-ligand to increase BMD
  • HRT in early post-menopausal women
  • Teriparatide (recombinant human parathyroid peptide)
184
Q

OSTEOPOROSIS

What are the benefits and risks of HRT?

A
  • Reduces # risk, stops bone loss + prevents menopausal Sx

- Increased risk of breast cancer, stroke, CV disease + VTE

185
Q

OSTEOPOROSIS

What is an alternative to HRT?

A
  • Selective oestrogen-receptor modulators (SERMs) like raloxifene
  • Less breast cancer risk as stimulates oestrogen receptors just on bone
186
Q

OSTEOPOROSIS

How do bisphosphonates, denosumab, HRT + SERMs compare to teriparatide?

A
  • First lot are anti-resorptive meds which inhibits osteoclast activity + bone turnover
  • Teriparatide is anabolic which increases osteoblast activity + bone formation
187
Q

OSTEOPOROSIS

Give some examples of bisphosphonate regimes

A
  • PO 70mg alendronate once weekly
  • PO 35mg risedronate once weekly
  • IV 5mg zoledronate once yearly
188
Q

OSTEOPOROSIS

What is the mechanism of action of bisphosphonates?

A
  • Analogues of pyrophosphate, a molecule which decreases demineralisation in bone
  • Inhibit osteoclasts by reducing recruitment + promoting apoptosis
189
Q

OSTEOPOROSIS

What are some important instructions to patients taking bisphosphonates?

A
  • Take on empty stomach with plenty of water

- Stay upright (sitting/standing for 30m)

190
Q

OSTEOPOROSIS

What are some adverse effects of bisphosphonates?

A
  • Reflux + oesophagitis
  • Osteonecrosis of jaw
  • Atypical stress # (proximal femoral shaft)
191
Q

OSTEOPOROSIS
When should bisphosphonates be reviewed?
What is the process?
When should they be stopped?

A
  • After 5y on PO or 3y on IV
  • Reassess Rx, update FRAX score + DEXA scan
  • Consider holiday (18m-3y) if BMD improved + no fragility #
192
Q

OSTEOPOROSIS

What factors would make you have to continue bisphosphonate treatment?

A
  • On steroids
  • > 75y
  • Previous hip/vertebral # or further # on Rx
  • High risk FRAX
  • DEXA T score -2.5 or less after Rx
193
Q

COTE PHARMACOLOGY
What is the mechanism of action of acetylcholinesterase inhibitors?
Give some examples
What are the side effects?

A
  • Increase ACh as ACh is depleted in Alzheimer’s to slow disease progression + aid cognitive issues
  • Donepezil, rivastigmine
  • D+V, nausea, abdo pain (work systemically so GI upset), bradycardia
194
Q

COTE PHARMACOLOGY

What is the mechanism of action of N-methyl D receptor antagonists (NMDA)?

A
  • Protects brain cells from excess glutamate (excitatory neurotransmitter) released from cells affected by Alzheimer’s to prevent further damage, good for agitation + BPSD
195
Q

COTE PHARMACOLOGY
Give an example of NMDA?
What are some side effects?
When should it be avoided?

A
  • Memantine
  • Confusion, hallucinations, agitation, paranoid delusions
  • Do not give in renal failure (low GFR) as nephrotoxic
196
Q

INCONTINENCE

What is incontinence?

A
  • Involuntary leakage of urine/faeces at a time which is not socially acceptable
197
Q

INCONTINENCE

What are some causes of incontinence?

A
  • MS
  • Stroke
  • Parkinson’s
  • Spinal trauma
  • Cauda equina/cord compression
  • Brian tumour
  • Normal pressure hydrocephalus
198
Q

INCONTINENCE

What investigations would you do for incontinence?

A
  • Urine MC&S for infections
  • MRI spine of ?cord compression
  • MRI head if ?MS or Parkinson’s
  • Treat underlying cause if find one
199
Q

INCONTINENCE

What is the management of incontinence?

A
  • Pads, intermittent self-catheterisation or indwelling catheter
  • Permanent catheter if spinal cord damage/paralysis, surgery option if severe
200
Q

URINARY RETENTION

What is urinary retention?

A
  • Inability to empty the bladder due to obstruction or decreased detrusor power
201
Q

URINARY RETENTION

What are some causes of urinary retention?

A
  • BPH (#1 cause in men)
  • Urethral strictures
  • Anticholinergics
  • Alcohol
  • Constipation
  • Infection
  • Cancer
202
Q

URINARY RETENTION

How does acute urinary retention present?

A
  • Inability to pass urine, elderly may become agitated
  • Bladder tender on abdo exam
  • Contains around 600ml urine
203
Q

URINARY RETENTION

How does chronic urinary retention present?

A
  • More insidious onset, often painless
  • Bladder capacity may be >1.5L
  • Can present with overflow incontinence, acute-on-chronic retention, lower abdo mass, UTI or renal failure
204
Q

URINARY RETENTION

What might you find on clinical examination in urinary retention?

A
  • Abdo = palpate + percuss bladder to assess extent of retention + if tender
  • PR = ?enlarged prostate, check tone for ?cauda equina
205
Q

URINARY RETENTION

What other investigations would you do in urinary retention?

A
  • FBC, U+E, CRP/ESR, LFTs, TFTs, PSA
  • Urine MC&S for infections
  • CT if concerned about cancer
206
Q

URINARY RETENTION

What is the conservative management of urinary retention?

A

(Tips to aid voiding)

  • Analgesia
  • Walk around
  • Stand to void
  • Sound of running water
  • Hot bath
207
Q

URINARY RETENTION

What other management is there for urinary retention?

A
  • Catheterise acutely with ?intermittent self-catheterisation at home needed
  • Alpha-blocker tamsulosin to relax muscles in bladder neck making easier to urinate (+ effect on prostate for BPH)
208
Q

END OF LIFE CARE
What is palliative care?
What are the aims?
What does it involve?

A
  • Holistic Mx of a pt in whom death is likely to be soon + where curative Tx no longer possible
  • Help pt + relatives come to terms with death whilst optimising the quality of time left
  • MDT approach – physical Sx relief, social, psychological, spiritual + family support
209
Q

END OF LIFE CARE

What care should be given to an end of life patient?

A
  • Basic care ALWAYS (warmth, comfort, shelter, freedom from pain, cleanliness, PO nutrition + hydration)
  • Artificial nutrition + hydration is considered treatment so may be withheld
  • Simplify meds, s/c if possible
  • Communication v important
210
Q

END OF LIFE CARE

How does a patient at the end of their life present?

A
  • Sleepy, agitated, drifting in/out consciousness, confusion
  • Change in breathing pattern or dyspnoea
  • Decreased need for food + fluids
  • Loss of bladder or bowel control
  • Cold/bluish extremities, mottled skin
  • Death rattle
211
Q

END OF LIFE CARE
What is the death rattle?
Is this dangerous?
How is it managed?

A
  • Reduced ability to clear saliva + mucous from back of throat + hypersecretion leading to noisy airway
  • No, not painful or uncomfortable
  • Hyoscine butylbromide if distressing
212
Q

END OF LIFE CARE

What issues presenting at the end of life can be managed pharmacologically?

A
  • Pain
  • Dyspnoea
  • Agitation + anxiety
  • Nausea
  • Constipation
213
Q

END OF LIFE CARE
In terms of managing end of life care, what should be given for…

i) regular medication?
ii) pain + dyspnoea?
iii) agitation, anxiety, dyspnoea?
iv) Nausea, agitation?
v) Constipation?

A

i) Syringe driver
ii) Morphine or oxycodone
iii) Midazolam
iv) Haloperidol (other anti-emetics can be used like ondansetron)
v) Start with stimulant laxative (senna) as opiates decrease peristalsis or stool softener if not on opiates, if not suppositories, enemas, PR evacuation

Phase 3a Revision (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions