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Y4 OPIC > OPMH > Flashcards

OPMH Flashcards

1
Q

AD

A

Chronic, neurodegenerative disorder characterised by the progressive accumulation of abnormal protein deposits, primarily amyloid plaques and tau tangles, in the brain

Leads to deterioration of cognitive function, memory loss & various behavioural and psychological symptoms

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2
Q

AD risk factors

A

Increasing age

FHx of Alzheimer’s disease

Genetic predisposition

  • mutations in the amyloid precursor protein, presenilin 1 & presenilin 2

Apoprotein E allele E4

Caucasian ethnicity

Down’s syndrome

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3
Q

AD pathological changes

A

Macroscopic: widespread cerebral atrophy, particularly involving the cortex & hippocampus

Microscopic: cortical plaques due to deposition of type A-beta-amyloid protein & intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein

Biochemical: deficit of acetylcholine from damage to an ascending forebrain projection

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4
Q

AD clinical features

A

Memory impairment - early in the disease → difficulties in recalling recent events & conversations

Language impairment - difficultly finding words, struggling to express oneself & aphasia

Executive dysfunction - impaired ability to plan, organize & carry out tasks → difficulties in activities of daily living

Behavioural changes - agitation, aggression or apathy

Psychological symptoms - hallucinations, delusions & paranoia can occur

Disorientation - unable to recognize places or people

Loss of motor skills - motor skills decline, leading to difficulties with mobility and self-care

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5
Q

AD ix

A

History - Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) / Functional Activities Questionnaire (FAQ)

  • assess cognitive decline using an approved scoring tool eg. MMSE, MOCA

Examination - neuro

Bloods - confusion screen → FBC, U&E, LFT, CRP/ESR, Ca2+, TFTs, B12, folate, syphilis, HIV

Neuroimaging

Cerebrospinal fluid analysis

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6
Q

AD general management principles

A

Non-pharmacological approaches - psychological interventions, cognitive stimulation therapy & OT

Support for carers

Patient-centred care

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7
Q

AD pharmacological mx

A

Acetylcholinesterase inhibitors (donepezil, galantamine & rivastigmine) options for managing mild to moderate AD

  • donepezil is relatively contraindicated in patients with bradycardia
    • adverse effects include insomnia

Memantine = 2nd line

  • moderate AD for those who have contraindication to first line
  • add-on drug
  • monotherapy in severe AD

Antipsychotics should only be used for patients at risk/agitation causing severe distress

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8
Q

FTD

A

Heterogenous group of neurodegenerative disorders characterised by progressive atrophy of the frontal and/or temporal lobes of the brain → impairments in behaviour, personality, language & motor functions

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9
Q

FTD clinical features

A

Personality changes - disinhibited behaviour and apathy early on

Language impairments - early language difficulties to severe aphasia

Cognitive decline - executive function is frequently impaired

Motor abnormalities - features of MND

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10
Q

FTD ix

A

Neuroimaging - atrophy of frontal and/or temporal lobes, focal gyral atrophy & knife-blade appearance

Genetic testing - if inherited form is suspected

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11
Q

FTD mx

A

Focused on alleviating symptoms and providing support

Behavioural interventions - counselling, behaviour modification strategies

Pharmacotherapy - SSRIs & antipsychotics

Supportive care - SALT, physio & OT to help manage the impacts of the disease on daily functioning

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12
Q

Vascular dementia

A

Umbrella term denoting a collection of cognitive impairment syndromes caused by cerebrovascular disease

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13
Q

Vascular dementia subtypes

A

Stroke-related VD - multi-infarct or single-infarct dementia

Subcortical VD - caused by small vessel disease

Mixed dementia - presence of both VD & Alzheimer’s disease

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14
Q

Vascular dementia risk factors

A

Hx of stroke or TIA

AF

HTN

DM

Hyperlipidaemia

Smoking

Obesity

Coronary heart disease

FHx of stroke or cardiovascular

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15
Q

Vascular dementia clinical features

A

Progressive, stepwise deterioration in cognition (over a span of several months to years)

Focal neurological abnormalities eg. visual disturbance, sensory or motor symptoms

Difficulty with attention & concentration

Seizures

Memory disturbance

Gait disturbance

Speech disturbance

Emotional disturbance

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16
Q

Vascular dementia ix

A

Comprehensive H&E

Formal cognition screening - MMSE or MoCA

Medication r/w to exclude medication-induced cognitive impairment

Exclusion of reversible organic causes

Neuroimaging (MRI head) - extensive white matter change & infarcts evident

17
Q

Vascular dementia mx

A

Detection of and addressing cardiovascular risk factors

Cognitive stimulation programmes - music & art therapy

Symptomatic treatment - cholinesterase inhibitors/memantine if co-morbid AD, PD, dwLD

Advanced care planning to prepare for progressive cognitive and physical decline

18
Q

DLB

A

Dementia with Lewy bodies (DLB) is a type of progressive dementia caused by deposits of an abnormal protein, alpha-synuclein, forming cytoplasmic inclusions known as Lewy bodies within brain cells

Aggregates disrupt normal cell functioning & eventually lead to neuronal death

19
Q

DLB clinical features

A

Progressive cognitive impairment

  • typically occurs before parkinsonism, but both features usually occur within a year of each other
  • in contrast to Parkinson’s disease → motor symptoms typically present at least one year before cognitive symptoms
  • cognition may be fluctuating
  • early impairments in attention & executive function

Parkinsonism

Visual hallucinations

20
Q

DLB ix

A

Diagnosis primarily clinical

DaT scan: can help distinguish DLB from other types of dementia

Neuropsychological testing: assess cognitive functioning and fluctuations

EEG: not diagnostic but a slowing background rhythm

21
Q

DLB mx

A

Cognitive stimulation, physical therapy & occupational therapy

Supportive care: palliative & EoL care considerations are essential

Medications: cholinesterase inhibitors can help manage cognitive symptoms

  • caution required with antipsychotic meds due to neuroleptic sensitivity
22
Q

DLB complications

A

Rapid disease progression

Severe neuroleptic activity

23
Q

Delirium

A

Acute and fluctuating disturbance in attention and cognition, often accompanied by a change in consciousness

Typically reversible & frequently seen in the elderly

24
Q

Delirium types

A

Hyperactive - marked by increased psychomotor activity, restlessness, agitation & hallucinations

Hypoactive - characterised by lethargy, reduced responsiveness & withdrawal

Mixed delirium - combines features of both hyperactive and hypoactive

25
Q

Delirium aetiology

A

DELIRIUMS

D - drugs and alcohol (anti-cholinergics, opiates, anti-convulsants, recreational)

E - eyes, ears and emotional disturbances

L - low output state (MI, ARDS, PE, CHF, COPD)

I - infection

R - retention (of urine/stool)

I - ictal (related to seizure activity)

U - under-hydration/under-nutrition

M - metabolic disorders

S - subdural haematoma, sleep deprivation

26
Q

Delirium clinical features

A

Disorientation

Hallucinations - visual or auditory

Inattention

Memory problems

Change in mood or personality

  • sundowning = agitation & confusion worsening in the late afternoon/evening

Disturbed sleep

27
Q

Delirium ix

A

4AT and CAM

Bedside - bladder scan, review meds, ECG, urine MC&S

Bloods - FBC, U&Es, LFTs, TFTs, blood cultures

Imaging - CXR, USS abdomen, neuroimaging

28
Q

Delirium mx

A

Treating the underlying cause

Non-pharmacological strategies

  • providing an environment with good lighting
  • maintaining a regular sleep-wake cycle
  • regular orientation and reassurance
  • ensuring the patient’s glasses & hearing aids are used if needed

Agitated/potential danger = small doses of haloperidol/lorazepam

Y4 OPIC (4 decks)

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