Dementia & Alzheimer's disease flashcards
23 high-yield MRCP Part 1 cards from the Intellect Medicos Geriatrics & Palliative Care course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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The most common cause of dementia is ______ (over 50%), followed by vascular dementia (about 20%).
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Alzheimer's disease
Why? Dementia with Lewy bodies (~15%) and frontotemporal dementia make up most of the rest.
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The most common cause of dementia is Alzheimer's disease (over 50%), followed by ______ (about 20%).
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vascular dementia
Why? Dementia with Lewy bodies (~15%) and frontotemporal dementia make up most of the rest.
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Name three brief cognitive tests NICE suggests for assessing suspected dementia in non-specialist settings.
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Any three of: 6CIT, 10-point cognitive screener (10-CS), 6-item screener, Memory Impairment Screen, Mini-Cog, Test Your Memory.
Why? These are quick, validated screens. Specialist clinics use fuller tests such as ACE-III or MMSE.
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Name four blood tests in the reversible-cause screen for suspected dementia.
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Any four of: FBC, U&E, LFTs, calcium, TFTs, B12 and folate, glucose, ESR/CRP.
Why? Hypothyroidism, B12 deficiency, hypercalcaemia and other metabolic problems can cause treatable cognitive decline.
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Name three structural causes that CT or MRI aims to exclude in suspected dementia.
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Normal pressure hydrocephalus, tumour and subdural haematoma.
Why? These are potentially treatable, so structural imaging is part of the standard work-up.
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What is the classic triad of normal pressure hydrocephalus?
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Gait disturbance (magnetic, broad-based), urinary incontinence and dementia.
Why? Enlarged ventricles stretch periventricular fibres to the legs and bladder; gait problems usually come first.
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Which peptide forms the extracellular plaques in Alzheimer's disease, and from which protein?
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Amyloid-β 42 (Aβ42), from amyloid precursor protein (APP).
Why? In AD, APP is cleaved by β- and γ-secretase instead of α-secretase, producing sticky neurotoxic Aβ42 that aggregates into plaques.
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Neurofibrillary tangles in Alzheimer's disease are made of ______ protein inside neurons.
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hyperphosphorylated tau
Why? Tau normally stabilises microtubules; once hyperphosphorylated it clumps into tangles and the neuron dies.
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Loss of neurons in which nucleus causes the acetylcholine deficit in Alzheimer's disease?
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The nucleus basalis of Meynert.
Why? This cholinergic nucleus projects to the cortex; its loss is the rationale for cholinesterase inhibitors.
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Which brain region is the earliest and most marked site of atrophy in Alzheimer's disease?
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The hippocampus (medial temporal lobe), then temporal and parietal lobes.
Why? The hippocampus is the memory centre, which is why short-term memory loss is the first symptom.
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Name the three genes linked to familial early-onset Alzheimer's disease.
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APP, PSEN1 (presenilin 1) and PSEN2 (presenilin 2).
Why? All three increase production of Aβ42. They are autosomal dominant and cause early-onset disease.
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What is the strongest genetic risk factor for late-onset Alzheimer's disease?
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The ApoE4 (apolipoprotein E ε4) allele.
Why? ApoE4 is a susceptibility gene (chromosome 19); it raises risk but does not make AD certain.
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Why do people with Down syndrome develop Alzheimer's disease early?
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They have three copies of chromosome 21, which carries the APP gene, so they overproduce amyloid.
Why? Extra APP means more Aβ42 and earlier plaque formation, often from the 40s.
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What is the first-line non-drug intervention for mild to moderate Alzheimer's disease?
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Cognitive stimulation (group cognitive stimulation therapy), with memory aids and structured routines.
Why? NICE recommends offering group cognitive stimulation therapy to people with mild to moderate dementia.
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What is the first-line drug class for mild to moderate Alzheimer's disease?
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Acetylcholinesterase inhibitors: donepezil, rivastigmine or galantamine.
Why? They boost cholinergic transmission to compensate for the loss of cholinergic neurons. NICE NG97 recommends them as monotherapy for mild to moderate AD.
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What is the mechanism of action of donepezil?
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Reversible inhibition of acetylcholinesterase, raising acetylcholine in the synapse.
Why? Less breakdown of acetylcholine improves cholinergic signalling for memory and learning.
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Name three side effects of acetylcholinesterase inhibitors.
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Any three of: nausea, vomiting/diarrhoea, bradycardia, weight loss (also insomnia/vivid dreams).
Why? These are cholinergic (parasympathetic) effects on the gut and the heart.
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Which cardiac problems are a caution or reason to avoid donepezil?
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Bradycardia and heart block (including sick sinus syndrome).
Why? The vagotonic effect slows the heart and can cause syncope and falls.
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What is the mechanism of action of memantine?
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NMDA (glutamate) receptor antagonist.
Why? It blocks excess glutamate-driven excitotoxicity.
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When is memantine used in Alzheimer's disease?
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Moderate AD if cholinesterase inhibitors are not tolerated or contraindicated; severe AD (alone or added to a cholinesterase inhibitor).
Why? NICE NG97: memantine monotherapy for moderate disease when AChE inhibitors cannot be used, and for severe disease; consider adding it in moderate disease, offer it in severe.
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When should antipsychotics be used for behavioural symptoms in dementia?
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Only if there is risk of harm to self/others or severe distress from agitation, hallucinations or delusions — lowest dose, shortest time.
Why? They raise the risk of stroke and death in dementia. NICE NG97 advises reassessing at least every 6 weeks.
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What is the target of lecanemab and donanemab?
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Amyloid-β — they are anti-amyloid monoclonal antibodies that clear plaques.
Why? They are disease-modifying drugs for early Alzheimer's disease (mild cognitive impairment or mild dementia).
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What is the main serious adverse effect of anti-amyloid antibodies such as lecanemab?
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Amyloid-related imaging abnormalities (ARIA): brain oedema/swelling and microhaemorrhages.
Why? Clearing amyloid from vessel walls makes them leaky. MRI monitoring is needed and the risk is higher in ApoE4 carriers.