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Medicine Year 2 > People and Illness Week 4 > Flashcards

People and Illness Week 4 Flashcards

1
Q

Describe mild cognitive impairment

A
  • Subjective awareness of cognition problem (e.g. memory), doesn’t impact on day-to-day function, would perform below expected on neuropsychological testing
  • Higher risk of progressing to frank dementia
  • Lifestyle and medical intervention to prevent progression
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2
Q

Describe the pathology of Pick’s disease

A
  • Phosphorylated Tau accummulation causing Pick body formation
  • Walnut brain, knife edge atrophy - very severe atrophy, advanced in frontal region
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3
Q

Compare CJD to Alzheimer’s disease

A
  • Similarities
    • Both fatal neurodegenerative diseases
    • Inherited and sporadic forms
    • Amyloid deposits
    • Increased beta-sheet secondary structures
  • Differences
    • Unrelated protein aggregates - APP vs PrPc
    • PrPsc is infectious
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4
Q

Describe the protein aggregation which causes dementia with Lewy bodies

A
  • Alpha synuclein aggregates
  • Misfolding into beta-pleated sheet structure of alpha-synuclein (dimers, trimers and oligomers) that further aggregate into higher-order insoluble structures (fibrils) - building blocks for Lewy bodies
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5
Q

Define delirium

A

Acute neuropsychiatric syndrome characterised by confusion

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6
Q

Compare Tau in a physiological state to Tau in a pathological state

A
  • Physiological Tau - balance between phosphorylated and non-phosphorylated Tau, allows neurite growth, axonal transport, microtubule dynamics
  • Pathological Tau - too much phosphorylated Tau = Tau filament formation (neurofibrillary tangles), microtubule dysfunction, cell death
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7
Q

List the risk factors for Alzheimer’s disease

A
  • Increasing age - 2x risk every 5 years from 60
  • Genetics -
    • Early onset familial - amyloid precursor protein (APP), presenilin-1/2
    • Sporadic - apolipoprotein 4 allele (APOE4)
  • Down syndrome
  • Female gender (2/3 are female)
  • Head injury
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8
Q

Describe the tertiary structure of proteins

A
  • Overall conformation of protein/3D arrangement
  • Stabilised by interactions between R groups
    • Hydrophobic interactions between non-polar R groups
    • Hydrogen bonds between polar R groups
    • Disulfide bonds
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9
Q

Give examples of disorders of praxis

A
  • Dyspraxia/apraxia - errors of action conception (knowledge of actions/item function), action production (production/control of movement)
  • E.g. ideational apraxia, imitation of gestures, orobuccal movement, use of imagined objects, lower limb apraxia
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10
Q

List the hallmark features of delirium

A
  • Impaired consciousness
  • Hyperactivity (active, tachycardic) or hypoactive subtype (reduced alertness, may look depressed) - can alternate between
  • Fluctuation in mental state - more disturbed overnight
  • Acute onset - hours to days
  • Change in cognition from baseline, cognitive deficits
  • Visual hallucinations (and other pyschiatric symptoms e.g. delusions)
  • Sleep-wake cycle disruption
  • Affect changes
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11
Q

How is glutamate involved in Alzheimer’s disease?

A
  • Major excitatory neurotransmitter, acts on NMDA and AMPA receptors
  • NMDA - permeable to calcium ions, blocked by magnesium (voltage-dependent blockade), long-term potentiation (slow gated kinetic)
  • Memtantine replaces glutamate to stimulate NMDA receptor
  • Long-term potentiation - long-lasting enhancement of the effectiveness of synaptic transmission
  • Calcium activated kinases - increase effectiveness of existing receptors, increase number of receptors
  • In Alzheimer’s
    • Reduced glutamate clearance - chronic over-activity (excitotoxicity) could be part of pathology - disrupts memory formation via NMDA
    • Glutamate loss - reduction of pyramidal neurons - entorhinal cortex, CA1 and subiculum areas of hippocampus (glutamate containing)
    • Reduction in NMDA receptors in the hippocampus and neocortex
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12
Q

How common is Alzheimer’s disease

A

60% of neurodegenerative dementias

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13
Q

List the types of dementia

A
  1. Alzheimer’s - most common
  2. Vascular
  3. Dementia with Lewy bodies
  4. Frontotemporal
  5. Mixed - common but not often diagnosed (two distinct/discreet patholgies within brain)
  6. Other
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14
Q

Describe frontotemporal dementias

A
  • Sporadic/inherited
  • Heterogenous group of dementias
  • Younger patients - 45-65
  • Frontal lobe dysfunction - behavioural/personality changes, disinhibition, depression, agitation
  • Cognitive and memory impairment
  • E.g. Pick’s disease
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15
Q

Describe the differential psychiatric diagnosis for dementia

A
  • Normal aging
  • Delirium
  • Mild cognitive impairment
  • Amnestic syndrome - Korsakoff’s
  • Chronic brain damage e.g. head injury or anoxia (static level of impairment)
  • Depression - pseudo-dementia
  • Late onset schizophrenia or other psychosis
  • Learning disability - same level of impaired function throughout life
  • Malingering presentation - feigns illness for secondary gain
  • Dissociation - after psychological trauma
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16
Q

List the further investigations done in dementia diagnosis

A
  • HIV + syphillus serology
  • Chest X-ray
  • CT/MRI - atrophy of brain, vascular disease
  • EEG - electrical activity in brain (delirium = diffuse slowing)
  • Lumbar puncture
  • ECG
  • SPECT - blood flow in brain, also dopamine (for Lewy body dementia/Parkinson’s disease dementia)
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17
Q

How do proteinopathies cause disease?

A

Accumulation of misfolded proteins results in aggregates, thereby gaining toxic activity or losing the normal function

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18
Q

Describe the pharmacological treatment of dementia with Lewy bodies

A
  • Antipsychotics cause significant mortality/morbidity
  • Rivastigmine (cholinesterase inhibitor) improves
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19
Q

Which area of the brain is responsible for praxis?

A

Usually L hemisphere - parietal and frontal lobe

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20
Q

What causes the behavioural and psychiatric symptoms of dementia?

A
  • Complex cortical-subcortical circuits that affect behaviour and areas of brain atrophy/dysfunction
  • Depression associated with reduced monoaminergic function
  • Agitation and aggression associated with cholinergic deficit and increased D2/3 receptor availability in striatum
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21
Q

List types of proteinopathies, aggregated proteins involved and the neurodegenerative diseases which result

A
  • Amyloidosis
    • A-beta accumulates
    • Causes Alzheimer’s disease
  • Prionopathy
    • PrP accumulates
    • Causes Crutzfeldt-Jakob disease
  • Tauopathy
    • Hyperphosphorylated Tau accumulates
    • Causes frontotemporal lobar degeneration, Alzheimer’s disease, progressive supranuclear palsy and Pick’s disease
  • Synucleopathy
    • Alpha-synuclein accumulates
    • Causes Parkinson’s disease, Lewy body disease
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22
Q

Describe the mechanism of action of cholinesterase inhibitors

A

Low Ach causes cognitive symptoms (especially nucleus basalis of Meynert), cholinesterase breaks down acetyl choline from synapse - anticholinesterase inhibitors stop breakdown of acetyl choline, increase cholinergic action

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23
Q

List the routes of transmission in Prion diseases

A
  • Sporadic Creutzfeldt-Jakob disease – unknown
  • Iatrogenic CJD – exposure to contaminated hormones, tissues, blood products
  • Variant CJD – ingestion of contaminated food
  • Kuru – ritualistic cannibalism
  • Familial CJD – genetic (germline PRNP mutations)
  • Gerstmann-Straussler-Scheinkler syndrome – genetic (germline PRNP mutations)
  • Fatal familial insomnia – genetic (germline PRNP mutations)
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24
Q

Which area of the brain is responsible for calculation?

A

L hemisphere - angular gyrus in parietal lobe crucial

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25
Q

List the pharmacological treatments of dementia

A
  • Cognition enhancers, 2 classes
    • Cholinesterase inhibitors e.g. rivastigmine, donepezil, galantamine - liscensed for mild to moderate Alzheimer’s disease and Parkinson’s disease dementia
    • Partial glutamine agonist - memantine, licensed for moderate to severe Alzheimer’s disease
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26
Q

Describe the control of protein folding by the ER

A
  • Newly synthesised glycoprotein, gets glycosylated (add sugar groups)
  • Glucosidase I and II cleave off sugar groups
  • Gives binding sites for chaperones e.g. calnexin and calreticulin, allow time for protein to fold and find correct conformation
  • Glucosyltransferase determines if it is correctly folded or not
  • Correctly folded à exits ER
  • Incorrectly folded à glucosyltransferase adds sugar groups, try to refold
  • Eventually will stop trying to refold – must have mutation, removed by ER-associated protein degradation (proteasome)
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27
Q

Describe the aetiology of delirium

A

Predisposing factors (age, dementia, vascular disease, drugs) + precipitating factors

Precipitating factors

  • Infection
  • Stroke
  • Drugs e.g. opioids, steroids, digoxin
  • MI
  • Fractures
  • Cancer
  • Electrolyte/fluid balance problems
  • Heart failure
  • Diabetes
  • PVD
  • Alcohol withdrawal
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28
Q

Describe the normal brain changes which occur with aging

A
  • Loss of brain volume, atrophy with age
  • Increase in forgetfulness after age 50, slowing of response times, physical changes (vision, hearing, sensory/motor impairment)
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29
Q

What are molecular chaperones?

A
  • Any protein that interacts with, stabilises or helps another protein acquire its functionally active conformation, without being present in its final structure
  • Selectively binds to short stretches of hydrophobic amino acids, provides safe environment for folding
  • Different classes of structurally unrelated chaperones exist, forming cooperative pathways/networks
  • Proteome-maintenance functions - de novo folding, refolding, oligomeric assembly, protein trafficking, proteolytic degradation
  • Can also use chaperonin - form cylinder into which new polypeptide is placed, safe environment for folding
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30
Q

Describe transmissible spongiform encephalopathies/Prion diseases

A
  • Family of rare, progressive and fatal neurodegenerative diseases
  • Loss of motor coordination and behavioural changes
  • Can be inherited, sporadic, acquired
  • Long incubation periods
  • Characteristic spongiform changes associated with neuronal loss, and a failure to induce an inflammatory response
  • Aetiological agent = prion
    • PrPc (normal) à PrPsc (infectious)
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31
Q

Describe the secondary structure of proteins

A
  • Alpha helices
    • Results from H bonds forming between carbonyl oxygen atom of each peptide bone with the amide H atom from an amino acid 4 positions towards the C-terminus
    • Results in periodic spiral, 3.6 amino acids per turn
    • Confers directionality on the helix
    • R groups face outwards, covering the helix
  • Beta pleated sheets
    • Each strand is 5-8 amino acid residues
    • Hydrogen bonding between strands of polypeptides forms the planar sheet
    • Directionality - parallel or anti-parallel
    • R groups project from both faces of the sheet
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32
Q

Describe the prevalence of dementia

A

65+ prevalence is 7.1%

1 in 79 of entire UK population

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33
Q

Describe the structure of neurofibrillary tangles

A
  • Main components of tangles are paired helical filaments - long fibrous proteins ‘braided’ together, typical flame shape
  • Consists of the microtubule-associated protein Tau
34
Q

Describe the non-pharmacological treatment/prevention of delirium

A
  • Control noise and lighting
  • Orientating influences - calendars, clocks, familiar objects, family
  • Fluid balance, diet, bowel habit, pain control
  • Regular communication/reassurance from staff, address sensory impairment
  • Limit variation in staff
  • Encourage normal sleep cycle and side room if possible
  • Early mobilisation
  • Avoid ward transfers
  • Consider necessity of some procedures
  • Recognise frailty
35
Q

Describe the use of antipsychotics in dementia

A
  • Use in
    • Severe agitation
    • Risk of harm to themselves or others - usually physical aggression
    • Psychosis - watchful waiting first
  • Not for - insomnia, wandering, abnormal vocalisations
  • If stable for 3 months then cautiously withdraw, lowest possible effective dose for shortest possible time
36
Q

When are cholinesterase inhibitors used/not used?

A

1st line treatment for Alzheimer’s, small improvement in Parkinson’s disease dementia, not useful in frontotemporal dementia, vascular dementia or mild cognitive impairment

37
Q

Describe the amyloid hypothesis

A
  1. A beta monomers
  2. A beta oligomers
  3. A beta fibrils and plaques
  4. Inflammatory response - Tau aggregates and tangles
  5. Synaptic and neuronal loss
  6. Inflammatory responses - cognitive decline and disability

Secondary structure changes - alpha helix to beta sheets

38
Q

Describe the structure of proteins

A
  • Primary - sequence of amino acids in polypeptide chain
  • Secondary - local folding, hydrogen bonds, alpha helices and beta pleated sheets
  • Tertiary - long range folding
  • Quaternary - multimeric organisation, subunits (e.g. haemaglobin)
  • Supramolecular - large scale assemblies (e.g. collagen)
  • Structure determines function - regulation, movement, signalling, transport, catalysis
39
Q

List causes of dementia/apparent dementia

A
  • Parenchymal/degeneration
    • Alzheimer’s disease, vascular dementia, fronto-temporal dementia, Parkinson’s disease, Huntington’s disease, Wilson’s disease, MS, progressive supranuclear palsy
  • Intracranial
    • Tumour, head injury, subdural haematoma, cerebrovascular accident, normal pressure hydrocephalus
  • Infection
    • Crutzfeldt-Jakob disease, neurosyphillus, HIV associated dementia, TB
  • Endocrine
    • Hypothyroidism, hyperparathyroidism, Cushing’s and Addison’s
  • Metabolic
    • Uraemia, hepatic encephalopathy, hypogylycaemia, hypo/hypercalcaemia, hyper/hypomagnaesmia
  • Vitamin deficiency
    • B12, folate, thiamine, niacin
  • Toxins
    • Alcohol, lead
40
Q

List the standard blood tests done in diagnosis of dementia

A
  • Full blood count
  • Inflammatory markers - ESR, CRP
  • Glucose
  • U + E (renal)
  • LFTs
  • Thyroid function
  • Bone profile - calcium
  • Urinalysis
  • B12, folate
41
Q

Describe visuospatial skills

A
  • Process and identify what is around you and link this to position in space
  • Visual cortex, projects to parietal lobe (sensory - spatial positioning and orientation) and temporal lobe (recognising things)
42
Q

Describe the cause of vascular dementia

A
  • Not neurodegenerative, underlying vascular pathology
    • Small vessel disease - subcortical infarcts
    • Large vessel disease - cortical multi-infarcts
  • Hypertension
  • Vascular risk factors - smoking, diabetes
43
Q

When are proteins degraded by proteosomes?

A

Short half-life

Key metabolic enzymes

Defective proteins

44
Q

Give examples of disorders of language

A

Aphasia - speaking

Agraphia - writing

Alexia - reading

Dysphasia (e.g. Wernicke’s and Broca’s) - speech

45
Q

Describe the pathology of vascular dementia

A
  • Brain weight normal, no significant atrophy
  • Areas of cystic disruption - previous infarcts
  • Mild ventriculomegaly
  • Loss of white matter
  • Red eosinophilic neurons - normally more basophillic (= red dead neurons - one of the earliest changes seen in brain in ischaemia, within 30 minutes)
46
Q

Describe the clinical features of dementia with Lewy bodies

A
  • Progressive cognitive decline
  • Fluctuating consciousness
  • Visual hallucinations
  • Parkinsonism - motor disorders
47
Q

Define anterograde and retrograde amnesia

A

Anterograde amnesia - not able to recall newly experienced information/memories from after disease process has set in

Retrograde amnesia - past information/before disease process has set in

48
Q

How are the behavioural and psychiatric symptoms of dementia treated?

A
  • Antidepressants - SSRIs sertraline and citalopram reduce agitation
  • Cholinesterase inhibitors - reduce severity of neuropsychiatric symptoms, greatest effect on apathy
  • Memtantine - slightly less likely to develop agitation, larger effect in moderate to severe AD
  • Antipsychotics - atypical especially risperidone (licensed) and aripiprazole mainly for severe agitation/aggression, harmful - increase CV risk and mortality
49
Q

Describe the ubiquitin-proteasome system

A
  • Proteasomal degradation of proteins
  1. Polyubiquitination - minimum of 4 polyubiquitin tags
  2. PolyUb protein recognised by CAP of proteasome
  3. PolyUb removed, protein unfolded
  4. Protein threaded through proteasome
  5. Proteolysis
50
Q

Describe the effects of mild, moderate and severe cortical atrophy in Alzheimer’s

A
  • Mild - memory loss, confusion, trouble handling money, poor judgement, mood changes, anxiety
  • Moderate - increased memory loss and confusion, problems recognising people, difficulty with language and thoughts, restlessness, agitation, wandering and repetitive statements
  • Severe - completely dependent requiring nursing home care, weight loss, seizures, increased sleeping, loss of bladder and bowel control, death usually occurs from pneumonia
51
Q

When are proteins degraded by lysosomes?

A

Long half-life, membrane proteins, extracellular proteins

52
Q

Describe the pathology of Alzheimer’s disease

A
  • Reduced brain weight (normal = 1250-1500g, 96g less in Alzheimer’s)
  • Forebrain:hindbrain, normal is 8-10:1
  • Macroscopic
    • Enlarged ventricles - bilateral ventriculomegaly (due to atrophy)
    • Temporal lobe atrophy (sulcal widening)
    • Neocortical grey matter thinned
    • Entorhinal cortex then hippocampus affected first
  • Microscopic
    • Two types of lesion - neurofibrillary tangles, amyloid plaques
    • Neurofibrillary tangles - phosphorylated Tau, in cytoplasm
    • Amyloid plaques - neuritic plaques (cerebral amyloid angiopathy, vessels hard and prone to rupture) in extracellular space
53
Q

Compare the pathology of Parkinson’s disease to dementia with Lewy bodies

A
  • Parkinson’s - pathology in nigrostriatal system, clinical effect = extrapyramidal movement disorder
    • Alpha-synucleinopathy in cortex, SN/LC, dorsal vagal nucleus, myenteric plexus, autonomic ganglia
  • Dementia with Lewy bodies - pathology in cerebral cortex, clinical effect = dementia
    • Alpha-synucleinopathy in cortex, SN/LC, dorsal vagal nucleus and myenteric plexus
54
Q

What determines protein folding?

A
  • Proteins self-assemble into 3D conformation
  • Protein conformation determined by primary structure
  • Hydrophobicity important - some R groups are very hydrophobic, in a hydrophilic environment so need hydrophilic groups on outside
  • Tendency for proteins to aggregate - folding takes time, environment is highly crowded (concentrations 300-400g/l)
55
Q

Define proteostasis

A

Protein homeostasis - synthesis, folding, processing, assembly, degradation, localisation, trafficking

Loss of proteostasis contributes to pathogenesis of many human pathologies (including Alzheimer’s disease)

56
Q

Describe the cognitive testing done in dementia diagnosis

A
  • Addenbrooke’s cognitive examination - 100-point test, more senitive than MMSE in early disease, covers executive function, time consuming (cut-off scores - 88/82)
  • MMSE - easier, faster, shouldn’t have variation in scoring, insensitive to early impairments, poorly covers executive function, influenced by age/education/socioeconomic status, useful screening tool and good for monitoring change
57
Q

List the side effects of cholinesterase inhibitors

A

Nausea, vomiting, diarrhoea, muscle cramps, dizziness, fatigue, anorexia, cardiac adverse events, peptic ulcers/GI bleeding

Monitor BP, HR and GI side effects

58
Q

Describe the pharmacological management of delirium

A
  • Used if non-pharmacological methods ineffective, risk to self or others, actively hallucinating/psychosis
  • Treat medical problem
  • Treat delirium
    • Antipsychotics - haloperidol, olanzapine, risperidone, aripipoazole, quetiapine
    • Benzodiazepines - lorazepam, diazepam (in alcohol/substance abuse withdrawal or seizure disorders)
    • Other - melatonin (sleep), trazodone (anti-depressant - low doses manage agitation and correct sleep cycle/affect)
59
Q

Define executive reasoning

A

Group of cognitive skills e.g. planning, decision making, motivation, setting goals

Controlled by the frontal lobes

60
Q

Describe the normal and abnormal function of APP

A
  • Normal function unclear, widespread in CNS
    • Normal cleavage (non-amyloidogenic) - cleaved just above transmembrane domain by alpha secretases to give sAPP alpha
  • Abnormal cleavage (amyloidogenic)
    • Cleaved by beta secretases above transmembrane domain to give sAPP beta, then in the transmembrane domain by gamma secretases (contain presenilin) to give A beta
61
Q

What are the methods of protein degredation?

A

Lysosomal or proteosomal

62
Q

List causes of Tau aggregation

A
  • Imbalances of kinases and phosphatases (Cdk5 and GSK3 beta)
  • Tau gene mutations
  • Covalent modifications of Tau - change in conformation, dissociation from microtubules
  • = detachment of Tau from microtubules, increased unbound Tau, misfolded Tau, pretangles, beta-sheet containing structures, neurofibrillary tangles
63
Q

Describe the general clinical features of dementia

A
  • Syndrome with chronic, progressive (usually irreversible) cognitive impairment due to brain disease
  • Deterioration from higher level of function
  • Multiple cognitive deficits
  • Chronic duration >6 months
  • Impact on social/occuptational function
  • Personality change/disintegration (more in some types than others, especially frontotemporal)
  • Decline in emotional control/motivation
64
Q

Describe the pathology of prion diseases

A
  • Neuronal loss, ‘vacuolation’ – spongiform cerebral cortex
  • Amyloid plaques
65
Q

Describe the structure and function of proteasomes

A
  • Protein degrading machines
  • Cytosol and nucleus
  • Hollow, cylindrical structures + CAP, 60 subunits
    • Alpha subunits - non-enzymatic
    • Beta subunits - proteolytic activity
  • Degrade proteins via the ubiquitin-proteasome system
66
Q

Describe the aetiology of common neurodegenerative diseases

A
  • Often genetic - cerebellar ataxia, frontotemporal dementia
  • Often sporadic - Alzheimer’s disease, Parkinson’s disease, ALS
  • Always genetic - Huntington’s disease
  • Always sporadic - PSP, MSA
67
Q

Describe the pathology of dementia with Lewy bodies

A
  • Pallor of brainstem pigmented nuclei - substantia nigra
  • Classical Lewy bodies - bright eosinophilic structures, alpha synuclein aggregates
68
Q

Compare delirium and dementia

A
  • Delirium
    • Rapid onset
    • Acute medical cause
    • Consciousness impaired
    • Major sleep-wake cycle disturbance
    • Considerable fluctuation in 24 hour period
    • Agitation, restlessness
    • More prominent visual hallucinations
    • Prominent labile affect, distress
  • Dementia
    • Slow progression, insidious
    • Chronic progressive cause
    • Clear consciousness (usually)
    • Relatively less disturbance
    • Worse in evening - ‘sun-downing’
    • Relatively more settled
    • Lability less common
69
Q

Describe the diagnosis of dementia

A
  • Clinical assessment
  • Corroborative history - family members
  • General physical examinations
  • Standard (+/- specialised) bloods
  • Structured cognitive testing
70
Q

Describe the clinical features of vascular dementia

A
  • Stepwise progression
  • Memory impairments
  • Lack of insight
71
Q

What kind of memory loss occurs in dementia?

A

Ribot’s gradient - pattern of memory loss, will forget more recent material first then more long term as time goes on

Hippocampal atrophy in Alzheimer’s disease - loss of anterograde episodic memory

72
Q

Describe the mechanism of action of memtantine

A
  • NMDA receptor agonist, improves memory by restoration of homeostais in the glutaminergic system - used in combination with cholinesterase inhibitors or if they are ineffective/not tolerated
  • No significant effect in mild dementia, vascular dementia or frontotemporal dementia
  • Possible small effect in DLB but case reports of pyschosis
  • Side effects - dizziness, headache, constipation, drowsiness and hypertension
73
Q

Define cognition and list the aspects of cognition

A

Thinking, knowing, understanding

Includes - attention/orientation, memory, executive functioning, language, calculation, praxis and visuospatial ability

74
Q

Describe the structure of amino acids

A
75
Q

Describe the normal function of Tau protein

A
  • Normal function - microtubule associated protein (transport of vesicles etc.), coats microtubules and stabilises
  • Phosphorylation - Tau dissociates from microtubules, depolymerised - breaks microtubule function
76
Q

Describe the prevalence of delirium

A

Occurs in 15-30% of hospital inpatients aged over 65

77
Q

Describe the features of a neurodegenerative disease

A
  • Neuronal death, systematic (symmetrical) loss
    • Cortex - Alzheimer’s, frontotemporal dementia
    • Basal ganglia - movment disorder (Parkinson’s/Huntington’s)
    • Cerebellum and spinal cord - ataxia
  • Protein accumulation and inclusions are primary pathology
    • Beta-amyloid, Tau, alpha-synuclein, TDP-43
  • Secondary changes - reaction (inflammation)
  • Unremitting progression
  • Unkown or genetic cause
78
Q

Give examples of disorders of calculation

A

Acalculia - can’t comprehend/write numbers

Anarithmetria - can’t manipulate numbers to do arithmetic

79
Q

Describe the spectrum of cognitive impairment

A

Age related cognitive impairment < mild cognitive impairment < dementia

80
Q

Give examples of visuospatial skill disorders

A
  • Topographical disorientation - difficulty moving around previously familiar environment
  • Difficulties dressing - dressing apraxia
  • Mis-reaching for objects
  • Visual neglect - only eat one half of plate, draw clock face on one side
  • Visual object agnosia - can’t recognise objects
  • Prosopagnosia - don’t recognise familiar faces
  • Constructional dyspraxia - can’t draw cube (R parietal lobe)
81
Q

Define dementia

A

An overall term that describes a group of symptoms associated with a decline in memory or other cognitive skills severe enough to reduce a person’s ability to perform everyday activities

82
Q

Describe the features of Alzheimer’s disease

A
  • Significant decline in cognition, cognitive defects interfere with independence in everyday activities
  • Clear history of worsening
  • Initial and most prominent deficits are:
    • Amnestic - episodic memory alteration
    • Non-amnestic - progressive aphasia, visuospatial deficit, executive dysfunction
  • Not always homogenous, may vary in:
    • Age at onset
    • Disease progression
    • Disease duration
    • Symptoms at onset - predominantly frontal (behavioural), predominantly occipital (visuospatial)

Medicine Year 2 (41 decks)

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