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Old Age Flashcards

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1
Q

What is the definition of dementia according to DSM?

A

‘loss of intellectual abilities of sufficicent severity to interfere with social or occupational functioning’

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2
Q

How long has the relationship between olda ge and memory been considered?

A

Ancient greeks and egyptians were aware that increased age is associated with memory disorders

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3
Q

Who is a case study for dementia?

A

Ronald Reagan - Mother died from AD. FAther = alcoholic. Childhood = alcoholism and financially struggling. actor –> president. STRESSFUL

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4
Q

What do we know about the gene apoE-4?

A

It is carried by 4-8% of people aand appears to determine the age at which some forms of late onset AD emerge

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5
Q

Who came up with Alzheimer’s Disease?

A

Alois Alzheimer (1907)

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6
Q

what is the prevalance of AD?

A

over 65s = 5-7%

Over 85s = 29%

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7
Q

What about diagnosis of AD?

A

Definitive diagnosis can only be done post-mortem - microscopic changes in brain tissue.
LAter starges diagnositc guidelines= 85%-90% accurate (1984)

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8
Q

How do AD patients act in a mental state exxam?

A

Circumstantial, repeat themselves and lack richeness of detail

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9
Q

What two microsopic signs are involved in AD?

A

Neurofibrillary tangles - and amyloid plaques

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10
Q

What are neurofibillary tanlges?

A

webs of abnormal filaments within a nerve cell

Filaments = made up of protein tau. If tau = misshaped or tangled = neuron tube colapses.

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11
Q

What did Sham & Morris, 2011 show?

A

Although abnormal tau aggression can occur indepenently, there is reason to beleive that build up of tau protein = accelerated by an increasing burden of amyloid in the brain

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12
Q

What are amyloid plaques?

A

Neurons in the brain secrete a sticky protein substance called beta amyloid. It is produced faster than it can be cleared away and broken down. Amyloid accumlates – makes amyloid plaques. These interfere with synaptic funcioning and set off a cascade of events –> death of brain cells

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13
Q

What di Jalburt et al, 2008 find?

A

Having apoE-E4 form of APOE gene = associated with the more rapid build up of amyloid in the brain

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14
Q

What is the caspase theory?

A

beta amyloid stimulates caspases (type of protease) whihc become enzymes that destroy neurons.
Primary disturbanec = in the acetylcholine (Ach) system - involved in learning and memory
AD people have insufficient choline acetyltransferase (enzyme that catalyses synthesis of Ach)

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15
Q

What dot he genes involvedin late onset familial AD lead to ?

A

Excess beta amyloid

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16
Q

Where is the apoE gene found?

A

chromosome 19 - 3 common forms = e3, e4. e2

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17
Q

What does the e4 allele do?

A

Production of E4 – damages neurone microtubules

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18
Q

What do apoE2 and apoE3 do?

A

Protect the tau protein – stabilises microtubules

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19
Q

What gene is inovoled in early onset familial AD?

A

Defective presenilin gene – involved in premature brain ageing

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20
Q

How many genes do research estimate account for genetic risk of AD

A

4 genes account for 1/2 the genetic risk of AD

Presinilin 1 & 2, AP and apoE

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21
Q

What did the Honolulu-ageing study involve?

A

longitudinal study on Japenese American males mid-late adulthood
Heavy smoking in mid life = increased risk of AD
Men who walked 2 miles a day = decreased risk of AD compared to those who walked 1/4 - 1 mile

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22
Q

What did the experiment involving older adults in sweden involve?

A

36% increase in risk of AD by age 79 for every unit increase of BMI age 70

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23
Q

Who did an experiment involving nuns and what did htey show?

A

Snowdon et al, 1998 – elderly nuns whosing signs of AD – decades earlier had written essays low in idea density and grammatical complexity

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24
Q

What two drugs? can be used to inhibit anticholinesterase and what does tha tenzyme do?

A

THA + DH

The enzyme destroys Ach after synaptic release

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25
Q

What effects can THA have?

A

Toxic effects in liver and the required does = too much for some

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26
Q

What effects can DT have?

A

Gastrointestinal effects but required dose = lower and no interference with liver function

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27
Q

What does clioquinol do?

A

antibiotic which breaks up chemical bonds holding amyloid together

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28
Q

What do anti-oxidants do?

A

When beta-amyloid breaks into fragments, free radicals form that damage neurons???

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29
Q

Quote on complexity of the brain?

A

Thompson (2000) – the brain is the most complex structure in the human universe

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30
Q

What can episodes of dperession cause?

A

Speck et al (1999) – can double risk of AD up to 20 years later

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31
Q

What is delirium

A

State of acute brain failure that lies between normal wakefulness and stupor or coma

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32
Q

What does delirum involve?

A

sudden onset, fluctuatitng state of awareness. Essentially unable to carry out purpose mental activity of any kind. elderly = particularly at risk

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33
Q

Who else are particularly at risk from delirium and why?

A

children = maybe because brains aren’t develope dfully yet

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34
Q

Other risk factors for delirium?

A

Dementia, depression, tobacco use (Fricchione et al, 2008)

35
Q

Delirium criteria?

A

Disturbance of concousness, change in cognition (e.g. memory deficits), develops over short period of time.
Distrubance tends to be caused by the direct physiological consequences of a general medical condition

36
Q

What horrible stat is there for elderly delirium and death?

A

Witlox et al, 2010 – 25% of elderly die within following 6 months

37
Q

What’s dementia about?

A

No sudden onset, symptoms do not wax and wane. Gradual onset.
Memory = affected irst. Then, amrked deficicts in abstract think ing, acquiring of new knowledge, problem solving and judgement
Can be reversible if underlying cause = removed/trated (e.g. vitamin deficiency)

38
Q

Hwo many differnet disorders have ben found to cause dementia ?

A

Bonde and LAnge (2001) – at least 50.

39
Q

What are the most common neurogenerative disorders and according to who?

A

JAlbert et al, 2008 – AD then PD

40
Q

Prevalence of PD?

A

65-69 = 0.5 -1 %. over 80 = 1 -3 %

41
Q

What are the symptoms?

A

Motor - resting tremors or rigid movements. Underlying cause = loss of dopamine neurons in the substantia nigra.

42
Q

How can symptoms be temporarily reuduced?

A

Miraplex medication - increases availblaility of dopamine in brain. Symptoms return wehen meds wear off

43
Q

When are genetic factors and enviornmental facros mroe important?

A

Wirdefelt et al (2011) - genetic factors = more important in earlier development. Enviornmental = later development

44
Q

What is huntingdon’s disease?

A

Rare degerneative disease of CNS. 1/10000 Mid life start (40 ish). Men and women = affected equally. Chronoic, progressive chorea (involumtary and irregular mvements that flow randoml from one area of body to another)

45
Q

What is the relationship between cog problems and motro problesm re HD?

A

Shoulson and Young 2011 – cognitive problems due to the progressive loss of brain tissue that occurs as muh as a decade before the formal onset of the illlness

46
Q

What happens to HD patients eventaully?

A

Dementia and death - normally 10/20 years after level of illness

47
Q

Where is the dominant gene for Huntingdons?

A

Chromosome 4

48
Q

Do people want to be tested for the dominant HD gene?

A

Shoolson & Young, 2011 – in US, about 10% of those eliggible for testing choose to be tested. HAyden (2000) – majority of those who ask to be tested = women

49
Q

What is AD??

A

Progreessive and fatal degenerative disease. Inperceptible onset and usually slow but progressively deteriorating cause. Terminating in delirium and death.

50
Q

When is diagnosis normally given for AD?

A

Post-mortem for sure

Normally only given out after all other potential causes of dementia = ruled out

51
Q

When does AD normally begin?

A

About 45 – Malaspine et al, 2002

52
Q

Horrible statistic re death after AD diagnosis?

A

Jalbert et al, 2008 – median time to death = 5.7 years after time of 1st clinical contact. Women = slightly higher risk at developing AD

53
Q

AGe related risk statistic re AD?

A

Hendrie, 1998 – estimated that rate of AD doubles ever 5 years after a person reaches 40.

54
Q

How many will be living with AD by 2030 ?

A

Vrengdenhil et al, 2011 – 66 million

55
Q

Loneliness and AD?

A

Wilson et al, 2001 – 800 PPs. If lonely = twice the risk of developing AD over course of 4 years. May explain higher prevalence in women – outlive husbands.

56
Q

What other other risk factors of AD

A

JAlbert et al, 2008 – current smokers, fewer years of formal education, lower income, lower occupational status

57
Q

Where is prevalence higher for AD?

A

Ballart et al (2011), north america, europe, lower in se asia, india and africa

58
Q

Is there a relationship between diet and AD?

A

Sjognen & Blennous 2005 – high fat/high chol diet = implicated in development of AD

59
Q

Cholesterol improving drugs?

A

Sparks et al, 2005 - taking statin drugs to lower cholesterol also seems to offer some protection against AD

60
Q

How many gene mutations contribute to early onset AD?

A

Ballard et al 2011 – 3
APP
PS1/PS2
APOE gene

61
Q

APP gene mutations

A

chromosome 21. associated with 55-60 years.
Janichi & Dalton, 1993 – down syndrome people (Tripling of chrom 21) = who live past 40 = likely to develop illness like dementia

62
Q

How much of cases do APP, PS1 and PS2 mutations account for?

A

5%

63
Q

Where is PS1 and PS2 mutations?

A

Chrom 14. 30-50 years onset

64
Q

What chromosome is the APOE gene on

A

Chromosome 19. apoliprotein

65
Q

What does APOE gene code for?

A

Blood protein that helps carry cholesterol through bloodstream.
A person can inherit 0 1 or 2 of APOE-E4 gene == risk increasies accordingly

66
Q

What did Ballard et al (2011) find re APOE?

A

HAving 2 APOE-E4 allleles results in 7 fold increase in person’s chance of developing disease

67
Q

What did MAlaspine eta l 2002 find?

A

Approx 65% of patients have at least one copy of the APOE-E4 allele
4 fold increase in dvelopment of AD up to 5 years after traumatic brain injury

68
Q

What did Myers et al, 2006 find?

A

Only 55% of patients with 2 APOE-E4 alleles had developed AD by 80

69
Q

Weggen et al 2001

A

Exposure to non-steroiidal anti-inflammatory drugs e.g. ibuprofen may be protective and lead to lower risk of AD

70
Q

What did FDA issue a warning about?

A

Schultz 2008 – patients with dementia who receive atypical anti-psychotic meds = incerased risk of death

71
Q

Hiippocampal size and AD?

A

Heijer et al, 2006 – reduction in HIIP size predicts later development of AD in certain cases
Sperling et al 2003 – HIP = less active when patients with AD = enganged in mem tasks

72
Q

What evidence is there against HIP size reduction and AD?

A

Smith et al 2002 – people at genetic high risk = incrased activity in various brain areas including the HIP when they engage in memory tasks
Maybe because APOE-E4 carriers have to work harder to manage cog tasks

73
Q

Brain weight sta?

A

Perl, 1999 — by age 80, our brain has lost about 15% of original weight

74
Q

Cost of dementia annualy?

A

Alzheimer’s association, 2010 – $172 billion. estimated

75
Q

Caregivers of AD patients~?

A

Cummings et al, 2002 – caregivers sufffer from increased rates of depression and physical illness

76
Q

Reducing length of stay of deliours patients?

A

Levkoff et al (1986) – reducing lenght of stay of delirous patients in hospital by a day = $1-2 billion savings annually.

77
Q

Experiment in a cardiac intensive care unit?

A

Uguz et al, 2010 – cardiact intensive care unit, acute myocardial infections. 3 independently related predicitve factors
Old age
Higher serum potassium on admission
Cardiac arrest during myocardial infection

78
Q

Which anti-depressant has been succesfully used to treat delirium?

A

Furose et al, 2010 –> fluvoxamine – rapid decrease in symptoms

79
Q

When is the full benefit of disease modifying treatment posisble?

A

Carillo et al, 2009 – only obtainable if drugs = digven to paople so early in teh ‘pathological process’ of AD that clinical symptoms of thsi disease have not yet surfaced.

80
Q

What can HIV and AIDS cause?

A

Irreversible dementia

81
Q

Name three types of dementia?

A

Lews Body dementia
Vascular dementia
Dementia Pugilistic

82
Q

What is Lews Body dementia?

A

1/7 dementia cases. Visual hallucinations. Parkinsonism symptoms. Lwo qualtiy of life. Dififcult to plan ahead.
Variable experineces from indivdiual to indivdiual

83
Q

What is vascular dementia?

A

67000 people die from strokes each year.
Onset = more sudden than in AP. Outcome = similar to AP
Entirely different disease to AD in terms of underlying neuropathology = series of circumcised cerebal infarcts - ‘smal strokes’
Treatment = more encouraging than AD - basic problem of cerebral arteriosclerosis can me medially managed to some extent – decreases likelihood of further strokes

84
Q

What is dementia pugilistics ?

A

Career boxers/people who receive multiple blows to head.
AVerage time of onset = 16 years after start of boxing
Muhammed Ali
Chris Beneit (WWE) killed wife and son and hung himself in June 07
Symptoms = dementia, parkinsonism or tremors, lack of co-ordination
Drake & Cifo (2004) – not well understood why it occurs

Abnormal Psychology (3 decks)

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