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BMS3052 > ND > Flashcards

ND Flashcards

1
Q

What is the difference between upstream and downstream prevention strategies?

A

Upstream: large government campaigns that affect populations, e.g. quit smoking or wipe off 5.
Downstream: individual lifestyle, e.g. smoking, drinking, speeding, etc.

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2
Q

What are the 11 obstacles to prevention in health?

A
  1. Not enough drama
  2. Success is invisible
  3. Requires persistent behaviour change
  4. May be long delayed
  5. Statistical lives have low emotional effect
  6. Benefits do not accrue to the payer (e.g. a hospital who runs successful prevention programs will see less patients)
  7. Avoidable harm is accepted as normal (e.g. smoking)
  8. Preventive advice may be inconsistent (e.g. harmfulness of butter)
  9. bias against errors of commission may be a deterrent (mistakes made by those “in the know”)
  10. prevention is expected to produce a financial return whereas treatment is only expected to be worth its cost
  11. commercial interests and personal, cultural and religious beliefs may conflict with disease prevention
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3
Q

Examples of prevention strategies; identify steps involved

A

Stop smoking campaign; increasing legal buying age to 18; increasing tax on cigarettes; stopping

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4
Q

Outline 9 hallmarks of ageing

A
  1. Telomere attrition - reduction of telomeres over multiple replications.
  2. Mitochondrial dysfunction - build-up of ROS due to ineffectiveness of ETC (particularly I and IV).
  3. Epigenetic modifications - during ageing, histones are lost and hypomethylation (global) and hypermethylation (focal) occur.
  4. Loss of proteostasis - loss of mechanisms that dispose of misfolded proteins; e.g. proteosomes and autophagy.
  5. Deregulated nutrient sensing - mechanistic target of rapamycin (mTOR) pathway inhibition extends lifespan; IGF-1 signalling pathway attenuation also extends life span.
    Calorie restriction also extends lifespan.
    Candidate longevity genes in humans:
    - Sir 1, 2 and 3
    - FOXO1 and 3 TF
    - Akt1
  6. Cellular sensescence
  7. Stem cell exhaustion
  8. Altered intercellular communication
  9. Genomic instability
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5
Q

Describe the phenotype and common neuropathological features of neurodegenerative diseases (5)

A
  • delayed onset (age)
  • selective neuronal vulnerability: Alzheimer’s (cholinergic neurons spanning from basal forebrain to hippocampus); Parkinson’s (dopaminergic neurons spanning from substantia nigra to striatum)
  • abnormal protein processing and aggregation
  • cellular toxic effects involving both cell-autonomous and cell-cell interaction mechanisms
  • most neurodegenerative mechanisms have unknown aetiology
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6
Q

Outline diagnostic steps for Alzheimer’s Disease (4)

A 
Cognitive performance (dementia):
* ADAS-cog scale
* MMSE
* CDR scores
No reliable biomarkers of disease in CSF
* total tau/ phosphoTau
* amyloid beta42
Neuroimaging
* PIB-PET (amloid pathology)
* 18FDG-PET (hypometabolism)
* MRI (hippocampal atrophy)
Post-mortem confirmation of pathology
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7
Q

Outline steps involved in the processing and deposition of amyloid beta

A

Normal: APP protein is cleaved by alpha-secretase to result in C83, which is then cleaved by gamma-secretase to p3 (neuroprotective)
Amyloidogenic: APP protein cleaved by beta secretase to C99, which is then cleaved by gamma secretase to amyloid beta 1-40 or amyloid beta 1-42.
* amyloid beta 1-40 has a lower tendency to aggregate and thought to have neurotrohic tendency
* amyloid beta 1-42 prone to formation of oligomers, main form in amyloid fibrils

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8
Q

Describe how tau-hyperphosphorylation causes synaptic dysfunction

A

Hyperphosporylated tau detaches from microtubules; soluble tau aggregates and with increasing phosphorylation forms NEUROFIBRILLARY TANGLES which aggregate in the hippocampus

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9
Q

List genetic and environmental risk factors of AD

A

Genetic
Early onset - Familial AD (FAD)
* mutations in APP (amyloid precursor), presenelin 1 and 2 (components of gamma secretase)
Late onset AD (LOAD)
* ApoE, clusterin, ABCA7 - cholesterol metabolism
* complement receptor 1, CD33, TREM2 - immune response
* BIN1, PICALM, CD2AP, EPHA1, SORL1 - endocytosis
* rare variants APP, presenellin 1 and 2
TAU protein
* silent mutations of MAPT gene = hyperphosphorylation
* missense mutations of MAPT = inherited cases of frontotemporal dementia, NOT AD
Environmental
* age
* head trauma
* vascular health
* obesity & diabetes
* physical and mental inactivity
* smoking
* low education attainment

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10
Q

Agents currently being used in treatment of AD, including mechanisms of action

A

Symptomatic
* cholinesterase inhibitors (increase cholinesterases)
* NMDA receptor antagonist
Disease-modifying (4)
* amyloid plaque formation - amyloid beta vaccine, gamma secretase inhibitors
* tau hyperphosphorylation - kinase inhibitors, phosphatases
* synaptic dysfunction - neuroprotective agents
* hippocampal atrophy
The ONLY approved therapies are cholinergic neuron-treating symptoms

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11
Q

Describe the animals models used to study AD

A

Single transgenic - APP mutations
Double transgenic - APP and PS1 mutations
Triple transgenic - APP, PS and tau [unpredictable; mutation can drop out during transbreeding]
Tau transgenic - tau mutations
Problem: animals that express tau tangles have frontotemporal disease, not AD
animals that express amyloid have plaques, no tau tangles

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12
Q

Outline clinical features and diagnostic steps for Parkinson’s disease

A 
TRAP:
T: tremors
R: rigidity
A: akinesia
P: postural instability
Post-mortem pathology:
- Degeneration of the substantia nigra pars compacta
- Lewy bodies [accumulation of degenerated alpha synuclein bodies] and Lewy neurites
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13
Q

Susceptible pathway in PD?

A

Nigro-striatal dopaminergic neurons - depletion

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14
Q

% of people in AU that experienced some form of a MD in their lifetime?

A

45.5%

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15
Q

% of people who experienced major depression?

A

6%

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16
Q

To which category does depression belong?

A

Affective/ mood disorders

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17
Q

Female: male ratio of major depression?

A

1.5-3:1

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18
Q

% of people who experienced bipolar?

A

1-2%

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19
Q

Female: male ratio of bipolar?

A

1:1

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20
Q

Causes of bipolar? (5)

A
  1. genetics
  2. serotonin abnormality (main)
  3. environmental
  4. medical illness
  5. pregnancy
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21
Q

What duration of persistence applies to GAD (generalised anxiety disorder)?

A

> 6 months

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22
Q

Female:male ratio of GAD?

A

2:1

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23
Q

% of AU who reported PTSD?

24
Q

% of women with PTSD? Men?

A

W: 8.3%: men 4.6%

25
Q

of people with psychotic illnesses?

A

64,000 (18-64)

26
Q

Fraction of people with schizophrenia who experience only one or a few “episodes” of psychosis?

27
Q

Lifetime prevalence of schizophrenia?

28
Q

Peak incidence of schizophrenia?

A

15-25y, with a peak at 40

29
Q

Annual cost of schizophrenia?

A

661m or 18k/person

30
Q

How many people worldwide are living with dementia?

A

46.8m (18th largest economy if that was a country)

31
Q

How many AU are living with dementia?

A

353,000 (expected to almost triple by 2050)

32
Q

Total expenditure on dementia in 2009-10?

33
Q

What is the most common form of dementia? What % of people with dementia have this disease?

34
Q

How many people in Australia have autism?

A

1/100 - 242,000

35
Q

What % of unemployed people had a 12-month mental disorder?

36
Q

What % of employed people had a 12-month mental disorder?

37
Q

What % homeless people had a 12-month mental disorder?

38
Q

What % of countries have NO mental health policy?

39
Q

What % of countries have no mental health programme?

40
Q

What % of countries have no mental health legislation?

41
Q

% of AU people who made use of mental health services?

42
Q

% who consulted a GP?

43
Q

% who consulted a psychologist?

44
Q

% who consulted a psychiatrist?

45
Q

What processes in brain development happen AFTER birth? (3)

A
  • pruning
  • circuit formation
  • synapse formation
46
Q

Neural migration is complete by birth in all but these (2) areas of the brain:

A
  • hippocampus

- cerebellum

47
Q

During what period of neural development do the vast majority of congenital abnormalities occur?

A

Embryonic - 1st 8 weeks

48
Q

During what period of neural development does the brain grow the most?

49
Q

Pruning of synapses is associated with a ____ in gray matter/ increased myelination and connectivity is associated with ____ in white matter

A

decrease, increase

50
Q

Name 2 monogenic neurodevelopmental disorders.

A

Angelman’s (ubiquitin ligase UBE3A) and Fragile X Syndromes (FMRP)

51
Q

What are the 3 core symptoms of ASD?

A

Persistent deficits in:
* social communications
* social interactions
Repetitive behaviour and restricted interests.

52
Q

What % of deaths in 2015 AU were due to CVD?

53
Q

How is efficacy of a new treatment measured?

A

Using relative risk

54
Q

How is effectiveness of a new treatment measured?

A

Absolute changes in risk

55
Q

What does allocative efficiency in healthcare consider?

A
  • efficient distribution of available resources

- opportunity costs

56
Q

What does technical efficiency in healthcare consider?

A
  • efficient management of a single condition

- cost effectiveness

BMS3052 (2 decks)

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