Lifespan Psych- Later Life Chap 15, Lec 3

Front 1

What are the trends in aging for industrialized nations?

Back 1

The population of older adults in industrialized nations has been increasing rapidly in the 20th century

Front 2

By 2030 how many people will be over the age of 65 in comparison to other age groups.

Back 2

Predicted that by 2030 the number of people over 65 will equal the number in other age groups

Front 3

Who represents the fastest growing population in canada?

Back 3

In Canada, seniors (> 65 years) represent the fastest growing population group (Health Canada, 2003)

Front 4

What is Longevity? how is it determined?

Back 4

Longevity is the number of years a person is expected to live.
Determined by genetic and environmental factors.

Front 5

What are the 3 types of longevity?

Back 5

Average
Useful
Max

Front 6

Average life expectancy refers to?

Back 6

the age half of the people born in a year will have died.

Front 7

Useful life expectancy refers to?

Back 7

the number of years that a person is free from debilitating chronic disease and impairment

Front 8

Max life expectancy refers to?

Back 8

oldest age any person lives
- current estimates 120 yrs.

Front 9

Why has life expectancy risen so much?

Back 9

- significant declines in infant mortality and women dying in childbirth
- elimination of major diseases like small pox
- polio
- improvements in med tech that prolong lives of people with chronic disease

Front 10

What are some majors factors in genetic and environmental factors for life expectancy?

Back 10

Heredity: old parents your more likely to live longer

Environment: plays a role by the effects of disease and toxins
- bacteria, pollutant, clean water

Social Class:

Front 11

What are the four groups of biological theories of aging?

Back 11

1. Wear and tear theory
2. Cellular theories
3. Metabolic theories
4. Programmed cell death theories

Front 12

What is the wear and tear theory?

Back 12

the body much like any machine, gradually deteriorates and finally wears out.
- explains things like osteoporosis well.

Front 13

What are the three Cellular theories?

Back 13

1. Absolute limit
2. free radical damage
3. Cross linking

Front 14

Absolute limit

Back 14

Hayflick limit, cellular divisions become less and less, until they don’t divide anymore

- telomers

Front 15

Free radical damage

Back 15

occurs through metabolism, cells loose an electron, become positively charged, and they become election hungry, and attack other cells. Antioxidants will stabilize these unstable electrons

Front 16

Cross linking

Back 16

some proteins start to metabolize differently and start adhering to various tissues, makes them stiff and inflexable. Ex: if this happens to a heart muscle

Front 17

Metabolic theories:

Back 17

: result in produces stress, diabetes, many many health problems. As you get older, unable to regulate hormonal reactions to stress

- caloric intake


examine the interaction between caloric intake and stress

Front 18

Programmed cell death theories

Back 18

points to evidence that aging is gentically programmed


. Apart of DNA strand that have nothing happening, but that may be proteins that turn on certain processes at a certain time in life. Abnormal repeats.

Front 19

What is a Cerebrovascular accident?

Back 19

- Stroke
- Blockage, breaking or bleeding of the blood vessels in the brain results in injury to brain tissue

Front 20

What are the three majors types of CVAs?

Back 20

1. Ischemic attacks (TIA)
2. Infarctions
4. Hemorrhage

Front 21

Ischemic attacks(TIA)

Back 21

Trans ischemic attack. Mini strokes. May not even know your having one. May be sudden dizziness
-no necrosis. May be hypoxia (lack of O2)
if it occurs many times, they build up. May have all over the brain problems. May result in major stroke

Insufficient blood supply to focal area

Temporary loss of function (transient)

Front 22

What can symptoms of a TIA tell someone?

Back 22

location of attack

Front 23

Anterior will show as?

Back 23

brief dysarthia, aphasia, weakness

Front 24

Posterior will show as?

Back 24

brief dizziness, vision, numbness

Front 25

What does it look like on MRI?

Back 25

Little black spots on MRI, dead brain tissue is filled with cerebral spinal fluid, CSF, not dense shows black

Front 26

Whats an infarction?

Back 26

Blood to the brain cut off (blockage/occlusion)
Results in the death of brain tissue (infarct)

- real stroke

Front 27

What can cause an infarct?

Back 27

Thrombosis
Atherosclerosis/ platelets
Embolism

Front 28

Thrombosis:

Back 28

chronic: clot within the artery

Front 29

Atherosclerosis/platelets:

Back 29

platlets stick to sides, could be caused by stress

Front 30

Embolism

Back 30

acute= travelling clot/ fatty plaque, heart arrhythmia, sudden onset/acute

Front 31

Lacunar infarctions:

Back 31

lakes of CSF

Front 32

Which place is highly vulnerable to an infarction?

Back 32

Left Middle Cerebral Artery highly vulnerable

Front 33

What happens when the LMCA is lost?

Back 33

Language lost, and paralysis of right side.

Front 34

What are the 3 diagnostic imaging techniques for CVA?

Back 34

CT
Angiography
Doppler imaging

Front 35

CT Scan:

Back 35

May not always show a problem, if its super early, not sensitive for small things

computerizes tomography

Front 36

Angiography

Back 36

: high risk people, or had a previous stroke, family history
Side effect: having a stroke
- Iodine contrast injected

Front 37

Doppler Imaging

Back 37

: less invasive. May be a screening for angiography. – uses sound waves, and if obstruction it will cause a difference in the sound waves.

Front 38

What are the effects of a right hemisphere stroke? Why is this often downplayed?

Back 38

Visual-Spatial
Visual-Constructional
Often downplayed, may be worst, because people don’t understand their disabilities
Could get lost in your own home,

Front 39

What are the effects of a left hemisphere stroke.

Back 39

Language

Front 40

What test is used to test visuospatial abilities?

Back 40

Rey figure: this is so complex to pick up subtle nuances

Front 41

What does the prognosis of a stroke depend on?

Back 41

Vessel Size
Collateral Channels
Premorbid factors
Location


Going to be different for each person

Front 42

Vessel size

Back 42

the more damage the bigger

Front 43

Collateral ChAnnels: what is this also called? describe?

Back 43

(anastomosis): more then one root, then if one is blocked, then you have another root. This is better

Front 44

Premorbid factors

Back 44

lifestyle variables age, smoking, diabetes, fatty……. Gender

Front 45

Location

Back 45

L Language/Depression
R Spatial/Emotion

Front 46

Right damage would show how? global or detail?

Back 46

Global deficits. Wouldnt see an M. Just the little shapes it is made up of

Front 47

Left damage would show how?

Back 47

detail
- Would draw M, no small shapes

Front 48

What are the 2 categories of treatment for CVAs?

Back 48

Medications
Surgical Procedures

Front 49

Medications?

Back 49

Anticoagulants (if no bleeding)
Vasodilators
Lower Blood Pressure

Front 50

Surgical Procedures

Back 50

Clipping/coiling: block off damaged vessel.
Aneurisms

Front 51

What is normal aging vs. dementia? Whats one way to tell?

Back 51

A lot of dementia signs are seen in all old people.

Cue vs. not. Alzheimer's or not. Do you benefit from the cue?

Front 52

What kind of cognitive changes are seen?

Back 52

Crystallized intelligence remains, however fluid intelligence (new learning, abstract resoning, processing speeds) are decreased.

Front 53

How does the speed of info processing change? Study by brenda. Describe. results?

Back 53

Is performance difference across age groups
The effects of age 3 groups (Young, middle, older)
Predict longer latencies for more complex tasks (semantic, A-PASAT= math test = 2+3= 6 +4= 10 would see where you are most efficient, however older people did better, because it is crystallized)
- Complexity effect most pronounced in older group

Front 54

What are brain changes in normal aging? (7)

Back 54

Structural changes
Thinning of white matter
Neuronal loss (prefrontal)
Neurofibrillary tangles
Senile plaques
Neurotransmitter changes
Cortical atrophy: shrinking, loss of size

Front 55

Neurofibrillary tangles:

Back 55

: within neuron everyone has microtubules, in normal people they are in parallel lines. And in dementia, they cause twisted filaments. Tau

Front 56

Senile plaques

Back 56

: accumulation in synapse of anrnoild. Occur in hippocampus, parietal lobe. Causes disconnections

Front 57

Neurotransmitter changes

Back 57

acetyl choline, concentration

Front 58

What 2 things mean dementia?

Back 58

1. Memory and learning impairment

2. Impairment in 1 or more cognitive functions, resulting in a decline from a higher level of performance that compromises a person’s occupational or social functioning


Umbrella term. Lots of subtypes

Front 59

How is dementia diagnosed?

Back 59

according to cause/site
(trauma, infection, poisoning, ..)

Cant look at average. Must compare their previous level. Premorbid factors

Front 60

What is the diagnostic criteria for demenitia according to specific cognitive impairments?

Back 60

learning and memory:

attention and arousal
language function
visual-perception function
motor skills
executive function

Front 61

How are the major subtypes of dementia separated according to part of brain effected?

Back 61

Cortical vs. Subcortical

Front 62

Cortical:

Back 62

(gray matter) higher cell bodies memory

Front 63

Sub cortical:

Back 63

(white matter) basal ganglia motar

Front 64

What dementia is it when the cortical area is damaged? (2)

Back 64

Alzhemiers
Vascular Dementia

Front 65

Vascular Dementia:

Back 65

(multi-infarct): mini strokes don’t know always, accumulates, TIA

Front 66

What is it when the subcortical is damaged?

Back 66

Parkinson’s Disease, substencia nigra
Huntington's’ Disease

Front 67

What is lewey body disease

Back 67

LBD: second to alzheimers: protein gone rye, encrusted inside dead neurons, accumulates in neurons. Looks like specks. Everywhere. Hallucinations, both symptoms

Front 68

Whats in common with the dementias in relation to areas effected?

Back 68

Parkinson’s Disease: problems don’t start mentally, but show in tremors, or muscles. Works way up
L dopamine
stem cells
Alzheimers: could go to subcortical, and you get motor


- can travel through brain and damage more

Front 69

How can you tell the difference between delirium and dementia?

Back 69

Acute vs. Chronic

Front 70

Delirium:

Back 70

A transient, global disorder of cognition and attention (alertness)
Acute onset: one period of time, can pinpoint start
Sundowning: gets worst at night


: can be fixed, metabolic function disrupt. May show confusion, disoriented
Underlying metabolic dysfunction

Front 71

Dementia:

Back 71

Static/Progressive/Course:
Chronic. Subtle onset

Front 72

Vascular dementia symptoms? cause? risk factors?

Back 72

Accumulation of TIA (infarcts)
Blackouts/heart problems
Memory/language impairment
Mood swings

Hypertension/Sex a risk factor

Front 73

What is Alzheimer's? Disease (AFS) general cause? specifcs? how is it diagnoses?

Back 73

Cognitive result of neurofibrillary tangles (tau)
Senile plaques (β-amyloid)
Reduced acetylcholine

No single or known cause
Chromosome 21
ApoE4
Diagnosed post-mortem (MRI rules out)
SDAT only diagnosis

Front 74

Senile plaques (β-amyloid):

Back 74

build up, and make crusted pieces of neuronal deposits, inbetween neurons, at synapse

Front 75

Acetylcholine:

Back 75

: helps pay attention
Drugs help prevent reuptake of acetycolina

Front 76

ApoE4, derivative of ApoE3 .

Back 76

Varies cholesterol around the brain lippoprotein in all normal cells. People who have this have high instance of senile plauqes

Front 77

What are the Memory clinical presentation of ADS?

Back 77

Declarative learning (anterograde amnesia)
(encoding, storage, retrieval)
Failure to “cue”
Temporal gradient (retrograde amnesia)
Intrusions/ perseverations: when things move over lists,
perseverations: repeating things
Anomic aphasia:

Front 78

Anomic aphasia:

Back 78

when you cant name something

Front 79

Declarative:

Back 79

things you can say “I did this yesterday”

Front 80

anterograde amnesia

Back 80

unable to learn new information after a certain time

Front 81

Failure to cue:

Back 81

: the cake example. Retrieval problem in normal, storage in dementia

Front 82

retrograde amnesia

Back 82

forgetting old information

Front 83

What are the spatial clinical presentation of ADS?

Back 83

Spatial Disorientation & construction (recall & copy)

Front 84

How can you test the spatial symptoms of ADS

Back 84

complex ray

Front 85

What does the trails B test?

Back 85

Need cognitive flexibility

Front 86

What is the best way to remediate

Back 86

focus on strengths! Don’t keep saying it will just get better.

Front 87

What part of of the subcortical is effected in Parkinson's disease

Back 87

substantia nigra

-area that produces dopamine,

Front 88

What part of of the subcortical is effected in Huntingtons's disease

Back 88

Caudate nucleus
-dominate autosomal, genetic. Caudate nucleus, bilateral deterioration

Front 89

What is in common with all of them?

Back 89

All affect motor function but in a different way

Front 90

What is the neuropathology of PD?

Back 90

Damage to the basal ganglia, particularly in the substantia nigra
Dopaminergic system
Lewy bodies

Front 91

What are the Primary Symptoms of PD

Back 91

motor


resting tremors (pill-rolling)
Bradykinesia (slow), hypokinesia (reduced), micrographia
masklike countenance, rigidity, slow stiff gait, crouching

Front 92

Bradykinesia

Back 92

movements slow and diminished

Front 93

hypokinesia

Back 93

they don’t have full movement of a particular limb

Front 94

Micrographia:

Back 94

when you write things start to get smaller and smaller

Front 95

masklike countenance:

Back 95

seems like no facial expression, lack of affect bc of lack of motor movement

Front 96

What are the memory symptoms of PD?

Back 96

Declarative/ nondeclarative dissociation

Front 97

Declarative/ nondeclarative dissociation

Back 97

memory you can talk about is okay. Implicit, procedural memory, driving, motpr memory is affected

Front 98

What is the name of the test that tests spatial memory called?

Back 98

Benton line orientation test

PD suffers would have trouble

Front 99

What is the course of PD

Back 99

Unlike stroke, onset is chronic

Aches/Tiredness

Subtle motor deficits (weakness)

Facial/Voice: bc speech is motor

Front 100

What are the (5) treatments for PD?

Back 100

Pallidotomy
Anticholingerics
L-dopa
Neurostimulators
Stem cells

Front 101

Pallidotomy

Back 101

Pallidotomy (Heat lesioning): not used much anymore. Using electric prob to destroy tissue. Forms scar tissue. Inhibits tremors

Front 102

Anticholinergics

Back 102

Anticholinergics (Ach blockers): prevents Ach from casuing tremors

Front 103

L-dopa:

Back 103

crosses blood brain barriers. Show a stop in tremors. But a resistance builds up. Dosnt work anymore

Front 104

Neurostimulators:

Back 104

send impulses to parts in brain that are infected

Front 105

Stem cells:

Back 105

Looking for stem cell research, can regenerate dopamine neruons
controversial

Front 106

What is the neuropathology of Huntington's disease?

Back 106

Bilateral deterioration (caudate nucleus)
Striatum: Limbic/prefrontal

Front 107

What are the primary symptoms of HD?

Back 107

Motor:


Twisting, writhing, grimacing
Timing, ordering, sequencing
Perseveration, direct recall
Depression, aggression, impulsivity, irritability
Wide gait, clumsy
Dysarthic speech (erratic rate)

Becomes problem to integrate fluid movements

Front 108

What are some first signs of HD

Back 108

First signs: depression, change in personality

Front 109

What causes Huntingtons?

Back 109

Hereditary chorea (dominant)

Gene ITI-5 chromosome 4

Repeats of CAG (trinucleotide)
- Normal people have 28, people with over 28 have a predisposition

Front 110

Depression in older adults: because? treatments?

Back 110

May be due to imbalances in neurotransmitters
Internal belief systems may play a role in how people interpret things that happen to them

Treatment:
Drugs that affect the levels of neurotransmitters
Monamine oxidase inhibiters (MAOs) and selective serotonin reuptake inhibitors (SSRIs)