Psychology Flashcards

1
Q

What are the 3 CNS units of Luria’s brain behaviour theory?

In terms of functional systens how does he define pluripotentiality?

A
  1. Regulation of arousal and muscle tone via brainstem
  2. Reception and integration of sensory information via posterior cortical areas
  3. Planning and executing behaviour via anterior cortical areas

That each area of the main may play a role for many behaviour and will interact with other areas. No area is singuarly responsible for behaviour.

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2
Q

Within the limbic system, what are some of the roles of the following:
Amygdala
Orbitofrontal cortex
Hippocampus

A

Amydala; related to fear, emotional learning and clinically anxiety and depression if dysregulated
Orbitofrontal cortex; identification and expression of emotion
Hippocampus; role in affective disorders

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3
Q

Can an affective response be separate to a cognitive one? Give an example of separate and together

A

They can be independent but they usually work together e.g. Separate; immediate fear preceding cognition
Together; cognitive appraisal influencing an emotional response, so thinking something will be bad and so you experience it as bad

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4
Q

What is executive function?

What part of the frontal cortex is traditionally ascribed to be responsible for it?

A

Inter-related processes responsible for goal directed, purposeful behaviour; inc cognitive, emotional and social.
Such as; working memory, planning, insight an moral judgement
Pre frontal cortex, the dorso-lateral prefrontal cortex has the ‘traditional’ functions above. But prefrontal cortex just like coordination of EF, lots of brain regions involved and any injury to them could disrupt it

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5
Q

What is the medial prefrontal cortex’s and the orbitofrontal PFC role within executive function? what is their blood supplies?

A

Medial PFC; emotional-motivation interface; initiative and self awareness. Supplied by ACA
OFPFC; Inhibition and impulsivity of cog/em/soc. supplied by ACA and MCA

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6
Q

What is the difference between fluent and non fluent aphasia in terms of:

  • Area
  • Artery
  • Language effect
A

Non- fluent

  • Superior division of MCA
  • Brocas
  • Impaired grammatical construction of sentences
  • Content selection in tact
  • Motor weakness in right arm and face

Fluent

  • Inferior division of MCA
  • Wernickes
  • Impaired selection of content
  • Grammatical structure in tact
  • Impaired comprehension
  • Right quadrantanopsia
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7
Q

What are the two main gyrus’ associated with Broca’s and Wernicke’s area?
What white matter tract is hypothesised to run between them?

A
  • Pars triangularis
  • Pars opercularis
    In frontal lobe
  • Supramarginal gyrus
  • Angular gyrus
    In temporoparietal association neocortex

Arcuate fasciculus running between

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8
Q

What are the parts of long term memory?

A

Declarative; episodic and semantic

Non-declarative; procedural/skills/habbits and priming/classical conditioning

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9
Q

What brain structures are associated with the hippocampal system?
What are the main function of the right vs left hippocampus

A

Hippocampus, entorhinal cortex, perirhinal cortex
Left; verbal, so lists and stories for eg.
Right; non-verbal, so visuospatial and faces

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10
Q

Someone presents with partial complex seizures and declarative memory loss, what could be the underlying pathology?

A

Hippocampal sclerosis; get CA1 loss and gliosis

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11
Q

What are some causes of transient amnesia

A

Transient global amnesia; not sure why but things like stress, sex and the cold can trigger
Post-epiletptic amnesia; after a seizure
Post-traumatic amnesia; after trauma
All resolve

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12
Q

What is the major risk factor for alzheimers?

Braak and Braak staging of AD define it in terms of 3 sequential structures being affected, what are they?

A

Age
Starts in transenterhinal cortex (asymptomatic)
Entorhinal cortex (incipient)
Neocortical (full blown AD)

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13
Q

What is mild cognitive impairment and how does it present

A

Transition between normal ageing and Alzheimer’s.

  • Subjective memory complain
  • Objective memory impairment
  • But in tact general functioning
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14
Q

What is long term potentiation in the hippocampus? what is the difference between early and late LTP
What receptors are implicated and what do they do?

A

LTP is strengthening of a synapse from recent patterns of activity. Nerves more sensitive to input, and as they fire together create memories.
Early LTP is protein independent, fast and the EPSP isn’t as great
Late LTP is the opposite
AMPA and NMDA receptor implicated as working together . Get more AMPA receptors within LTP, makes more excitable. But NMDA responsible for initiating longer term protein changes.

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15
Q

What is the transactional model of development?

A

That development takes place through transacting factors; genetic, environment, psychological etc. operating together

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16
Q

In terms of risk factors what is multifinality and equifinality?

A

Multifinality- one risk factor can lead to multiple endings

Equifinality- many risk factors can lead to same ending

17
Q

What is the compression of morbidity?

A

Compression in time between chronic disease onset and death- makes more rectangular life curve

18
Q

What is frailty?

What model do we generally use to measure it?

A

Dysregulated homeostasis increasing chance of morbidity and mortality. Associated with chronic inflammation
Phenotype model

19
Q

What is sarcopenia? Which muscle fibre type do you lose more of?

A

Loss of muscle mass and strength.

Lose more type 2 then type 1, so less ability for fast precise movement

20
Q

What is geriatric syndrome?

A

Accumulated effect of impairments in multiple domains that lead to one particular adverse outcome e.g. a fall

21
Q

What are the two categories of cognitive interventions?

A

Environmental modifications e.g. reduce stimulation

Compensatory strategies e.g. mnemonics and cues