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AQA A2 Psychology PSYA3/PSYA4 Revision Thread 2016 Watch

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    (Original post by NHM)
    I think you could probably gain credit for ethics and reductionism?
    my teacher said that A03 marks still count and they still give you them
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    for schizophrenia can we get 4+8 mark questions?
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    (Original post by ThatGirlJemma)
    Damn I praise you! It seems quite challenging! I am struggling so bad rn with my teachers help.. And yeah, I hate it when teachers purely only put on movies or the such, like I need to be learning and doing exam papers?!?!

    Soo were you doing addiction then? Then switched to media? What else did you learn?
    Aw thank you . No, it's not as difficult as it sounds. Read a few things online and put them together into one set of notes.
    I know right! We watched Shutter Island for Schizophrenia, interesting movie but, come on.

    I was supposed to do anomalistic behaviours.
    I've done relationships (switched from sleep), aggression, eating behaviours, schizophrenia and media (switched from anomalistic). Addiction sounds interesting too though. What else have you learnt?
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    Guys, for addiction the 3 approaches, could we get asked a question like

    Discuss the role of relapse for the biological explanation of smoking, if So how are we supposed to fricken get 6 marks of Evaluation for the RELAPSE part of smoking as an explanation?
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    (Original post by SunDun111)
    Guys, for addiction the 3 approaches, could we get asked a question like

    Discuss the role of relapse for the biological explanation of smoking, if So how are we supposed to fricken get 6 marks of Evaluation for the RELAPSE part of smoking as an explanation?
    omg this is exactly what im thinking!!- same with initiation - im really stuck for studies- are you just gonna talk about genetic predispositions for initiation or talk about 2 factors e.g the dopamine reward system?
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    (Original post by keepdreaming-)
    How long are your 10 marks essays generally? In terms of essay length - so number of pages.
    About 1.5 sides hand written
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    (Original post by artymaniac)
    omg this is exactly what im thinking!!- same with initiation - im really stuck for studies- are you just gonna talk about genetic predispositions for initiation or talk about 2 factors e.g the dopamine reward system?
    It will only be 4 marks so ill talk about genetics, but if a 6 marker of evaluation for something like maintence and relapse comes up im screwed, its so stupid, its to specific if that would come up, it would mean i have to LEARN 9 AO2 points for each approach.
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    (Original post by Alisahussain1)
    probably 3/4 but evaluate them and expand on them
    Thanks
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    (Original post by mosahra)
    for schizophrenia can we get 4+8 mark questions?
    yes, jan 2013 asked for 2 4+8 markers
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    yeah i get you, but cant initiation come up as a 6 marker or 10 marker too. Is genetics enough to talk about? like all ive got is Vink et al and Cummings et al- would you recommend any other studys?
    (Original post by SunDun111)
    It will only be 4 marks so ill talk about genetics, but if a 6 marker of evaluation for something like maintence and relapse comes up im screwed, its so stupid, its to specific if that would come up, it would mean i have to LEARN 9 AO2 points for each approach.
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    anyone doing phobic disorders?
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    (Original post by artymaniac)
    Is it possible for someone to explain to me the dopamine hypothesis and what studies you would use.. ive spent an 3hours on this and still dont understand it!;( It wud b great if sum1 could explain it! thanks
    Hey I'm not sure if anyone has already answered you but this is from what I understand of the Dopamine Hypothesis so far, I hope it helps in some way!


    So first start by thinking - More dopamine = Induces Schizophrenic episodes

    Also, it would be important to note that from PSY3 - dopamine is associated with the reward pathway in the brain (if you did aggression that is haha) and I think it is also linked with motor activity and cognition (how brain controls movement).

    The original dopamine hypothesis suggested that schizophreniais associated with an excess of the dopamine. So because dopamine is a neurotransmitter (produces an electrical impulse from neuron to neuron - also called an action potential) it causes these neurons to fire too often so they are constantly being stimulated and become over sensitive. They transmit too many impulses along axons of these neurons.

    But a more recent version says that rather than an excess of dopamine it is an excess of dopamine receptor cells (D2 receptors). If you don't do biology, basically what receptors do is they want to take back in the dopamine which are on the cell surface membrane of cells, so because dopamine is a complementary shape to the receptors it can bind to the receptor and be taken into the body- via the receptors... the result of hyper-stimulation of D2 receptors gives a sufferer positive symptoms of Schizophrenia e.g. hallucinations and delusions (symptoms added). Whereas problems with dopamine function in the mesocortical pathway may be responsible for the 'negative symptoms' of schizophrenia,e.g. as avolition and alogia.

    Evidence for and against (from what I have) is mainly drugs which can even act as competitive inhibitors (blocking the binding site on receptors so Dopamine isn't taken in because it cannot bind) or drugs that increase dopamine -
    -L-Dopa
    -Parkinson's disease - caused by a lack of dopamine in basal ganglia (brain region).
    -Amphetamines cause schizophrenic symptoms in a disorder called "amphetamine psychosis.
    -Antipsychotics
    -Post-Morton
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    (Original post by Tinksy)
    Hey I'm not sure if anyone has already answered you but this is from what I understand of the Dopamine Hypothesis so far, I hope it helps in some way!


    So first start by thinking - More dopamine = Induces Schizophrenic episodes

    Also, it would be important to note that from PSY3 - dopamine is associated with the reward pathway in the brain (if you did aggression that is haha) and I think it is also linked with motor activity and cognition (how brain controls movement).

    The original dopamine hypothesis suggested that schizophreniais associated with an excess of the dopamine. So because dopamine is a neurotransmitter (produces an electrical impulse from neuron to neuron - also called an action potential) it causes these neurons to fire too often so they are constantly being stimulated and become over sensitive. They transmit too many impulses along axons of these neurons.

    But a more recent version says that rather than an excess of dopamine it is an excess of dopamine receptor cells (D2 receptors). If you don't do biology, basically what receptors do is they want to take back in the dopamine which are on the cell surface membrane of cells, so because dopamine is a complementary shape to the receptors it can bind to the receptor and be taken into the body- via the receptors... the result of hyper-stimulation of D2 receptors gives a sufferer positive symptoms of Schizophrenia e.g. hallucinations and delusions (symptoms added). Whereas problems with dopamine function in the mesocortical pathway may be responsible for the 'negative symptoms' of schizophrenia,e.g. as avolition and alogia.

    Evidence for and against (from what I have) is mainly drugs which can even act as competitive inhibitors (blocking the binding site on receptors so Dopamine isn't taken in because it cannot bind) or drugs that increase dopamine -
    -L-Dopa
    -Parkinson's disease - caused by a lack of dopamine in basal ganglia (brain region).
    -Amphetamines cause schizophrenic symptoms in a disorder called "amphetamine psychosis.
    -Antipsychotics
    -Post-Morton
    You can also use:
    -the fact that PET scans have shown that drugs that block D2 receptors dont always reduce the symptoms of schizophrenia and the use of L-Dopa dont worsen or induce the symptoms for everyone
    -Lloyd et al 1984 suggests it could be stress or family environment which alter dopamine levels and trigger symptoms
    -Copolov and Crook (2000) Neuroimaging studies have so far failed to provide convincing evidence of altered DA activity in the brain of ppl with schizophrenia which would have been credible evidence
    -Also causality? Could be a consequence rather than the cause
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    Thank you so much for taking the time to do this! im doing addiction and was looking at it in relation to the initiation of smoking- but there are bits of this that are useful!
    thx again its much appreciated
    (Original post by Tinksy)
    Hey I'm not sure if anyone has already answered you but this is from what I understand of the Dopamine Hypothesis so far, I hope it helps in some way!


    So first start by thinking - More dopamine = Induces Schizophrenic episodes

    Also, it would be important to note that from PSY3 - dopamine is associated with the reward pathway in the brain (if you did aggression that is haha) and I think it is also linked with motor activity and cognition (how brain controls movement).

    The original dopamine hypothesis suggested that schizophreniais associated with an excess of the dopamine. So because dopamine is a neurotransmitter (produces an electrical impulse from neuron to neuron - also called an action potential) it causes these neurons to fire too often so they are constantly being stimulated and become over sensitive. They transmit too many impulses along axons of these neurons.

    But a more recent version says that rather than an excess of dopamine it is an excess of dopamine receptor cells (D2 receptors). If you don't do biology, basically what receptors do is they want to take back in the dopamine which are on the cell surface membrane of cells, so because dopamine is a complementary shape to the receptors it can bind to the receptor and be taken into the body- via the receptors... the result of hyper-stimulation of D2 receptors gives a sufferer positive symptoms of Schizophrenia e.g. hallucinations and delusions (symptoms added). Whereas problems with dopamine function in the mesocortical pathway may be responsible for the 'negative symptoms' of schizophrenia,e.g. as avolition and alogia.

    Evidence for and against (from what I have) is mainly drugs which can even act as competitive inhibitors (blocking the binding site on receptors so Dopamine isn't taken in because it cannot bind) or drugs that increase dopamine -
    -L-Dopa
    -Parkinson's disease - caused by a lack of dopamine in basal ganglia (brain region).
    -Amphetamines cause schizophrenic symptoms in a disorder called "amphetamine psychosis.
    -Antipsychotics
    -Post-Morton
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    can someone please let me know how many researchers we need to include for an addiction essay!
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    (Original post by carli97)
    About 1.5 sides hand written
    Thank you
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    (Original post by Alisahussain1)
    yes, jan 2013 asked for 2 4+8 markers
    ok thanks
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    Hi guys!

    Can anyone help me or have a model essay for 'Discussone or more explanations for the effectiveness of television in persuasion'?
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    I am very confused

    If a question asks to outline on biological therapy of schizophrenia (4 marks) do I just write about drugs; both atypical and conventional, OR both?
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    (Original post by Marli-Ruth)
    Hey! It was a decent paper I thought
    Except gender schema 🙄😑 but luckily I read some notes on it just in case so I was able to answer it!
    How did you find it xx
    oh yeah I heard about the gender topic...did they repeat the question from last year? and I thought it was okay but I think I might have screwed up a bit in the aggression question....oh well xxx
 
 
 
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