Lesson 8.6.1
8.6.1 Brain chemicals in Parkinson's and depression Quiz: Pearson Edexcel Biology A (Salters-Nuffield), Unit 8
20 questions
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Lesson 8.6.1, Brain chemicals in Parkinson's and depression: 20 multiple choice questions for the Pearson Edexcel Biology A (Salters-Nuffield) (9BI0), Unit 8: Grey Matter, written with Revision Ninja.
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The 20 questions
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Which neurotransmitter is deficient in Parkinson's disease?
- Glutamate in the cerebellum only, which is lost from the cerebellar cortex as the disease progresses
- Dopamine, whose loss from the substantia nigra underlies the movement symptoms of Parkinson's disease
- Acetylcholine at all synapses, which is depleted throughout the brain and the spinal cord in the disease
- Serotonin only, which is the main chemical deficient in Parkinson's and is replaced by dopamine therapy
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Which neurotransmitter is most closely linked to the low-mood hypothesis of depression?
- Adrenaline only, which is released at low levels in people with depression and affects mood directly
- Insulin, which is linked to depression because low insulin levels in the brain reduce the motivation to act
- Oxytocin only, which is the hormone that is consistently reduced in every form of depression in the body
- Serotonin, since reduced serotonin activity in the brain is proposed to contribute to depression
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Which region of the brain contains the neurones that are lost in Parkinson's disease?
- Cerebellum, which co-ordinates movement and is the main site of dopamine loss in the disease
- Corpus callosum, which connects the two hemispheres and is where most of the lost neurones are found
- Medulla oblongata, which controls breathing and heart rate and is damaged in the early stages of the disease
- Substantia nigra, where dopamine-producing neurones degenerate, reducing dopamine supply to the striatum
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Which symptom is characteristic of Parkinson's disease?
- Loss of hearing in both ears, which is caused by damage to the auditory nerve in the brainstem
- Tremor and rigidity of muscles, along with slowed movement, caused by a deficiency of dopamine
- Increased appetite only, which is caused by excess dopamine and leads to rapid weight gain
- Excess production of insulin, which causes a sharp fall in blood glucose and loss of consciousness
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Why is L-Dopa used to treat Parkinson's disease?
- It kills the substantia nigra to stop tremors, by removing the source of the abnormal electrical activity
- It blocks all synapses in the brain, which stops the uncontrolled movements that the disease causes
- It is converted into dopamine in the brain, replacing the lost neurotransmitter and easing the symptoms
- It increases the production of insulin, which lowers the level of dopamine released in the brain
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Why does L-Dopa, rather than dopamine itself, get used as a treatment?
- Dopamine is always toxic to neurones, so it can never be used as a medicine in any form or dose
- L-Dopa is more expensive, so it is preferred by doctors even though it has the same effect as dopamine
- Dopamine is found only in the liver, so it cannot reach the brain from the blood in any amount
- Dopamine cannot cross the blood-brain barrier, but L-Dopa can, and is then converted into dopamine in the brain
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Which statement describes a limitation of L-Dopa treatment for Parkinson's disease?
- It treats symptoms but does not stop the progressive loss of neurones, so its effect declines over time
- It has no effect on movement, since it only changes the mood of patients with Parkinson's disease
- It cures the disease permanently, so patients do not need to take it once they have started the treatment
- It prevents all tremor in every patient, which means that no further monitoring is needed during treatment
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A patient with depression has low serotonin activity in synapses. Which drug type could help by increasing serotonin in the synapse?
- Anticoagulant that thins the blood, which reduces clotting and is used to treat clots in the veins
- Anti-diabetic drug that raises insulin, which lowers blood glucose but has no direct effect on serotonin
- Selective serotonin reuptake inhibitor (SSRI), which blocks reuptake so that more serotonin remains in the cleft
- Dopamine agonist that blocks serotonin, which reduces the serotonin signal and so worsens the symptoms
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Why might a drug that blocks serotonin reuptake raise serotonin activity?
- It increases the number of myelin sheaths on the serotonin neurones, which speeds up the impulses
- Serotonin stays in the cleft for longer, increasing the stimulation of postsynaptic receptors
- It prevents serotonin from being released, which causes it to accumulate inside the presynaptic neurone
- Serotonin is converted to insulin, which is then released into the blood and lowers the blood glucose level
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Which statement best describes the chemical basis of Parkinson's disease?
- Deficiency of red blood cells, which reduces the oxygen supply to the brain and damages the motor pathways
- Imbalance or loss of dopamine due to degeneration of dopamine-producing neurones
- Blockage of the optic nerve, which prevents the visual signals from reaching the regions that control movement
- Excess serotonin in the cerebellum, which blocks the movement signals sent by the motor cortex
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A student says that depression is caused only by low serotonin. Which evaluation is most appropriate?
- Correct, because serotonin is the only brain chemical involved, so every form of depression has the same cause
- Incorrect, because serotonin has no effect on the brain, so it cannot contribute to depression in any way
- Overstated, because depression is multi-factorial, and serotonin is one of several factors that may contribute
- Correct, because serotonin is a hormone secreted by the thyroid, which is the main cause of all mood disorders
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Which of the following is a function of dopamine in the brain?
- Control of blood glucose in the liver only, since dopamine acts as a hormone in the liver's metabolism
- Control of voluntary movement and reward pathways, with its loss underlying the motor symptoms of Parkinson's
- Production of red blood cells in the bone marrow, which dopamine stimulates through the blood circulation
- Breakdown of myelin in the axons of the peripheral nerves, which is the main role of dopamine in the body
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Which of these best explains why SSRIs take several weeks to show benefits in depression?
- The patient's kidneys must regrow before the drug can be processed, which takes a long period of treatment
- SSRIs take effect immediately, so the delay is a mistake in the way the drug is prescribed to patients
- Changes in receptor sensitivity and neural adaptation take time, not just the immediate rise in serotonin
- The drug must be stored in the myelin sheath before it can act, which takes several weeks in every patient
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A researcher measures dopamine levels in post-mortem tissue from people with Parkinson's disease and healthy controls. What result would support the dopamine hypothesis?
- Dopamine levels are identical in both groups, which would show that dopamine is not involved in the disease
- Dopamine levels are lower in the substantia nigra of Parkinson's patients than in healthy controls
- Dopamine levels are higher in Parkinson's patients, which would show that dopamine causes the disease
- Dopamine is absent in healthy controls only, which would show that the disease is caused by excess dopamine
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Which statement best describes the role of serotonin in mood regulation?
- It is a hormone that is produced only in muscle, where it controls the mood of the individual
- It is a neurotransmitter that influences mood and behaviour through receptors in the brain
- It is a structural protein in bones, which affects mood by changing the strength of the skeleton
- It is an enzyme that digests glucose, which changes the mood by altering the energy supply to the brain
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A drug is designed to block dopamine receptors and is found to worsen tremor in Parkinson's patients. Which explanation is most consistent?
- Blocking receptors reduces dopamine signalling further in an already dopamine-deficient system
- Blocking receptors increases dopamine production in the substantia nigra, which then causes the tremor
- The drug has no effect on receptors, so the tremor must come from an unrelated cause in the patient
- Blocking dopamine receptors cures Parkinson's, so the worsening tremor must be a rare side effect of recovery
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A patient with Parkinson's disease responds well to L-Dopa at first but later develops involuntary movements. Which evaluation is most reasonable?
- Long-term L-Dopa can cause side effects, so dose and monitoring must be balanced against symptom control
- L-Dopa has no effect on dopamine levels in any patient, so the movements must be caused by another drug
- Involuntary movements prove the disease has been cured, since the drug has restored normal dopamine signalling
- The L-Dopa is useless and should be stopped immediately with no further assessment of the patient's condition
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Which of these is a correct link between brain chemicals and disease?
- Imbalance of naturally occurring brain chemicals can contribute to ill health, such as dopamine in Parkinson's
- Brain chemicals cannot be linked to any disease, since they are only used for normal communication between cells
- Only hormones from the pituitary cause brain disease, which is why brain chemicals are never involved in illness
- Parkinson's is caused by a bacterial infection of the spinal cord only, with no role for any brain chemical
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Which pair correctly matches a condition with its chemical imbalance?
- Depression: insulin deficiency, which lowers the level of serotonin in the brain and causes low mood
- Parkinson's disease: dopamine deficiency, caused by loss of dopamine-producing neurones
- Depression: dopamine excess only, which is the main chemical imbalance seen in people with low mood
- Parkinson's disease: serotonin excess only, which causes the tremor and the rigidity of the muscles
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A student estimates that dopamine neurone loss in Parkinson's disease is 60 per cent. If a patient originally had 1000 units of dopamine-producing activity, how many units remain?
- 40 units, found by taking 4 per cent of the original 1000 units that remain in the substantia nigra
- 600 units, which is the amount lost, found by taking 60 per cent of the original 1000 units
- 400 units, found by taking 40 per cent of the original 1000 units that remain after the loss
- 160 units, found by taking 16 per cent of the original 1000 units after the loss of the neurones
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