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Y2 BB PBL Questions
Medicine (A100)
Queen Mary University of London
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med year 2Preview text
PBL1: Mr Body
- Name the neurotransmitters released by the corticostriatal and striatopallidal pathways (1 mark)
● Glutamate and GABA respectively
- Describe the effects of D1 receptor activation on striatal efferent circuitry (2 marks)
● D1 receptor activation causes the activation of the direct pathway (½ mark) by which the GPi is inhibited (½ mark). This causes the disinhibition of the thalamus (½ mark) and hence the activation of the cortex (½ mark)
- What is cognitive behavioural therapy (CBT)? (2 marks)
● It’s a behavioural and cognitive approach that looks at how we think about a situation and how this affects the way we act (1 mark) ● Method: therapist and patient work together in changing the patient’s behaviours, their thinking patterns or both of these, resulting in more positive thoughts (1mark)
- List and briefly describe three long-term complications of L-DOPA therapy (3 marks)
● Motor fluctuations: include “on-off” phenomena in which sudden and dramatic fluctuations of motor performance occur; periods of normal mobility (on) followed by sudden ‘freezing’ (off). End of dose deterioration and delayed (or ‘no on’- freezing) responses also occur (1 mark)
● Dyskinesias: include choreiform movements (purposeless involuntary dance-like movements) and dystonias (sustained intense muscle contractions) (1 mark)
● Neuro-psychiatric problems: hallucinations, delirium, mood changes, sleep disturbance and nightmares (1 mark)
- What is rotigotine and what is its route of administration? (2 marks)
● Dopamine receptor agonist (non-selective) with affinity for both D 1 and D 2 family receptors ● Applied transdermally as a patch
- In Parkinson’s disease striatal dopamine signalling is gradually lost. How can this loss be monitored using imaging? (1 mark)
● The gradual loss of dopaminergic innervation of the striatum can be monitored by imaging the dopamine transporter, using the DaTScan (1 mark)
- What is alpha-synuclein, where is it found and what is its link with Parkinson’s? (2 marks)
● Alpha-synuclein is a protein found in the cytoplasm in Lewy bodies (major histopathological feature of Parkinson’s disease) (1 mark) ● Certain genes associated with alpha-synuclein (PARK1/4, SNCA gene) have been identified as a genetic risk factor for Parkinson’s disease (1 mark)
- Selegiline was considered to be added to Mr Body’s medication. What is the mechanism of action of selegiline and why might this improve Mr Body’s symptoms? (2 marks)
● Selegiline is a monoamine oxidase B inhibitor (1 mark) ● MAOB breaks down dopamine so inhibiting this enzyme will increase the available levels of dopamine in the brain (1 mark)
PBL2: Aches and Pains
- Hyperalgesia and allodynia commonly occur in neuropathic pain. What is meant by hyperalgesia and allodynia? (2 marks)
● Hyperalgesia occurs when one’s perception of the intensity of painful stimuli is increased, i. increased pain in response to a noxious stimulus (1 mark). ● Allodynia occurs when a normally innocuous (non-painful) stimulus is felt as painful, i. pain experienced as light clothes brushing the skin (1 mark).
- Describe the pathway, starting with the nociceptive afferents, with terminals in the lower back, through the spinal cord and ultimately to the cerebral cortex, for the transmission of pain sensation, specifically responsible for localization of the noxious stimulus. Ensure that you give the name of a) the sites where the neuronal cell bodies are located and b) the projection taken by their axons.
● Nociceptive afferents with cell bodies in the dorsal root ganglia (½ mark), project axons which synapse in laminae I, II and V of the spinal cord (½ mark). ● Axons from projection neurons in lamina I and V cross over at this segment (or 1-2 segments above) (½ mark) and ascend in the spinal cord contralaterally in the spinothalamic tract (½ mark). ● The axons synapse in the ventroposterolateral (VPL) nucleus of the thalamus (½ mark), which projects to the primary somatosensory cortex (½ mark) where the localization of the stimulus is perceived.
- Explain the likely cause, the location of the injury and mechanism that generates the pain radiating down the side of Jerry’s leg to his toes. (4 marks)
● It is likely due to herniation of the L4/L5 vertebral disc or vertebral degeneration (1 mark) ● Compression or irritation of the nerve root/ dorsal root ganglion (1 mark) causes sensitisation and spontaneous activity in the affected fibres and thus the radiating pain (1 mark). ● The nerve root affected is L5 as suggested from the distribution of the shock-like pains, which correspond to its peripheral distribution (1 mark)
- What class of drug is pregabalin and what is its mechanism of action? (2 marks)
● It is an anticonvulsant drug used in the treatment of neuropathic pain (1 mark). ● It works on the α2δ1 subunit of N-type voltage gated calcium channel (½ mark) ● The α2δ1 subunit on primary afferents and other central terminals is upregulated in neuropathic pain conditions (½ mark) ● Pregabalin causes decreased release of neurotransmitters linked to hyperexcitability (e. glutamate, substance P, noradrenaline) (½ mark)
- Opioid analgesics are often prescribed for severe pain. How do opioid drugs reduce neuronal excitability? (2 marks)
● They hyperpolarise neurones by opening potassium (K+) channels (1 mark) and inhibit neurotransmitter release by inhibiting calcium (Ca2+) entry into the presynaptic terminal (1 mark) o Most opioid receptors are on nociceptive primary afferents (presynaptic)
Note: In the scenario it is likely that there is nerve root and/or sensory ganglion compression or irritation occurring. This can lead to ectopic neural activity originating from the site of the compression. Compression can also lead to severing of axons within the nerve roots or spinal nerves. While this may cause a loss of sensitivity through death of sensory neurons and decreased neurotransmission in some neurons, it causes other changes, including inflammatory responses within the nerve which sensitise other cells. Neurons show altered biophysical properties including membrane instability also leading to ectopic activity. Changes may also take place in the spinal cord at the first synapse and produce spontaneous activity in these central neurons. Such activation in the nerve or spinal cord may be perceived as ‘electric shocks’. Burning sensations are often associated with alterations in nociceptor function as a result of injury. These can result from both peripheral sensitisation (affecting threshold of activation of the sensory neurons themselves) and central sensitisation after injury.
PBL4: A difficult decision
- Briefly describe 3 possible cellular mechanisms which are implicated in the generation of seizures. ( marks)
● Increased excitation (e. hyperactivity of glutamatergic transmission) (1 mark) ● Decreased inhibition (e. deficit in GABAergic transmission) (1 mark) ● Intrinsic neuronal hyperexcitability (related to altered electrical properties of the neuronal membrane) (1 mark)
- What is a paroxysmal depolarising shift and how is it caused? (2 marks)
● The resting membrane potential of neurons becomes depolarised by 30-40mV causing a sustained burst of action potentials for several seconds (1 mark) ● This is most likely due to activation of NMDA glutamate receptors (elevated glutamate levels are associated with epileptic foci) (1 mark)
- Explain why it is not advisable for the mother to stop taking the anti-epileptic medication during her pregnancy? (2 marks)
● Prolonged or frequent seizures could promote fetal hypoxia or apnoea (1 mark), which could damage the baby’s brain and result in neurological deficits (1 mark)
- There are non-pharmacological treatments for epilepsy. What is the major role of the corpus callosum and the rationale for carrying out corpus callosotomy in epilepsy? (2 marks)
● The corpus callosum is involved in inter-hemispheric communication (1 mark). ● Corpus callosotomy reduces the spread of seizures to the other cerebral hemisphere by cutting the corpus callosum (1 mark).
- Name the cellular target of the drug tiagabine. (1 mark)
● The GAT-1 GABA transporter
PBL5: The will to live
- Selective serotonin reuptake inhibitors are used to treat depression. Give an example of such a drug and briefly outline “the monoamine theory” of depression. Why is there a delay in the onset of action of these drugs? (3 marks)
● Any from: citalopram, escitalopram, fluoxetine, paroxetine, sertraline (1 mark) ● Depression is associated with decreased aminergic (serotonin, noradrenaline and/or dopamine) transmission in the CNS (1 mark). ● It is thought that, for example, the delay in onset of action is due to the time taken to downregulate presynaptic 5HT1A receptors (1 mark)
- Explain the rationale of cognitive behavioural therapy (CBT) (2 marks)
● CBT looks at how we think about a situation and how this affects the way we act. In turn our actions can affect how we think and feel. The therapist and client work together in changing the client’s behaviours, or their thinking patterns, or both of these. (1 mark for the thinking and 1 mark for the acting components of the answer)
- What is the “cheese effect” and why does it occur? What are its symptoms, and what class of drugs can induce this adverse effect? (3 marks)
● The “cheese effect” manifests as severe headaches, and also a massive hypertensive crisis may occur (1 mark). ● It is a reaction which reflects the interaction of irreversible monoamine oxidase inhibitors used in mood disorders, with food containing high levels of tyramine (1 mark). ● Normally tyramine is broken down in the gut and liver but if this is prevented then tyramine can lead to elevated levels of noradrenaline in the synaptic cleft (1 mark).
- Name two risk factors for depression-associated suicide. (2 marks)
● Male gender, older age, unemployed, concurrent mental disorders, previous suicide attempts, alcohol and drug abuse, low socio-economic status, previous psychiatric treatment, certain professions - doctors, students, low social support / living alone, significant life events (any two)
Y2 BB PBL Questions
Module: Medicine (A100)
University: Queen Mary University of London
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