pharmacology qs

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laurajane.price
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pharmacology qs
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2010-05-23 17:56:53
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pharmacology
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pharmacology
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  1. Where are glucocorticoid receptors located?
    Cell cytosol
  2. Where are the oestrogen receptors located?
    Cell nucleus
  3. State the differences between GABA A and GABA B receptors
    • GABA A:
    • ligand gated ion channel
    • located post synaptically
    • pentameric structure
    • activation opens Cl- channels

    • GABA B:
    • G protein coupled receptor
    • linked to adenylyl cyclase (inhibit cAMP)
    • found pre and post synaptically
    • prevent Ca2+ channel opening and increase K+ permeability
  4. Name the main inhibitory transmitters in the CNS and state how they are inactivated
    GABA - active uptake

    Glycine - active uptake and metabolism
  5. Name the main excitatory transmitters in the CNS and state how they are inactivated
    Glutamate - active uptake
  6. Name the four types of glutamate receptor
    Metabotropic

    and the 3 Ionotropic receptors:

    NMDA

    AMPA

    kainate
  7. Which ionotropic glutamate receptors are located post synaptically only?
    AMPA

    NMDA
  8. Which ionotropic glutamate receptor is located pre and post synaptically
    Kainate
  9. Acetylcholine in the CNS has a role in...
    Renshaw cell, alpha motor neurone moderation

    Interneurone in basal ganglia have excitatory actions on muscle control (Parkinsons)

    Involvement in pain perception

    Memory and learning (decreased function = dementia)
  10. What is Parkinson's Disease associated with?
    Loss of dopamine from the basal ganglia in the nigrostriatal pathway

    Disturbance of other CNS transmitters (ACh, GABA, NA, 5HT)
  11. What are the symptoms of Parkinson's Disease
    Muscle tremor at rest

    Muscle rigidity

    Difficulty with voluntary movements
  12. What are the four stages of anaesthesia and what do they entail?
    Stage I: analgesia - conscious but drowsy, reduced response to painful stimuli

    Stage II: excitement - loss of consciousness, no response to non-painful stimuli, reflexes to painful stimuli, exaggerated cough/gagging reflex - subject may move, hold breath, talk, choke or vomit)

    Stage III: surgical anaesthesia - spontaneous movement ceases, regular respiration

    Stage IV: medullary paralysis - cessation of respiratory control, vasomotor control ceases, leads to death
  13. Explain the lipid theory of anaesthetics and it's problems
    Anaesthetics may act by dissolving in the fatty fraction of the brain cells. These anaesthetics dissolve and remove fatty constituents from brains cells, changing their activity and inducing anaesthesia

    Strong correlation between lipid solubility and anaesthetic potency

    • However;
    • Anaesthetics can exist as active and inactive enantiomers, both will have same lipid solubility
    • Many compounds with high lipid solubility do not have anaesthetic effects
  14. Explain the protein theory of anaesthetics
    General anaesthetics interact with membrane proteins

    Explains inactive enantiomers as active site "lock and key" only active one will fi
  15. Explain the advantages and disadvantages of inhaled general anaesthetics
    • Advantages:
    • rapid control over anaesthesia depth as [inspired air] -> [arterial blood] -> [brain] (so long as BBB can be crossed
    • speedy recovery phase as expired out through lungs
    • shorter semi-comatose state

    • Disadvantages:
    • mask can be frightening
    • not as fast an induction as i.v.
  16. What are the advantages and disadvantages of i.v. anaesthetics
    • Advantages:
    • Rapid induction
    • No excitment phase
    • Simple apparatus
    • Pleasant induction
    • No atmospheric pollution
    • No psychological effects of mask

    • Disadvantages:
    • Difficult to control level of anaesthesia
    • Redistribution into skeletal muscle - slow recovery
    • Finite duration of anaesthesia
    • Damage to veins e.g. thrombophlebitis
    • Mechanically inflate lungs and give o2
    • Assessment of anaesthesia difficult
  17. What are the different opiod receptors and what do they do?
    • Mu
    • - open K+ channels (hyperpolarisation), reduce neuronal activity, inhibit neurotransmitter release, including substance P (pain transmission)
    • delta
    • - similar to mu receptors
    • kappa
    • - Reduce Ca2+ channel opening, inhibit neurotransmitter release as mu, delta
  18. Which opioid receptor is responsible for respiratory depression?
    • Mu
    • - Mu-2 only?
  19. How do the opioids cause repiratory depression?
    Decrease response to PCO2 which decreases respiratory rate and minute volum
  20. Name the main actions of glucocorticoid steroids
    • Metabolic effects
    • Anti-inflammatory
    • Immunosuppressive
  21. Name the main actions of mineralocorticoid steroids
    Water and electrolyte balance
  22. What is glucocorticoid activity associated with?
    beta-hydroxyl group at position 11

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