How do local anaesthetics prevent the conduction of action potentials in nerves?
Give a brief account of the mode of action of three different types of anti-cancer
agents. Why is it particularly important in the treatment of cancer to have
available a range of drugs acting by different mechanisms?
Explain why such a wide range of volatile organic compounds act as general
anaesthetics. Would it be sensible to attempt to develop a general anaesthetic
antagonist?
Describe the chemical transformations that drug substances undergo after absorption.
What is the clinical significance of genetically controlled variations in
the structure of drug transforming enzymes?
"It is now clear that antagonism at dopamine receptors is the main determinant
of antipsychotic drug action". Is that true? Is that sufficient?
Describe the electrical events at the neuromuscular junction. How are these
affected by drugs and toxins?
Give an account of the role of second messenger pathways in the flight-or-fight
response to adrenaline.
What physiochemical factors govern the interaction of a drug with its receptor?
What is the evidence for subtypes of beta-adrenergic receptors? Why is this
of relevance in the treatment of asthma and hypertension?
Describe the different modes of antagonism giving clinically relevant examples, where possible.