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Define the terms pharmacokinetics and pharmacodynamics



1. Define the terms ‘pharmacokinetics’ and ‘pharmacodynamics’.


2. What is meant by ‘plasma protein binding’? In your answer, explain the effects that plasma protein binding has on the metabolism and elimination of protein bound drugs.



3. Why should aspirin not normally be administered to a patient who is taking a course of the anticoagulant drug, warfarin?


4. Explain the ‘hepatic first pass effect’. Why is it important to consider this effect when administering drugs orally?


5. Morphine, a narcotic analgesic, has a half-life of about 2 -3 hours. The half-life of naloxone (Narcan), the “antidote” for narcotic overdose, is approximately 1 hour. What does the term ‘half-life’ mean, and what implications does this information have for the prescribers of these drugs?


6. What is meant by ‘steady state’ concentrations of a drug? Explain how and when a steady state is achieved.


7. Describe the characteristics and properties of enzymes. What is the difference between competitive and non-competitive enzyme inhibition? Give one example for each.


8. What happens when a drug acts as an ‘antagonist’? Explain how atropine, an anticholinergic, acts as an antagonist at cholinergic receptors. What are the effects of atropine on the human body?


9. Describe the drug interactions which may occur when the following drugs and/or other substances are administered concurrently:


a. phenelzine and broad beans or cheIDar cheese


b. tetracyclines and antacids


c. alcohol and diazepam




Fundamentals of Pharmacology


Mr FT is a 22-year-old man who has been admitted to your hospital emergency department. He has been working as a labourer at a nearby market garden that specialises in growing flowers. He was spraying the crops with the organophosphate insecticide Malathion when he collapsed. He was not wearing the appropriate protective clothing. You observe that he is conscious and complains of gastrointestinal cramps and nausea. He vomited a couple of times in the ambulance as he was transported to hospital. You note the manifestations: profuse sweating, drooling, lacrimation, bradycardia, agitation, muscle twitching and constricted pupils.


Supportive treatment is implemented, which involves respiratory support and the administration of antidotes. His progress is carefully monitored during this critical period. His recovery is without complications. He is discharged from hospital several days later.


1. Underlying this client’s condition is a change in the level of activity of a division of the autonomic nervous system. Which division is affected and what is the nature of the change? Provide examples of the physiological responses


2. Which type or types of tissue receptor are involved in this condition?


3. Explain the mechanism by which the organophosphate insecticides induce this state?


4. Which clinical drug group do the organophosphate insecticides closely resemble in terms of their action? Why?


5. Which drug group can be used as an antidote to oppose the effects of the insecticide? Why?





BB, a 5-year-old boy with a history of chronic asthma, has been admitted to hospital suffering a moderately severe asthma attack. Over a period of time his condition has been well managed using daily inhalation of the corticosteroid beclomethasone, coupled with inhalation of the Beta2 agonist salbutamol when required. His parents think that this particular attack was brought on by a mild respiratory infection that has been affecting the other members of the family.


Treatment begins with oxygen therapy and a dose of the Beta2 agonist salbutamol via an inhaler and spacer. A dose of hydrocortisone is administered intramuscularly soon after. Inhaler treatment is repeated hourly. After eight hours the acute attack is easing and by 12 hours post admission BB is ready for discharge.


1. Briefly outline the long-term aims of asthma management, the first-line therapy and the preferred treatment of an acute attach according to the National Asthma Campaign.



2. Explain why the mild respiratory infection would be considered a trigger for BB’s asthma attack.


3. What is the rationale for the use of inhaled corticosteroids in the long-term management of BB’s chronic asthma?




a. What short-term adverse effects would you expect to see with inhaled corticosteroids?

b. What short-term adverse effects would you  expect to see associated with inhaled B2 agonists?

5. What problem may be associated with the long-term use of inhaled corticosteroid therapy in young children?


6. Why has the health team managing BB’s acute attack used an inhaler and spacer to administer the bronchodilator therapy rather than a nebuliser?

7. How does the systemic administration of the corticosteroid hydrocortisone assist in the recovery after an acute asthma attack?


8. What aspects of your client’s condition would you monitor during this combined therapy? Why?



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