Pharmacology SCH3236 - Assignment Example

PHARMACOLOGY SCH3236 SEMESTER ONE 2017 ASSIGNMENT ONE Before midnight MUST INCLUDE YOUR NAME & STUDENT NUMBER ON THE ASSIGNMENT DOCUMENT PART A (Total 45 marks) 1. Define the terms 'pharmacokinetics' and 'pharmacodynamics'. Include in your answer an example of at least one drug. Pharmacokinetics refers to the study of the drugs motion in the body from intake to release. It involves four major steps. These are absorption, distribution, metabolism and excretion. Pharmacodynamics, on the other hand, refers to the biological changes of the drug that lead to its effects in the body (Bullock and Manias, 2013). These changes may be physical, chemical or based on receptor and enzyme interactions with the drug. In brief pharmacokinetics is what the body does to the drug and pharmacodynamics is what the drug does to the body. 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. Plasma protein binding is the reversible binding of drug components to circulating plasma proteins such as albumin. On binding, the plasma proteins act as the reservoir of the drugs as elimination and metabolism reduces the bioavailability. Free drug concentrations can, therefore, be maintained at a constant state as the drugs bound to protein are gradually released to circulate freely. Plasma binding properties of a drug has a direct proportion to its bioavailability (Edmunds, 2016). 3. Why should aspirin not normally be administered to a patient who is taking a course of the anticoagulant drug, warfarin? Aspirin is administered as aspirin phenylbutazone. The active ingredient of this compound inhibits platelet aggregation, a process that is involved in coagulation. Due to this property, aspirin potentiates the anticoagulation activity in blood. It also displaces warfarin from albumin, a plasma protein (Katzung and Trevor, 2015). Thromboxane pathway that is inhibited by aspirin is essential in the coagulation cascade and platelet activity on injured tissues. 4. Explain the 'hepatic first pass effect'. Why is it important to consider this effect when administering drugs orally? This refers to the process whereby a drug, on administration, enters the portal circulation before proceeding to the systemic circulation. Drugs that are taken orally undergo this first pass effect. This is why drugs that are rapidly metabolized in the liver should not be given orally since they will undergo the first pass effect, and less amounts will reach target tissues (Walsh, Schwartz-Bloom and Levine, 2010). There are other drugs that are administered parenterally and also undergo a first-pass effect since they also pass through the portal system and then they are released into the systemic circulation. If such drugs are very toxic to the liver, there may be associated impairments. 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? Half-life is a term used in determination of the excretion rate of a drug and it refers to the time it takes for the concentration of a drug at equilibrium to decrease from C to ½C or for it to change by 50%. Naloxone, with a shorter half-life will induce a more abrupt reaction that will aid in eliminating morphine (Walsh, Schwartz-Bloom and Levine, 2010). Half-life of the drugs can be easily determined in drugs that are solely eliminated via the kidney such as digoxin. It can also be determined in those that do not undergo metabolism and are excreted unchanged. The half-life of most drugs become altered in renal diseases and kidney failure. 6. What is meant by 'steady state' concentrations of a drug? Explain how and when a steady state is achieved. A steady state is a scenario where the elimination and absorption of drug in circulation is balanced, thereby there is a constant amount in circulation. It is achieved by exponentiation of the dose with preferred intervals until desired concentration is achieved. It is majorly done when the attainment of effective dose cannot be easily attained due to slow absorption or faster elimination (Clark, 2012). 7. Describe the characteristics and properties of enzymes. What is the difference between competitive and non-competitive enzyme inhibition? Give one example for each. The major properties of enzymes are specificity to substrate, catalytic properties, enzyme inhibition due to receptor blockers, engagement in reversible reactions, high molecular weight, colloidal and water solubility. Enzymes are targeted by many drugs. They can be inhibited reversibly or irreversibly. Some drugs act as substrates for other enzymes. Enzymes can also be used to convert a drug from a pro-drug to an active component. A competitive enzyme binds to a receptor instead of the normal ligand to prevent the normal ligand from binding. A non-competitive one binds to its own receptor and elicit its functions (Bullock and Manias, 2013). 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? A drug acts as an antagonist when it binds to a specific receptor to prevent the normal molecule of that receptor from binding. This leads to a reduction of the effect of such molecules. Atropine is an anticholinergic drug that binds cholinergic receptors of areas such as eye and salivary glands to prevent secretions hence drying. Atropine causes general drying of the body glands due to prevention of secretions (Bullock and Manias, 2013). 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 cheddar cheese Phenelzine is a monoamine oxidase inhibitor, a group of drugs that produce potentially fatal interactions with most foods. These are foods that contain tyramine; broad beans and cheddar cheese are examples. Tyramine present is broken down in tissues by monoamine oxidase which when inhibited causes a rapid blood pressure elevation which can be fatal (Clark 2012). b. tetracyclines and antacids Tetracycline absorption is reduced by aluminium and magnesium antacids. This is due to the formation of non-absorbable chelates with divalent and trivalent cations present in these antacids (Pazdernik and Kerecsen, 2011). c. alcohol and diazepam Diazepam is a benzodiazepine used as an anticonvulsant drug. Its interaction with alcohol or any other CNS depressant leads to the enhancement of its sedative-hypnotic effects that can eventually result into toxicity (Bullock and Manias, 2013). PART B (Total 20 marks) The treatment of pain and inflammation is a cornerstone of pharmacology research. a) Describe the actions and possible adverse effects of two analgesic, one narcotic and one non-narcotic and a (different) anti-inflammatory drug (10 marks). Analgesics Acetaminophen is a drug that blocks the synthesis of prostaglandins and has some antipyretic effects. It also has some weak anti-inflammatory effects since it has less effects on peripheral tissue cyclooxygenase pathway. The adverse effects of acetaminophen are not severe. They include skin rashes and minor hypersensitivity reactions that are rare. Other rare changes may be alteration in leukocyte counts, hypoglycemic coma and renal tubular necrosis that result from high dosage (Walsh, Schwartz-Bloom and Levine, 2010). With long term use, hepatic necrosis can easily occur; this is a life threatening condition all the same. It is therefore recommended that acetaminophen should be avoided in patients with liver diseases. Aspirin is a salicylic acid derivative and has been used for a long time in the management of pain – since 1939. The major effects of aspirin are analgesia, anti-inflammation and anti-pyrexia. This makes it qualify to be an anti-inflammatory drug as well. It converts the enzyme responsible for COX pathway (cyclooxygenase) to acetylated cyclooxygenase which is inactive. It decreases PGE2 synthesis leading to desensitization of the nerve endings to most of the chemical mediators (Edmunds, 2016). It manages pain of low to moderate intensities. The common adverse effects include gastrointestinal effects, reduction of platelete thromboxane levels, depression of the respiratory system, Reye’s syndrome, uncoupling of oxidative phosphorylation and hypersensitivity reactions. Narcotics Narcotics are also called opioids. They have morphine like actions and is derived from poppy plant. Methadone is a classic example of a narcotic drug. It is an opioid that is orally effective with a longer duration of action. This drug interacts with the µ receptors the receptors exist in the CNS, gut and the urinary bladder. It raises pain threshold at the spinal cord regions. It equally reduces the release of substance P, a substance that participates in the modulation of spinal cord pain perception (Bullock and Manias, 2013). Methadone also inhibit the release of some excitatory neurotransmitters involved in pain stimulation. The main significant adverse effect of methadone is physical dependence. This means that withdrawal may lead to either motor, autonomic or psychological responses that are characteristic of incapacitation (Gross, Aradi & Sibbing, 2017). Anti-Inflammatory Drug Celecoxib is an anti-inflammatory drug that inhibits majorly the COX-2 pathway rather than the COX-2. This inhibition is reversible and time-dependent. Fortunately, it does not result into GIT bleeding and ulcers as aspirin does (Biaggioni, 2017). This drug produces the following adverse effects: headache, abdominal pain, diarrhea, dyspepsia and anaphylactic reactions (Edmunds, 2016). It should also be avoided in patients with cardiovascular and CNS disorders. b) Provide examples of conditions/diseases that each drug could be used for and explain why they are effective for the treatment of that condition (10 marks). Acetaminophen – it is the best substitute of aspirin in the management of pyrexia and pain together with stomach problems (GIT bleeding). It can also be used for those who need to manage the two conditions without effects on inflammation. Chicken pox in children can be best managed using acetaminophen to alleviate pain and fever associated with the viral infection. It can be taken together with probenecid and glutathione without any drug interactions (Pazdernik and Kerecsen, 2011). Aspirin – for those with bleeding disorders with reduced bleeding time, aspirin prolongs bleeding. It is also used with anticlotting factors such as clopidogrel and heparin to increase their efficacy through synergy. It increases the alveolar ventilation in the respiratory tract. It inhibits gastric acid secretion in the stomach and enhance the production of a protective mucus layer to protect the stomach walls. Enhances the retention of water and sodium as it improves the renal blood flow. It manages pain and high temperatures as it depresses inflammation at various sites (Bullock and Manias, 2013). Methadone – it is an analgesic that can also be used to control the withdrawal symptoms and dependence of morphine and heroin. It also has a milder withdrawal symptom Celecoxib – treatment of rheumatoid arthritis, osteoarthritis and strong pain management without inducing gastrointestinal bleeding. PART C (Total 35 marks) Chapter 55, page 694 - Fundamentals of Pharmacology (7th Edition) 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. (7 marks) The long-term goals of asthma management include prevention of troublesome and chronic symptoms, maintenance of proper pulmonary function, maintenance of normal activities such as exercises, prevention of recurrent exacerbations of asthma, prevention of pulmonary dysfunction and minimized growth as well as therapeutic measures with non-severe adverse effects (Edmunds, 2016). The first line therapy of asthma include: i) Inhalation of β2 adrenergic agonist which are responsible for relaxation of smooth muscles of the airway and effective bronchodilation. These drugs include pirbuterol, terbutaline and albuterol for short term control and salmeterol xinophoate and formoterol for long-term bronchodilation (Clark, 2012). ii) Corticosteriods are the first line in any form of severe asthmatic attacks or persistent ones. However, oral glucocorticoid should accompany the drug. The inhaled corticosteroids are the most effective drugs in the long-term asthma management. They control inflammation of the airway that is a characteristic of asthma (Clark, 2012). In acute asthmatic attacks, epinephrine is administered to relieve the dyspnoeic effects that come with asthma. It also causes effective inhibition of release of mediators like histamine produced by mast cells (Scaglione, Donde, Hassan & Jannini, 2017). Isoproterenol is equally active in the management of acute asthmatic attacks when inhaled and the action persists for around an hour (Hilal-Dandan, Brunton and Goodman, 2014). Ephedrine and pseudoephedrine is also used for management of acute attacks, however, it is mostly used for chronic cases. Albuterol, pirbuterol, and terbutaline are also used for short term relief. 2. Explain why the mild respiratory infection would be considered a trigger for BB’s asthma attack. (3 marks) Infection of the respiratory tract results into inflammation. Inflammation plays a major role in the bronchoconstriction and an observable increase in mucus secretion by the goblet cells lining the airway. This can also be due to irritation of the tract whereby the stimulation will activate the mucociliary process (Bullock and Manias, 2013). This increase in bronchial activity and inflammation attenuates asthmatic attacks. This explains why cure of the infection cannot treat asthma itself. 3. What is the rationale for the use of inhaled corticosteroids in the long-term management of BB’s chronic asthma? (3 marks) Inhaled corticosteroids are the most preferred drugs for the management of persistent and chronic asthmatic attacks. In fact, there isn’t any preferred drug that is as effect as inhaled corticosteroids (Morgan, Aroke & Dungan, 2017). Even in patients with severe asthma, they are desirably potent and it will be unnecessary to use oral glucocorticoids. The National Heart, Lung and Blood Institute recommends that these drug class be used for patients who have not had the asthma classified (Apley and Smith, 2015). It decreases underlying airway inflammation through suppression of the inflammatory cascade. 4. a. What short-term adverse effects would you expect to see with inhaled corticosteroids? (2 marks) Osteoporosis, hyperglycaemia and hypokalaemia always exist with long term use of corticosteroids. Osteoporosis is the most common one since these drugs suppress intestinal Ca2+ absorption (Bullock and Manias, 2013). Symptoms that are characteristic of Cushing’s syndrome may occur due to long term use of corticosteroids (Gaston & Friedman, 2017). b. What short-term adverse effects would you expect to see associated with inhaled B2 agonists? (5 marks) The major adverse effects of inhaled corticosteroid use in children is retardation of vertical bone growth. The adverse effect becomes more alarming when the growth is secondary is secondary to low oxygen levels in blood (Clark, 2012). The latter frequently occurs in severe cases. 5. What problem may be associated with the long-term use of inhaled corticosteroid therapy in young children? (4 marks) As mentioned earlier, children who use corticosteroids for long term management of asthma may develop retarded growth due to retardation of vertical growth development. More serious problem may arise with development of Cushing-like syndrome (In Clark and In Kumar, 2017). Body fat is redistributed and a moon face is observable. This adverse effect is characterised by increased body hair growth, insomnia acne and increased appetite. Sex hormones may also fail to develop appropriately hence delayed maturation (Katzung and Trevor, 2015). 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? (2 marks) First, inhalers are preferred to such scenarios since they are more portable. This will allow BB to learn how to use it in any other subsequent attacks. Inhalers, unlike nebulizers, are easy to use and does not require any electric power in order to function (Hilal-Dandan, Brunton and Goodman, 2014). Another reason is that doses can be easily administered by number of puffs since the amount released are pre-measured. 7. How does the systemic administration of the corticosteroid hydrocortisone assist in the recovery after an acute asthma attack? (4 marks) Hydrocortisone is used to relieve inflammatory symptoms. The asthmatic attack was initiated by inflammation that followed a prior infection. They reduce inflammatory responses and also reduces the release of histamine from mast cells that will aggregate and cause inflammatory responses (In Clark and In Kumar, 2017). It is also used in the treatment of certain allergies. In addition, on topical application to the respiratory tract, it reduces systemic effects (Edmunds, 2016). 8. What aspects of your client’s condition would you monitor during this combined therapy? Why? (5 marks) The client should be observed often and carefully to ensure there are no incidences of exacerbations. It should also be ensured that the patient has no hypersensitivity to certain drugs or no drug-drug interactions (Hilal-Dandan, Brunton and Goodman, 2014). The acute management should be able to relieve the airway obstruction by mucus that clog them to ensure the drug is effective in the management. The patient should be assessed for circulation, airway and breathing to ensure that stability can be feasibly attained. As treatment occurs, it should be confirmed that there is no worsening of the condition. In case of worsening, the drug being administered should be immediately withdrawn (Walsh, Schwartz-Bloom and Levine, 2010). PART D - (Total 15 marks) Eva Bernstein, aged 58, comments how relieved she is now that her doctor has started her on the thiazide hydrochlorothiazide as part of her antihypertensive therapy. “Now I won’t have to worry about having food without salt. The water tablet will take care of it,” she explains. What would be your response to her? What other lifestyle issues will you explore with Ms Bernstein? Eva must be made aware of the action of hydrochlorothiazide (HCTZ) on her kidney. There is an increased excretion of water and sodium initially. Extracellular volume decreases consequently and cardiac output together with renal blood flow reduce. With time, plasma volume nears normal; it is only peripheral resistance that remains low (Bullock and Manias, 2013). This explains why they are always used together with potassium sparing agents. Use of normal or excessive intake of salt will initially cause renal dysfunction due to hyperactivity to eliminate sodium present in the blood. High salt intake will cause a faster achievement of normal plasma levels hence the drug will not be as effective as desired (Gauwitz, 2012). Finally, sodium cations present in table salt is likely to intensify hypertension and increases the risk of complications such as end organ damage and hypertension. It should therefore minimized or eliminated from the diet for the purposes of managing hypertension in such patients. The condition of the patient will require modification of lifestyle to prevent complications that may arise from the disease or worsen her prognosis (Insel, Amara, Blaschke & Meyer, 2017). i) She should avoid smoking at all costs. It is a gross risk factor of cardiovascular diseases. Quitting smoking has been an effective way of controlling the course of the disease. It entirely increases the heart rate and blood pressure (In Clark and In Kumar, 2017). ii) Nutrition as a modification factor requires the patient to take foods that are likely and more potent to modify the blood pressure to be within the desired range and they should avoid foods with high salt content as indicated in the explanations above (Katzung and Trevor, 2015). Other prime characteristics of dietary intake should be characterised by dietary potassium. Potassium in diet has the ability to decrease systolic blood pressure by up to 8mmHg and up to 2mmHg in normotensive individuals. Foods include bananas, potatoes, avocadoes, kiwi fruits and yoghurt. However, renal impairment can result into hyperkalaemia hence contraindicated in those with kidney problems. A healthy eating pattern is recommended to this group. iii) Such individuals always need to avoid alcohol. Lots of debate has seen the nullification of how beneficiary the consumption of less amounts of alcohol can help reduce blood pressure. Less amounts of alcohol always leads to addiction and later moderate or large intake. The two later quantities increase blood by more than 3.8 mmHg (Apley and Smith, 2015). Statistics show that reducing alcohol consumption among hypertensives reduces systolic blood pressure by an average of 3.8 mmHg. The risk increases among women. iv) Physical activities of 35 to 45 minutes daily have been associated with improvement in blood pressure and improving the state of hypertension (Gauwitz, 2012). However, isometric exercises should be avoided since it can raise blood pressure. v) Body weight should also be observed due to the positive association of obesity and hypertension (Bullock and Manias, 2013). Blood pressure reduction is always associated with loss of body weight – whether in hypertension or not. In this case, a reduction of body weight by 1% is equated to an average blood pressure drop by 1mmHg; so the more weight lost, the more hypertension is managed. The mechanisms and strategies above are not only for management of hypertension, but also for the prevention. The lifestyle practices mentioned are highly associated with healthy lives. Patients and general population are entitled to this information to curb hypertention, diabetes, arthritis and other lifestyle diseases. References Apley, M. D., & Smith, R. A. (2015). Bovine clinical pharmacology. Philadelphia, Pennsylvania: Elsevier. Biaggioni, I. (2017). The Pharmacology of Autonomic Failure: From Hypotension to Hypertension. Pharmacological Reviews, 69(1), 53-62. Bullock, S., & Manias, E. (2013). Fundamentals of Pharmacology VS. Sydney: Pearson Education Australia. Clark, M. A. (2012). Lippincott's illustrated reviews: Pharmacology. Philadelphia etc: Lipincott Williams and Wilkins. Edmunds, M. W. (2016). Introduction to clinical pharmacology. New York: Mcgraw-Hill. Gaston, T. E., & Friedman, D. (2017). Pharmacology of cannabinoids in the treatment of epilepsy. Epilepsy & Behavior. Gauwitz, D. F. (2012). Administering medications: Pharmacology for healthcare professionals. New York, NY: McGraw-Hill. Gross, L., Aradi, D., & Sibbing, D. (2017). Pharmacology: inhibitors of P2Y12. In Platelets in Thrombotic and Non-Thrombotic Disorders (pp. 1253-1267). Springer International Publishing. Hilal-Dandan, R., Brunton, L. L., & Goodman, L. S. (2014). Goodman and Gilman's manual of pharmacology and therapeutics. New York: Mcgraw-Hill. In Clark, M. L., & In Kumar, P. J. (2017). Kumar and Clark's Clinical medicine. Philadelphia, PA: Mosby/Elsevier. Insel, P. A., Amara, S. G., Blaschke, T. F., & Meyer, U. A. (2017). Introduction to the Theme “New Methods and Novel Therapeutic Approaches in Pharmacology and Toxicology”. Annual Review of Pharmacology and Toxicology, 57, 13-17. Katzung, B. G., & Trevor, A. J. (2015). Basic & clinical pharmacology. New York [etc.: McGraw-Hill Education. Morgan, B., Aroke, E. N., & Dungan, J. (2017). The Role of Pharmacogenomics in Anesthesia Pharmacology. Annual Review of Nursing Research, 35(1), 241-256. Pazdernik, T., & Kerecsen, L. (2011). Rapid review pharmacology. Philadelphia, PA: Mosby/Elsevier. Scaglione, F., Donde, S., Hassan, T. A., & Jannini, E. A. (2017). Phosphodiesterase Type 5 Inhibitors for the Treatment of Erectile Dysfunction: Pharmacology and Clinical Impact of the Sildenafil Citrate Orodispersible Tablet Formulation. Clinical Therapeutics. Walsh, C. T., Schwartz-Bloom, R. D., & Levine, R. R. (2010). Levine's pharmacology: Drug actions and reactions. London: Informa Healthcare. Read More

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? Half-life is a term used in determination of the excretion rate of a drug and it refers to the time it takes for the concentration of a drug at equilibrium to decrease from C to ½C or for it to change by 50%.

Naloxone, with a shorter half-life will induce a more abrupt reaction that will aid in eliminating morphine (Walsh, Schwartz-Bloom and Levine, 2010). Half-life of the drugs can be easily determined in drugs that are solely eliminated via the kidney such as digoxin. It can also be determined in those that do not undergo metabolism and are excreted unchanged. The half-life of most drugs become altered in renal diseases and kidney failure. 6. What is meant by 'steady state' concentrations of a drug?

Explain how and when a steady state is achieved. A steady state is a scenario where the elimination and absorption of drug in circulation is balanced, thereby there is a constant amount in circulation. It is achieved by exponentiation of the dose with preferred intervals until desired concentration is achieved. It is majorly done when the attainment of effective dose cannot be easily attained due to slow absorption or faster elimination (Clark, 2012). 7. Describe the characteristics and properties of enzymes.

What is the difference between competitive and non-competitive enzyme inhibition? Give one example for each. The major properties of enzymes are specificity to substrate, catalytic properties, enzyme inhibition due to receptor blockers, engagement in reversible reactions, high molecular weight, colloidal and water solubility. Enzymes are targeted by many drugs. They can be inhibited reversibly or irreversibly. Some drugs act as substrates for other enzymes. Enzymes can also be used to convert a drug from a pro-drug to an active component.

A competitive enzyme binds to a receptor instead of the normal ligand to prevent the normal ligand from binding. A non-competitive one binds to its own receptor and elicit its functions (Bullock and Manias, 2013). 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? A drug acts as an antagonist when it binds to a specific receptor to prevent the normal molecule of that receptor from binding.

This leads to a reduction of the effect of such molecules. Atropine is an anticholinergic drug that binds cholinergic receptors of areas such as eye and salivary glands to prevent secretions hence drying. Atropine causes general drying of the body glands due to prevention of secretions (Bullock and Manias, 2013). 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 cheddar cheese Phenelzine is a monoamine oxidase inhibitor, a group of drugs that produce potentially fatal interactions with most foods.

These are foods that contain tyramine; broad beans and cheddar cheese are examples. Tyramine present is broken down in tissues by monoamine oxidase which when inhibited causes a rapid blood pressure elevation which can be fatal (Clark 2012). b. tetracyclines and antacids Tetracycline absorption is reduced by aluminium and magnesium antacids. This is due to the formation of non-absorbable chelates with divalent and trivalent cations present in these antacids (Pazdernik and Kerecsen, 2011). c.

alcohol and diazepam Diazepam is a benzodiazepine used as an anticonvulsant drug. Its interaction with alcohol or any other CNS depressant leads to the enhancement of its sedative-hypnotic effects that can eventually result into toxicity (Bullock and Manias, 2013). PART B (Total 20 marks) The treatment of pain and inflammation is a cornerstone of pharmacology research.

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