Topics/Drug Classes – Page 7

Category: Topics/Drug Classes (page 7 of 7)

Why is guaifenesin so difficult to spell?

Even among drugs names that are often difficult to pronounce or spell, guaifenesin stands out for tripping up more students on spelling in exams than other drug names. Why is “guaifenesin” spelt this way?

Breaking “guaifenesin” up into “guai” and “fenesin” may help us to remember how to spell the word. It is the “guai” that in particular seems unnatural in English and is difficult to spell. Perhaps understanding the origins of the “guai” in “guaifenesin” can help us to remember how to spell the word.

The “guai” in “guaifenesin” comes from the word “guaiac”. Guaiac has been an English word since at least 1558, some say 1533. It is the common name for trees of the genus Guaiacum. The word originates from the Maipurean language spoken by the native Taínos people of the Bahamas. “Guaiac” has the honour of being the first American language word adopted into the English language. The guaiac is famous for being the source of the hardest wood known. The resin and bark of the guaiac were also used in traditional medicine for coughs and various other conditions. Guaifenesin is the active compound in the treatment of coughs isolated from guaiac resin and bark.

Guaifenesin was also formerly spelt “guaiphenesin”. It is one of the few drugs for which the American contraction of “ph” to “f” is now adopted for the official international nonproprietary name of the drug. The chemical name for guaifenesin is glyceryl guaiacolate.

Interestingly, guaiac resin also made another significant contribution to medicine. A phenolic compound derived from guaiac tree resin has also been used in the faecal occult blood test (FOBT). The presence of haeme from blood causes this compound to form a coloured product when exposed to hydrogen peroxide.

Adverse effects of guaifenesin and acetylcysteine

February 6, 2017 / phcdgs / 0 Comments

When the expectorant, guaifenesin, and the mucolytic, acetylcysteine, are prescribed together patients are monitored for bronchospasm and anaphylactoid reactions. Which of these two drugs is responsible for these serious adverse effects?

Guaifenesin is an expectorant. It increases the production of respiratory tract fluids. This helps to liquefy and reduce the viscosity of mucus in the respiratory tract. Generally, guaifenesin is a relatively safe drug, but it has been associated with dizziness, headache, vomiting, nausea, rash and urticaria.

Acetylcysteine can be used as a mucolytic. It possesses a free sulfhydryl group that splits disulphide bonds between mucoproteins. This reduces the viscosity of pulmonary secretions. Acetylcysteine can also be used to treat paracetamol overdose as it restores liver glutathione levels. However, acetylcysteine can trigger bronchospasm and severe anaphylactoid reactions, including rash, hypotension, dyspnoea, and wheezing. If they occur, these responses are usually observed within 30 to 60 minutes of starting intravenous infusion for the treatment of paracetamol poisoning. Anaphylactoid reactions are less likely in use as a mucolytic. Nevertheless, caution must be exercised when using acetylcysteine. Due to the risk of bronchospasm, the acetylcysteine must also be used with caution in elderly or debilitated patients with severe respiratory insufficiency and in patients with asthma.

Cromoglycate and Amiodarone

February 4, 2017 / phcdgs / 0 Comments

The surprising connection between cromoglycate and amiodarone

Cromoglycate is a mast cell stabiliser administered by inhalation as a preventer in the prophylactic control of asthma. It is also used for prophylactic control of allergic rhinitis and allergic conjunctivitis. Amiodarone is a class III antiarrhythmic agent, which prolongs repolarization of the cardiac action potential thus increasing the cardiac action potential duration.

Pharmacologically there is no obvious connection between cromoglycate and amiodarone. However, both drugs were first synthesised as derivatives of khellin the active ingredient obtained from plant extracts of khella (Ammi visnaga).

Low-dose aspirin plus glycine for anti-platelet drug therapy

February 3, 2017 / phcdgs / 3 Comments

Why do some low-dose aspirin formulations intended for use as anti-platelet medications contain glycine?

Aspirin has a potent anti-platelet action because it is an irreversible inhibitor of cyclooxygenase (COX). COX-1 is required for synthesis of the prothrombotic factor, thromboxane A2 (TXA2), in platelets. Platelets, being fragments of megakaryocytes, do not have a nucleus and therefore cannot synthesise more COX when it is irreversibly inhibited by aspirin. Thus, to recover from irreversible inhibition of COX-1 in the platelets, your body has to make new platelets. The average lifespan of a platelet is 8 to 9 days, so the anti-platelet effect aspirin is potent and long-lasting. However, in the stomach, inhibition of COX-1 prevents the production of protective prostaglandins and results in increased risk of gastrointestinal disturbance and peptic ulcers.

The combination of aspirin with glycine is reported to improve gastrointestinal tolerance to aspirin for anti-platelet drug therapy (1). Glycine is also itself reported to have an anti-platelet effect (2). The evidence to date for the efficacy of glycine both in improving gastrointestinal tolerance of aspirin and in having anti-platelet actions is limited. However, as glycine is a common dietary amino acid, there is little concern over the risk-to-benefit ratio of including glycine in aspirin formulations for use in anti-platelet drug therapy.

References:
(1) Kusche W, Paxinos R, Haselmann J, Schwantes U, Breddin HK. Acetylsalicylic acid tablets with glycine improve long-term tolerability in antiplatelet drug therapy: results of a noninterventional trial. Adv Ther. 2003 Sep-Oct;20(5):237-45.

(2) Schemmer P, Zhong Z, Galli U, Wheeler MD, Xiangli L, Bradford BU, Conzelmann LO, Forman D, Boyer J, Thurman RG. Glycine reduces platelet aggregation. Amino Acids. 2013 Mar;44(3):925-31. doi: 10.1007/s00726-012-1422-8.

Abuse potential of dextromethorphan?

February 2, 2017 / phcdgs / 0 Comments

When comparing dextromethorphan to the opioid antitussive (cough suppressant), codeine, it is often said that, while codeine is the more potent antitussive, the advantage of dextromethorphan is that it has no opioid-associated abuse potential. This is true but, unfortunately, detromethorphan is not completely free from potential for abuse.

Codeine is a weak opioid agonist. Low doses of codeine are sufficient to achieve the antitussive effect. Therefore, there is relatively little risk of abuse of codeine when used as an antitussive. However, up 15% of codeine is metabolised to morphine, which is a much more potent opioid agonist (1). Codeine has a well-known potential for abuse and abuse of codeine cough mixtures is a peristent problem.

Dextromethorphan is not an opioid receptor agonist and so does not have opioid-associated abuse potential. However, dextromethorphan is abused as a recreational drug. At very high doses, well above the label-specified maximum dosages for use as an antitussive, dextromethorphan acts as a dissociative anaesthetic. Like other dissociative anaesthetics, such as ketamine and phencyclidine (PCP), dextromethorphan is abused. The mechanisms of the dissociative anaesthetic effects of dextromethorphan are thought to involve actions as a nonselective serotonin reuptake inhibitor and an NMDA receptor antagonist.

References:

(1) “Codeine and Morphine Pathway, Pharmacokinetic”
https://www.pharmgkb.org/pathway/PA146123006 [accessed 2nd Feb 2017]