There are more opportunities to think about yourself now than ever before, and to care about yourself more. Knowing about the medications you are taking is now more important than ever. You and the physicians must be mindful of all the drugs that you are taking, whether you take multiple different prescriptions, consult more than one doctor, or have any complications of health. It will allow you to prevent future complications like interactions with drugs.
Drug interactions can decrease the effectiveness of your medication, cause unwanted side effects, or increase the effects of your drug. You may also witness certain drug reactions. Whenever you use a nonprescription product or prescribed drugs, it might be important for your wellbeing to read the label and to think about drug interactions. With a bit of experience and common sense, you will decrease the chance of potentially dangerous drugs and side effects.
Three broad definitions cover drug interactions:
- Drug-drug interactions It occurs as two or more medications used combinedly. You can develop an unwanted side effect from this drug-drug interaction. For instance, combining a medication you are taking to make you relax (sedative) with a medicine you take for allergies (antihistamine) can slow down your reactions and put a vehicle or computer at risk.
- Drug-food/beverage interactions Result from food or beverages reacting with medications being used. Mixing alcohol with some medications, for example, can make you feel sleepy and sluggish.
- Drug-condition interactions It can arise if such medications are actually detrimental to current medical conditions. For example, you may have an unexpected reaction when you are taking a nasal decongestant if you have high blood pressure.
1.Fluoxetine and Phenelzine:
A central syndrome of serotonin can result from the interaction. Changes in mental state, anxiety, diaphoresis, tachycardia, and death characterise this condition. When paired with phenelzine, these effects will progress rapidly with only 1 or 2 doses of fluoxetine. In conjunction with any medication that raises serotonin levels, such as dextromethorphan, meperidine, and other selective serotonin reuptake inhibitors ( SSRIs), serotonin syndrome is possible with any inhibitor of monoamine oxidases (MAOI), such as phenelzine or tranylcypromine sulphate. Owing to the long half-life of fluoxetine and its main metabolite, norfluoxetine, it is advised that fluoxetine be stopped at least 5 weeks before administering an MAOI. Also, 2 weeks should be required before beginning SSRI treatment after discontinuation of MAOI.
2.Digoxin and Quinidine:
For a long time, this critical drug interaction has been established, but it continues to be a problem, sometimes with disastrous effects. The association will lead to a marked rise in digoxin plasma concentration levels in over 90 % of patients. Important changes are noticed within 24 hours in serum digoxin. About 2-fold is the annual rise. The implications of this relationship vary from nausea and vomiting to death. A reduced amount of digoxin delivery secondary to its removal from binding sites in body tissues is the main mechanism for this relationship. Quinidine also reduces digoxin renal and nonrenal excretion rates, contributing to improved cardiac glycoside steady-state concentrations. Ideally, patients taking digoxin should prevent the use of quinidine, but the patient should be carefully supervised if the mixture is necessary. Pharmacists should consider a one-half reduction in the digoxin dosage to be necessary.
3.Sildenafil and Isosorbide Mononitrate:
For a long time, this critical drug interaction has been established, but it continues to be a problem, sometimes with disastrous effects. The association will lead to a marked rise in digoxin plasma concentration levels in over 90 % of patients. Important changes are noticed within 24 hours in serum digoxin. About 2-fold is the annual rise. The implications of this relationship vary from nausea and vomiting to death. A reduced amount of digoxin delivery secondary to its removal from binding sites in body tissues is the main mechanism for this relationship. Quinidine also reduces digoxin renal and nonrenal excretion rates, contributing to improved cardiac glycoside steady-state concentrations. Ideally, patients taking digoxin should prevent the use of quinidine, but the patient should be carefully supervised if the mixture is necessary. Pharmacists should consider a one-half reduction in the digoxin dosage to be necessary.
4. Potassium Chloride and Spironolactone:
This is another important interaction between drugs that has been recognised for a long time. Hyperkalemia can result from the combination. The resultant hyperkalemia can be extreme and can result in heart disease and death. Especially vulnerable to this effect are patients with renal dysfunction. Spironolactone is a competitive mineral corticoid antagonist, a potent example of which is aldosterone. In the distal section of the nephron, this process happens in the kidney and contributes to the excretion of sodium ions while saving potassium ions. This association can also be witnessed by patients undergoing potassium-depleting diuretics, such as amiloride or triamterene. All the absorbable sources of potassium bicarbonate, citrate, acetate, gluconate, and iodide salts can interfere with these diuretics. Extreme hyperkalemia is harmful and, thus, blood potassium levels must be tested in patients who are prescribed spironolactone.
5. Clonidine and Propranolol:
This interaction can create mysterious hypertension that, when treated separately, is irrelevant to either agent’s pharmacology. Fatal rebound hypertension can result from a sudden removal of clonidine from adjunctive therapy with propranolol.
Clonidine is a key adrenergic alpha-2 agonist that suppresses the brain’s sympathetic nervous system. This behaviour contributes to a reduction in the amount of norepinephrine available in the adrenergic neuron’s synaptic cleft. Due to less norepinephrine present in the cleft, alpha-1 receptors then become sensitised. A significant rise of norepinephrine in the synaptic cleft of the adrenergic neuron occurs when clonidine is unexpectedly removed. The sensitised alpha-1 receptors are activated, leading to vasoconstriction that is exaggerated. The body does not prepare for this reaction and when a patient is simultaneously taking propranolol, the beta-2 receptors are blocked. Dramatic rebound hypertension is found within 24 to 72 hours.
6. Warfarin and Diflunisal:
It has been shown that non-steroidal anti-inflammatory drugs (NSAIDs), such as diflunisal, raise the risk of gastrointestinal (GI) bleeding and warfarin anticoagulant reaction. Related reactions with warfarin have been seen in other NSAIDs, such as ketoprofen, piroxicam, sulindac, diclofenac, and ketorolac. However, indomethacin has no effect on hypo thrombinemic reaction in most patients. An alternative to diflunisal is recommended since the association between warfarin and diflunisal may lead to GI bleeding or even fatal haemorrhaging. The alternative of choice is acetaminophen. Yet, if an NSAID is needed, due to limited effects on platelets and gastric mucosa, non-acetylated salicylates such as magnesium salicylate or salsalate are safer.
7. Theophylline and Ciprofloxacin:
Simultaneous administration can result in toxic increases in theophylline. This issue arises because, through the cytochrome P-450 enzyme mechanism, ciprofloxacin inhibits the hepatic metabolism of theophylline. CYP1A2 and, to a lesser degree, CYP3A4 are metabolised by theophylline. All of the potent antagonists of CYP1A2 are ciprofloxacin and other drugs, including clarithromycin, erythromycin, fluvoxamine, and cimetidine. Levofloxacin or ofloxacin should be treated as an alternative to ciprofloxacin since they have no effect on CYP1A2. A dangerous condition is theophylline toxicity; some deaths have been related to serum concentrations as low as 25 mcg / mL. Headaches, dizziness, hypotension, hallucinations, tachycardia, and seizures are symptoms of theophylline toxicity.
8. Pimozide and Ketoconazole:
The QT interval can be prolonged by Pimozide alone and it has been associated with ventricular arrhythmias (torsades de pointes). The mixture can be deadly when pimozide is mixed with ketoconazole. Pimozide is a substrate of the CYP3A4 enzyme and ketoconazole is a potent CYP3A4 inhibitor. This contributes to marked changes in serum levels of pimozide. Some drugs are also potent antagonists of CYP3A4, such as itraconazole, clarithromycin, erythromycin, diltiazem, which nefazodone, and should not be treated with pimozide. Fluconazole is slower but it still reduces CYP3A4 in higher doses. Terbinafine, since it does not impact CYP3A4, is a better alternative.
9. Methotrexate and Probenecid:
The effect might be a 2- to 3-fold increase in methotrexate levels when probenecid is supplied with antineoplastic doses of methotrexate. Probenecid functions as an aggressive inhibitor of tubular secretion and avoids the excretion of methotrexate, thereby possibly inducing toxicity. Diarrhoea, vomiting, diaphoresis, and kidney dysfunction are the signs of extreme methotrexate toxicity and may result in death. Penicillins (e.g. amoxicillin, carbenicillin) and salicylates also have this relationship with methotrexate. The chance of low-dose methotrexate (commonly used for arthritis) is lower; NSAIDs are also deliberately used in conjunction with low-dose methotrexate.
In comparison to salicylates or NSAIDs, potential substitutes include acetaminophen. Celecoxib should not control the pharmacokinetics of methotrexate and may be an option. Rofecoxib, however, causes some changes in serum concentrations of methotrexate and should thus be avoided.
10. Bromocriptine and Pseudoephedrine:
Extreme peripheral vasoconstriction, ventricular tachycardia, epilepsy and likely death can result from the interaction. Bromocriptine has many applications, including antiparkinsonian treatment, and is an ergot-derived dopamine agonist. A shift in first-line medication from levodopa to bromocriptine or other dopamine agonists such as ropinirole, pramipexole, or pergolide is recommended by current clinical recommendations for Parkinson’s disease. Bromocriptine’s notable side effects include thickening of bronchial secretions and nasal inflammation. This is important because it raises the risk of a patient taking bromocriptine using an OTC decongestant such as pseudoephedrine to self-medicate. Avoidance in all sympathomimetics should be recommended to those taking bromocriptine.
References:
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https://www.fda.gov/drugs/resources-you-drugs/drug-interactions-what-you-should-know
https://www.pharmacytimes.com/publications/issue/2002/2002-10/2002-10-6975
