Herb-Drug Interactions: Coffee

Coffea L. species. (Rubiaceae) Synonym(s) and related species Arabian coffee is from Coffea arabica. Robusta coffee is from Coffea canephora (Pierre ex Froehner) also known as Coffea robusta (Linden ex De Wild.). Other species include Coffea liberica. Constituents The kernel of the dried coffee bean contains xanthine derivatives, the main one being caffeine (1 to 2%), with some theobromine and theophylline. It also contains polyphenolic acids such as chlorogenic acids and various diterpenes (e.g. kahweol, cafestrol). Use and indications Coffee has been used as a stimulant and diuretic. However, when roasted, coffee beans are most commonly used as a beverage. Pharmacokinetics The pharmacokinetics of caffeine are discussed under caffeine. Evidence suggests that chlorogenic acid is hydrolysed in the gastrointestinal tract to free caffeic acid, which is then conjugated to form the glucuronate or sulphate. Interactions overview Coffee contains significant amounts of caffeine, so the interactions of caffeine, are relevant to coffee, unless the product is specified as decaffeinated. By virtue of its caffeine content, coffee may also cause serious adverse effects if used with other drugs or herbs with similar Read more […]

ANTITHYROID AGENTS

ANTITHYROID AGENTS are used in the treatment of overactivity of the thyroid gland — hyperthyroidism. thyrotoxicosis or Graves’ disease. In thyrotoxicosis there is excess secretion of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3; liothyronine). This excess results in an exaggerated version of the normal activity of the gland, so that there are the symptoms of increased metabolic rate, an increase in body temperature, sweating, increased sensitivity to heat, nervousness, tremor, raised heart rate, tendency to fatigue and sometimes loss of body weight with an increased appetite. The cause of thyrotoxicosis may be simple overactivity of the gland; or toxic nodular goitre where there is secretion from a benign tumour or a carcinoma of the thyroid; or diffuse toxic goitre (Graves’ disease; exothalmic goitre) in which there are additional symptoms, including a swelling of the neck (goitre) due to enlargement of the gland, and protrusion of the eyes (exothalmos). How the disease is treated depends on its origin, but one final therapy is surgical removal of part of the gland or, more commonly, treatment of the gland with radioactive iodine to reduce the number of cells. For this purpose 131I is given orally Read more […]

ANTISYMPATHETIC AGENTS

ANTISYMPATHETIC AGENTS is a grouping of convenience intended to encompass all agents acting by one of the many mechanisms that lead to a reduction in the actions of the sympathetic nervous system, including those of poorly defined mechanism that are known to have this overall action. Antisympathetics are of particular importance in reducing vasomotor tone, and thence blood pressure. There are many of them and they will be grouped by site and mechanism of action. See also ANTIHYPERTENSIVE AGENTS. Central mechanisms. Some agents may act within the CNS to modify autonomic control of sympathetic tone and blood pressure. Clonidine inhibits release of noradrenaline by an agonist action at the autoinhibitory alpha2-adrenoceptors on sympathetic nerve endings. Methyldopa is thought to work, at least in part, centrally, acting both as an inhibitory false substrate in the biosynthetic pathway, also producing an active metabolite with actions at α2-adrenoceptors. Rauwolfia alkaloids, especially reserpine, which inhibit the monoamine transporters, were at one time used to treat hypertension, but the side-effects are marked. Biosynthetic pathway inhibitors. In both the central and periphery nervous systems, the biosynthetic Read more […]

β-ADRENOCEPTOR ANTAGONISTS

β-ADRENOCEPTOR ANTAGONISTS (also known as β-adrenergic receptor blocking drugs, β-adrenoceptor blocking drugs or beta-blockers) are drugs that inhibit certain actions of the sympathetic nervous system by blocking the action of adrenaline and noradrenaline (catecholamine mediators acting predominantly as hormone or neurotransmitter respectively). Among other actions, β-adrenoceptors have cardiac stimulant actions, they dilate certain blood vessels, suppress motility within the gastrointestinal tract, stimulate certain aspects of metabolism causing an increase in glucose and free fatty acids in the blood. These actions, in concert with those of the α-adrenoceptors, help prepare the body for emergency action. However, in disease, some of these effects may be inappropriate, exaggerated and detrimental to health, so β-blockers may be used to restore the balance. Thus β-blockers are used to lower blood pressure when it is abnormally raised in cardiovascular disease (see ANTIHYPERTENSIVE AGENTS): to correct certain heartbeat irregularities and tachycardias (see ANTIARRHYTHMICS); to prevent the pain of angina pectoris during exercise by limiting cardiac stimulation (see ANTIANGINALS)’, to treat myocardial infarction, Read more […]

ANTIMIGRAINE DRUGS

ANTIMIGRAINE DRUGS are used to treat migraine attacks, which constitute a specific clinically recognized form of headache. Attacks vary in form, but common characteristics include: throbbing in the head confined to one side only (unilateral headache), nausea and vomiting, and a forewarning of the attack (an aura) consisting of visual disturbances and weakness or numbness of the limbs. Drugs are used to help migraine sufferers (and the related state called ‘cluster headache‘) in two quite distinct ways. One group of drugs is given chronically, and helps to prevent attacks (prophylactic use): such as CALCIUM-CHANNEL BLOCKERS. e.g. nifedipine and verapamil; the β-blockers, e.g. metoprolol, nadolol, propranolol and timolol (see β-ADRENOCEPTOR ANTAGONISTS); and also certain vasoactive drugs, including cyproheptadine and the ergot alkaloid methysergide. All these drugs affect blood vessels. In migraine attacks, cerebral vessels are thought to constrict before an attack, then dilate, causing pain during the attack. A second group of drugs may be used to treat acute attacks, either at the stage of the prewarning aura, or during the attack stage itself; and here speed of administration and subsequent absorption of the Read more […]

ANTIARRHYTHMIC AGENTS

ANTIARRHYTHMIC AGENTS (antidysrhythmic agents) are used to treat a number of heart conditions characterized by irregularities of heart beat. They have been classified under the Vaughan Williams Scheme, though not all clinically used agents neatly fit these classes. Class I (which has a number of subtypes) is mainly used to treat atrial and ventricular tachycardias, and contains a number of SODIUM-CHANNEL BLOCKERS, e.g. disopyramide, flecainide, lignocaine, procainamide and quinidine. Class II, which is valuable for stress-induced tachycardias, contains β-ADRENOCEPTOR ANTAGONISTS, e.g. metoprolol, propranolol. Class III, which is used for certain tachycardia syndromes, includes amiodarone (whose mechanism of action is not clear), POTASSIUM-CHANNEL BLOCKERS and the atypical β-blocker sotalol. Class IV is used for atrial tachyarrhythmias and contains certain CALCIUM-CHANNEL BLOCKERS, e.g. diltiazem and verapamil. In addition to drugs in these classes, others may be used for certain arrhythmias. Digoxin may be used for treatment of atrial fibrillation, adrenaline for asystolic cardiac arrest, atropine for sinus bradycardia, methacholine (rarely) for supraventricular tachycardia, magnesium salts for ventricular Read more […]

ANTIANGINAL AGENTS

ANTIANGINAL AGENTS are used to relieve angina pectoris, an intense pain due to cardiac ischaemia, which is especially pronounced in exercise angina. The disease state often results from atheroma; a degeneration of the lining of the arteries of the heart due to build-up of fatty deposits. The objective is to relieve the heart of work, and to prevent spasm or to dilate coronary arteries. Unloading can be achieved by stopping exercise, preventing the speeding of the heart and by dilating the coronary arteries. Beta-blockers, by inhibiting the effect of adrenaline and noradrenaline on the heart, prevent the normal increase in heart rate, and are very effective in preventing exercise angina. Examples of beta-blockers used for this purpose include acebutolol, atenolol, metoprolol, nadolol, oxprenolol, pindolol, propranolol, sotalol and timolol. See β-ADRENOCEPTOR ANTAGONISTS. Many VASODILATORS act directly to relax vascular smooth muscle, so dilating blood vessels and thereby increasing blood flow (see SMOOTH MUSCLE RELAXANTS). For the acute treatment of anginal pain (and to a lesser extent in preventing angina attacks) the nitrates are widely used, e.g. glyceryl trinitrate, isosorbide dinitrate, isosorbide mononitrate Read more […]