A medication is a licenced drug taken to cure or reduce symptoms of an illness or medical condition. Medications are generally divided into two groups -- over the counter (OTC) medications, which are available in pharmacies and supermarkets without special restrictions, and Prescription only medicines (POM), which must be prescribed by a physician. Most OTC medication is generally considered to be safe enough that most persons will not hurt themselves accidentally by taking it as instructed. Many countries, such as the UK have a third category of pharmacy medicines which can only be sold in registered pharmacies, by or under the supervision of a pharmacist. However, the precise distinction between OTC and prescription depends on the legal jurisdiction. Medications are typically produced by pharmaceutical companies and are often patented. Those that are not patented are called generic drugs.

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Drug design is the approach of finding drugs by design, based on what the drug is targeting. Typically a drug target is a key molecule involved in a particular metabolic or signaling pathway that is specific to a disease condition or pathology. Some approaches attempt to stop the functioning of the pathway in the diseased state by causing a key molecule to stop functioning. Drugs may be designed that bind to the active region and inhibit this key molecule. However these drugs would also have to be designed in such a way as not to affect any other important molecules that may be similar in appearance to the key molecules. Sequence homologies are often used to identify such..

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An aphrodisiac is an agent which causes the arousal of sexual desire. The name comes from the Greek goddess of love Aphrodite. Desire can be stimulated by a variety of events or situations (see sexual arousal), but this article focuses on foods and drugs to which an aphrodisiac effect has been attributed. Newly introduced exotic fruits or vegetables often acquire such a reputation, at least until they become more familiar. Some aphrodisiacs appear to gain their reputation from the principles of sympathetic magic, e.g. oysters, due to their shape. This also explains the trade in the phallic-looking rhinoceros horn, which is endangering this animal. (See Carl Hiaasen's 1999 novel Sick...

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Beta blockers

Beta blockers block the action of epinephrine and nor epinephrine on the β-adrenergic receptors in the body (primarily in the heart, peripheral blood vessels, bronchi, pancreas, and liver). The hormones and neurotransmitters stimulate the sympathetic nervous system by acting on these receptors.

There are three types of beta receptors: β1-receptors located mainly in the heart, and β2-receptors located all over the body, but mainly in the lungs, muscles and arterioles. β3-receptors are less well characterized, but have a role in fat metabolism.

Activation of β1-receptors by epinephrine increases the heart rate and the blood pressure, and the heart consumes more oxygen. Drugs that block these receptors therefore have the reverse effect: they lower the heart rate and blood pressure and hence are used in conditions when the heart itself is deprived of oxygen. They are routinely prescribed in patients with ischemic heart disease and hypertension. In addition, beta blockers prevent the release of renin, which is a hormone produced by the kidneys which leads to constriction of blood vessels.

Drugs that block β2 receptors generally have a calming effect and are prescribed for anxiety, migraine, esophageal varices and alcohol withdrawal syndrome, among others.

Many beta blockers affect both type 1 and type 2 receptors; these are termed non-selective blockers. Propranolol and nadolol are examples. Selective beta blockers primarily affect β1-receptors. Non-selective beta blockers should generally not be used in patients with asthma or any reactive airway disease. Doing so can precipitate bronchospasm by blocking the β2 mediated relaxation of the bronchiole muscles.

Selective beta blockers generally only block the type 1 receptor. They gradually become less selective at higher doses. Examples of selective beta1 blockers in common use include atenolol and metoprolol.

Since they lower heart rate, beta blockers have been used by some Olympic marksmen to provide more aiming time between heart beats. Some musicians use beta blockers to avoid stage fright and tremor during auditions and performances. Beta blockers decrease nocturnal melatonin release.

NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)

Non-steroidal anti-inflammatory drugs, usually abbreviated to NSAIDs, are drugs with analgesic, antipyretic and anti-inflammatory effects - they reduce pain, fever and inflammation. The term "non-steroidal" is used to distinguish these drugs from steroids, which (amongst a broad range of other effects) have a similar eicosanoid-depressing, anti-inflammatory action. NSAIDs are sometimes also referred to as non-steroidal anti-inflammatory agents/analgesics (NSAIAs). The most prominent members of this group of drugs are aspirin and ibuprofen. Paracetamol (acetaminophen) has negligible anti-inflammatory activity, and is strictly speaking not an NSAID.

Beginning in 1829, with the isolation of salicylic acid from the folk remedy willow bark, NSAIDs have become an important part of the pharmaceutical treatment of pain (at low doses) and inflammation (at higher doses). Part of the popularity of NSAIDs is that, unlike opioids, they do not produce sedation, respiratory depression, or addiction. NSAIDs, however, are not without their own problems (see below). Certain NSAIDs, including ibuprofen and aspirin, have become accepted as relatively safe and are available over-the-counter without prescription.

Most NSAIDs act as non-selective inhibitors of the enzyme cyclooxygenase, inhibiting both the cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) isoenzymes. Cyclooxygenase catalyses the formation of prostaglandins and thromboxane from arachidonic acid (itself derived from the cellular phospholipid bilayer by phospholipase A2). Prostaglandins act (among other things) as messenger molecules in the process of inflammation. This mechanism of action was elucidated by John Vane, who later received a Nobel Prize for his work.

NSAIDs can be broadly classified based on their chemical structure. NSAIDs within a group will tend to have similar characteristics and tolerability. There is little difference in clinical efficacy between the NSAIDs when used at equivalent doses. Rather, differences between compounds tended to be with regards to dosing regimens (related to half-life), route of administration, and tolerability profile. Some more common examples are given below.

Paracetamol (acetaminophen), owing to its inhibitory action on cyclooxygenase, is sometimes grouped together with the NSAIDs. Paracetamol, however, does not have any significant anti-inflammatory properties and is not a true NSAID. Though it has not been clearly elucidated, it is suspected that this lack of anti-inflammatory action may be due to the paracetamol inhibiting cyclooxygenase predominantly in the central nervous system.

Calcium Channel Blockers

Calcium channel blockers are a class of drugs with effects on the muscle of the heart and the muscles of the rest of the body. The main action of calcium channel blockers is to lower the blood pressure. It is for this action that it is used in individuals with hypertension.

Most calcium channel blockers decrease the force of contraction of the myocardium (muscle of the heart). This is known as the negative inotropic effect of calcium channel blockers. It is because of the negative inotropic effects of most calcium channel blockers that they are avoided (or used with caution) in individuals with cardiomyopathy (weak muscle of the heart).

Many calcium channel blockers also slow down the conduction of electrical activity within the heart, by blocking the calcium channel during the plateau phase of the action potential of the heart (see: cardiac action potential). This causes a lowering of the heart rate and may cause heart blocks. This is known as the negative chronotropic effect of calcium channel blockers. The negative chronotropic effects of calcium channel blockers make them a commonly used class of agents in individuals with atrial fibrillation or flutter in whom control of the heart rate is an issue.

Calcium channel blockers work by blocking voltage-sensitive calcium channels in the heart and in the blood vessels. This prevents calcium levels from increasing as much in the cells when stimulated, leading to less contraction.

This decreases total peripheral resistance by dilating the blood vessels, and decreases cardiac output by lowering the force of contraction. Because resistance and output drop, so does blood pressure.

With low blood pressure, the heart does not have to work as hard, this can ease problems with cardiomyopathy and coronary disease.

Unlike with beta-blockers, the heart is still responsive to sympathetic nervous system stimulation, so blood pressure can be maintained more effectively.