BMA Concise Guide to Medicine & Drugs


The basic architecture of the human body comprises 206 bones, over 600 muscles, and a complex assortment of other tissues that enable the body to move efficiently.

Bones support the body, provide protection for organs, and enable movement.

Tendons attach the muscles that control body movement to the bones.

Muscles work bones that act as levers: when the muscle contracts, movement occurs at the joint.

Ligaments are bands of tough fibrous tissue that hold joints together.

Cartilage covers each bone end, reducing friction between the ends of two bones.


Although tough, these structures often suffer damage. Muscles, tendons, and ligaments can be strained or torn by violent movement, which may cause inflammation, making the affected tissue swollen and painful. Joints, especially those that bear the body’s weight – hips, knees, ankles, and vertebrae – are prone to wear and tear. The cartilage covering the bone ends may tear, causing pain and inflammation. Joint damage also occurs in rheumatoid arthritis, which is thought to be a form of autoimmune disorder. Gout, in which uric acid crystals form in some joints, may also cause inflammation, a condition known as gouty arthritis.

Another problem affecting the muscles and joints includes nerve injury or degeneration, which alters nerve control over muscle contraction. Myasthenia gravis, in which transmission of signals between nerves and muscles is reduced, affects muscle control as a result. Bones may also be weakened by vitamin, mineral, or hormone deficiencies.


A simple analgesic drug or one that has an anti-inflammatory effect will provide pain relief in most of the conditions described here. For severe inflammation, a doctor may inject a drug with a more powerful anti-inflammatory effect, such as a corticosteroid, into the affected site. In cases of severe progressive rheumatoid arthritis, antirheumatic drugs may halt the disease’s progression and relieve symptoms.

Drugs that help to eliminate excess uric acid from the body are often prescribed to treat gout. Muscle relaxants that inhibit transmission of nerve signals to the muscles are used to treat muscle spasm. Drugs that increase nervous stimulation of the muscle are prescribed for myasthenia gravis. Bone disorders in which the mineral content of the bone is reduced are treated with supplements of minerals, vitamins, and hormones.


· Non-steroidal anti-inflammatory drugs

· Antirheumatic drugs

· Corticosteroids for rheumatic disorders

· Drugs for gout

· Muscle relaxants

· Drugs used for myasthenia gravis

· Drugs for bone disorders

Non-steroidal anti-inflammatory drugs

Drugs in this group, often referred to as NSAIDs, are used to relieve the pain, stiffness, and inflammation of painful conditions affecting the muscles, bones, and joints. NSAIDs are called “non-steroidal” to distinguish them from corticosteroid drugs, which also damp down inflammation.


NSAIDs are widely prescribed for the treatment of osteoarthritis, rheumatoid arthritis, and other rheumatic conditions. They reduce pain and inflammation in the joints, but they do not alter the progress of these diseases.

The response to the various drugs in this group varies between individuals. It is sometimes necessary to try several different NSAIDs before finding the one that best suits a particular individual.

Because NSAIDs do not change the progress of a disease, additional treatment is often necessary, particularly for rheumatoid arthritis.

NSAIDs are also commonly prescribed to relieve back pain, headaches, gout, menstrual pain, mild pain following surgery, and pain from soft tissue injuries, such as sprains and strains (see also Analgesics).


Prostaglandins are chemicals released by the body at the site of injury. They are responsible for producing inflammation and pain following tissue damage. NSAIDs block an enzyme, cyclo-oxygenase (COX) which is involved in the production of prostaglandins, and thus reduce pain and inflammation (see Analgesics).


NSAIDs are rapidly absorbed from the digestive system and most start to relieve pain within an hour. When used regularly they reduce pain, inflammation, and stiffness and may restore or improve the function of a damaged or painful joint.

Most NSAIDs are short acting and need to be taken a few times a day for optimal pain relief. Some need to be taken only twice daily. Others, such as piroxicam, are very slowly eliminated from the body and are effective when taken once a day.


Most NSAIDs carry a low risk of serious adverse effects although nausea, indigestion, and altered bowel action are common. However, the main risk from NSAIDs is that, occasionally, they can cause bleeding in the stomach or duodenum. Therefore, the lowest effective dose is given for the shortest duration. NSAIDs should be avoided altogether by people who have suffered from peptic ulcers.

Most NSAIDs are not recommended during pregnancy or for breast-feeding mothers. Caution is also advised for people with kidney or liver abnormalities or heart disease, or those people with a history of hypersensitivity to other drugs.

NSAIDs may impair blood clotting and are, therefore, prescribed with caution to people with bleeding disorders or who are taking drugs that reduce blood clotting.


An NSAID may cause bleeding when its antiprostaglandin action occurs where it is not wanted, such as in the digestive tract. To protect against this side effect, a prostaglandin-like drug called misoprostol is sometimes prescribed with the NSAID. Preparations are available that incorporate both misoprostol and an NSAID. Misoprostol is also used to help heal peptic ulcers.


NSAIDs block two types of COX, COX-1 and COX-2, at different sites in the body; blocking COX-1 leads to the upper gastrointestinal tract irritation of NSAIDs, while blocking COX-2 leads to the anti-inflammatory effect. COX-2 inhibitors block COX-2 but not COX-1. COX-2 inhibitors are not prescribed to anyone who has had a heart attack or stroke, because they significantly increase the risk of recurrence, nor are they prescribed to people with peripheral artery disease (poor circulation). They are prescribed with caution to anyone at risk of any of these conditions.


Aceclofenac, Acemetacin, Aspirin, Diclofenac, Felbinac, Fenbufen, Fenoprofen, Flurbiprofen, Ibuprofen, Indometacin (indomethacin), Ketoprofen, Mefenamic acid, Meloxicam, Nabumetone, Naproxen, Piroxicam, Sulindac, Tenoxicam, Tiaprofenic acid

COX-2 inhibitors Celecoxib, Etodolac, Etoricoxib

Antirheumatic drugs

These drugs are used in the treatment of various rheumatic disorders, the most crippling and deforming being rheumatoid arthritis, an autoimmune disease in which the body’s mechanism for fighting infection contributes to the damage of its own joint tissue. There is pain, stiffness, and swelling of the joints that, over many months, can lead to deformity. Flare-ups of rheumatoid arthritis also cause a general feeling of being unwell, fatigue, and loss of appetite.

Treatments for rheumatoid arthritis include drugs, rest, physiotherapy, changes in diet, and immobilization of joints. The disorder cannot yet be cured, but in many cases it does not progress to permanent disability. It also sometimes subsides spontaneously for prolonged periods.


The aim of drug treatment is to relieve the symptoms of pain and stiffness, maintain mobility, and prevent deformity. Drugs for rheumatoid arthritis fall into two main categories: those that alleviate symptoms, and those that modify, halt, or slow the underlying disease process. Drugs in the first category include aspirin and other NSAIDs (see Non-steroidal anti-inflammatory drugs). These drugs are usually prescribed as a first treatment.

Drugs in the second category are known collectively as disease-modifying antirheumatic drugs (DMARDs). They may be given if the rheumatoid arthritis is severe or if initial drug treatment has proved to be ineffective. DMARDs may prevent further joint damage and disability, but they are not prescribed routinely because the disease may stop spontaneously and because they have potentially severe adverse effects (see Some types of disease-modifying antirheumatic drug, for further information on individual drugs).

Corticosteroids are sometimes used in the treatment of rheumatoid arthritis, but are used only for limited periods because they depress the immune system, increasing susceptibility to infection.


Chloroquine Originally developed to treat malaria, chloroquine and related drugs are less effective than penicillamine or gold. Prolonged use may cause eye damage, but only if too high a dose is used.

Immunosuppressants These are prescribed if other drugs do not provide relief and if the rheumatoid arthritis is severe and disabling. Regular observation and blood tests must be carried out because immunosuppressants can cause severe complications.

Sulfasalazine Used mainly for ulcerative colitis, sulfasalazine was originally introduced to treat mild to moderate rheumatoid arthritis. It slows the disease’s progress in some cases and has a low risk of serious adverse effects.

Gold-based drugs These are believed to be the most effective and may be given orally or by injection for many years. Side effects can include a rash and digestive disturbances. Gold may sometimes damage the kidneys, which recover once treatment is stopped; regular urine tests are usually carried out, however. Gold can also suppress blood cell production. Therefore, periodic blood tests are also carried out.

Monoclonal antibodies such as infliximab target a particular body protein that is responsible for rheumatoid arthritis. Monoclonal antibodies often cause allergy-type reactions, especially at the start of treatment. Infections, particularly of the upper respiratory and urinary tracts, are common.


It is not known precisely how most DMARDs stop or slow the disease process. Some may reduce the body’s immune response, which is thought to be partly responsible for the disease (see also Immunosuppressant drugs). Monoclonal antibodies such as infliximab combine with a body protein called tumour necrosis factor alpha (TNF), which is overactive in rheumatoid arthritis. By reducing the level of TNF activity, they can improve the arthritis. When effective, DMARDs prevent damage to the cartilage and bone, thereby reducing progressive deformity and disability. The effectiveness of each drug varies depending on individual response.


DMARDs are generally slow acting; it may be four to six months before benefit is noticed. So, treatment with aspirin or other NSAIDs is usually continued until remission occurs. Prolonged treatment with DMARDs can markedly improve symptoms. Arthritic pain is relieved, joint mobility increased, and general symptoms of ill health fade. Side effects (which vary between individual drugs) may be noticed before beneficial effects, so patience is required. Regular monitoring of the kidneys, liver, and bone marrow are needed. Severe adverse effects may require treatment to be abandoned.


Immunosuppressants Azathioprine, Ciclosporin, Cyclophosphamide, Leflunomide, Methotrexate


DMARDs Adalimumab, Chloroquine, Etanercept, Hydroxychloroquine, Infliximab, Penicillamine, Sodium aurothiomalate, Sulfasalazine

Corticosteroids for rheumatic disorders

The adrenal glands, which lie on the top of the kidneys, produce a number of important hormones. Among these are the corticosteroids, so named because they are made in the outer part (cortex) of the glands. The corticosteroids play an important role, influencing the immune system and regulating the carbohydrate and mineral metabolism of the body. A number of drugs that mimic the natural corticosteroids have been developed.

These drugs have many uses and are discussed in detail under Corticosteroids. This section concentrates on those corticosteroids injected into an affected site to treat joint disorders.


Corticosteroids given by injection are particularly useful for treating joint disorders – most notably rheumatoid arthritis and osteoarthritis – when one or only a few joints are involved, and when pain and inflammation have not been relieved by other drugs. In such cases, it is possible to relieve symptoms by injecting each of the affected joints individually. Corticosteroids may also be injected to relieve pain and inflammation caused by strained or contracted muscles, ligaments, and/or tendons – for example, in frozen shoulder or tennis elbow. They may also be given for bursitis, tendinitis, or swelling that is compressing a nerve. Corticosteroid injections are sometimes used in order to relieve pain and stiffness sufficiently to permit physiotherapy.


Corticosteroid drugs have two important actions that are believed to account for their effectiveness. They block the production of prostaglandins – chemicals responsible for triggering inflammation and pain – and depress the accumulation and activity of the white blood cells that cause the inflammation. An injection concentrates the corticosteroids, and their effects, at the site of the problem, thus giving the maximum benefit where it is most needed.


Corticosteroids usually produce dramatic relief from symptoms when the drug is injected into a joint. Often a single injection is sufficient to relieve pain and swelling, and to improve mobility. When used to treat muscle or tendon pain, they may not always be effective because it is difficult to position the needle so that the drug reaches the right spot. In some cases, repeated injections are necessary.

Because these drugs are concentrated in the affected area, rather than being dispersed in significant amounts in the body, the generalized adverse effects that sometimes occur when corticosteroids are taken by mouth are unlikely. Minor side effects, such as loss of skin pigment at the injection site, are uncommon. Occasionally, a temporary increase in pain (steroid flare) may occur. In such cases, rest, local application of ice, and analgesic medication may relieve the condition. Sterile injection technique is critically important.


Dexamethasone, Hydrocortisone, Methylprednisolone, Prednisolone, Triamcinolone

Drugs for gout

Gout is a disorder that arises when the blood contains increased levels of uric acid, which is a by-product of normal body metabolism. When its concentration in the blood is excessive, uric acid crystals may form in various parts of the body, especially in the joints of the foot (most often the big toe), the knee, and the hand, causing intense pain and inflammation known as gout. Crystals may form as white masses, known as tophi, in soft tissue, and in the kidneys as stones. Attacks of gout can recur, and may lead to damaged joints and deformity known as gouty arthritis. Kidney stones can cause kidney damage.

An excess of uric acid can be caused either by increased production or by decreased elimination by the kidneys, which remove it from the body. The disorder tends to run in families and is far more common in men than women. The risk of attack is increased by high alcohol intake, the consumption of certain foods (red meat, sardines, anchovies, yeast extract, and offal such as liver, brains, and sweetbreads), and obesity. An attack may be triggered by drugs such as thiazide diuretics or anticancer drugs, or excessive drinking. Changes in diet and a reduction in the consumption of alcohol may be an important part of treatment.

Drugs used to treat acute attacks of gout include NSAIDs (see Non-steroidal anti-inflammatory drugs), and colchicine. Other drugs, which lower the blood level of uric acid, are used for the long-term prevention of gout. These include uricosuric drugs (such as sulfinpyrazone) and allopurinol, the drug of choice. Aspirin is not prescribed for pain relief because it slows excretion of uric acid.


Drugs may be prescribed either to treat an attack of gout or to prevent recurrent attacks that could lead to deformity of affected joints and kidney damage. The NSAIDs and colchicine are both used to treat an attack of gout and should be taken as soon as an attack begins. Because colchicine is relatively specific in relieving the pain and inflammation arising from gout, doctors sometimes administer it in order to confirm their diagnosis of the condition before prescribing an NSAID.

If symptoms recur, your doctor may advise long-term treatment with either allopurinol or a uricosuric drug. One of these drugs must usually be taken indefinitely. Since they can trigger attacks of gout at the beginning of treatment, colchicine is sometimes given with these drugs for a few months.


Allopurinol and febuxostat reduce the level of uric acid in the blood by interfering with the activity of xanthine oxidase, an enzyme involved in the production of uric acid in the body. Sulfinpyrazone increases the rate at which uric acid is excreted by the kidneys. The process by which colchicine reduces inflammation and relieves pain is poorly understood. For the actions of non-steroidal anti-inflammatory drugs, see NSAIDs.


Drugs used in the long-term treatment of gout are usually successful in preventing attacks and joint deformity. However, response may be slow. Colchicine can disturb the digestive system, causing diarrhoea, in which case treatment is stopped.


Since they increase the output of uric acid through the kidneys, uricosuric drugs can cause uric acid crystals (urates) to form in the kidneys. They are not, therefore, usually prescribed for those people who already have impaired kidney function or urate stones. In such cases, allopurinol may be preferred. It is always important to drink plenty of fluids while taking drugs for gout in order to prevent kidney crystals from forming. Regular blood tests to monitor levels of uric acid in the blood may be required.


Drugs to treat attacks Colchicine, NSAIDs but not aspirin

Drugs to treat high uric acid caused by cytotoxic drugs Rasburicase

Drugs to prevent attacks Allopurinol, Febuxostat, Sulfinpyrazone

Muscle relaxants

Several drugs are available to treat muscle spasm – the involuntary, painful contraction of a muscle or a group of muscles that can stiffen an arm or leg or make it almost impossible to straighten your back. There are various causes. It can follow an injury, or come on without warning. It may also be brought on by a disorder like osteoarthritis, the pain in the affected joint triggering abnormal tension in a nearby muscle.

Spasticity is another form of muscle tightness seen in some neurological disorders, such as multiple sclerosis, stroke, or cerebral palsy. Spasticity can sometimes be helped by physiotherapy, but in severe cases drugs may be used to relieve symptoms.


Muscle spasm resulting from direct injury is usually treated with a non-steroidal anti-inflammatory drug or an analgesic. However, if the spasm is severe, a muscle relaxant may also be tried for a short period.

In spasticity, the person’s legs may become so stiff and uncontrollable that walking unaided is impossible. In such cases, a drug may be used to relax the muscles. Relaxation of the muscles often permits physiotherapy to be given for longer-term relief from spasms.

The muscle relaxant, botulinum toxin, may be injected locally to relieve muscle spasm in small groups of accessible muscles, such as those around the eye or in the neck.


Muscle-relaxant drugs work in one of several ways. The centrally acting drugs damp down the passage of the nerve signals from the brain and spinal cord that cause muscles to contract, thus reducing excessive stimulation of muscles as well as unwanted muscular contraction. Dantrolene reduces the sensitivity of the muscles to nerve signals. When injected locally, botulinum toxin prevents transmission of impulses between nerves and muscles.


Drugs taken regularly for a spastic disorder of the central nervous system usually reduce stiffness and improve mobility. They may restore the use of the arms and legs when this has been impaired by muscle spasm.

Unfortunately, most centrally acting drugs can have a generally depressant effect on nervous activity and produce drowsiness, particularly at the beginning of treatment. Too high a dosage can excessively reduce the muscles’ ability to contract and can therefore cause weakness. For this reason, the dosage needs to be carefully adjusted to find a level that controls symptoms but which, at the same time, maintains sufficient muscle strength.


The main long-term risk associated with centrally acting muscle relaxants is that the body becomes dependent. If the drugs are withdrawn suddenly, the stiffness may become worse than before drug treatment.

Rarely, dantrolene can cause serious liver damage. Anyone who is taking this drug should have his or her blood tested regularly to assess liver function.

Unless used very cautiously, botulinum toxin can paralyse unaffected muscles, and might interfere with functions such as speech and swallowing.


Centrally acting drugs Baclofen, Diazepam, Orphenadrine, Tizanidine

Other drugs Botulinum toxin, Dantrolene

Drugs used for myasthenia gravis

Myasthenia gravis is a disorder that occurs when the immune system becomes defective and produces antibodies that disrupt the signals being transmitted between the nervous system and muscles that are under voluntary control. As a result, the body’s muscular response is progressively weakened. The first muscles to be affected are those controlling the eyes, eyelids, face, pharynx, and larynx, with muscles in the arms and legs becoming involved as the disease progresses. Myasthenia gravis is often linked to a disorder of the thymus gland, which is the source of the destructive antibodies concerned.

Various methods can be used in the treatment of myasthenia gravis, including removal of the thymus gland (called a thymectomy) or temporarily clearing the blood of antibodies (a procedure known as plasmapheresis, or plasma exchange). Drugs that improve muscle function, principally neostigmine and pyridostigmine, may be prescribed. They may be used alone or together with other drugs that depress the immune system – usually azathioprine (see Immunosuppressant drugs) or corticosteroids. Intravenous immunoglobulins may also be used in severe cases where there are breathing and swallowing problems.


Drugs that improve the muscle response to nerve impulses have several uses. One such drug, edrophonium, acts very quickly and, once administered intravenously, it brings about a dramatic improvement in the symptoms. This effect is used to confirm the diagnosis of myasthenia gravis. However, because of its short duration of action, edrophonium is not used for long-term treatment. Pyridostigmine and neostigmine are preferred for long-term treatment, especially when removal of the thymus gland is not feasible or does not provide adequate relief. These drugs may be given to non-myasthenic patients after surgery to reverse the effects of a muscle-relaxant drug given as part of the general anaesthetic.


Normal muscle action occurs when a nerve impulse triggers a nerve ending to release a neurotransmitter, which combines with a specialized receptor on the muscle cells and causes the muscles to contract. In myasthenia gravis, the body’s immune system destroys many of these receptors, so that the muscle is less responsive to nervous stimulation. Drugs used to treat the disorder increase the amount of neurotransmitter at the nerve ending by blocking the action of an enzyme that normally breaks it down. Increased levels of the neurotransmitter permit the remaining receptors to function more efficiently.


These drugs usually restore the muscle function to a normal or near-normal level, particularly when the disease takes a mild form. Unfortunately, the drugs can produce unwanted muscular activity by enhancing the transmission of nerve impulses elsewhere in the body.

Common side effects include vomiting, nausea, diarrhoea, and muscle cramps in the arms, legs, and abdomen.


Muscle weakness can suddenly worsen even when it is being treated with drugs. Should this occur, it is important not to take larger doses of the drug to try to relieve the symptoms, because excessive drug levels can interfere with the transmission of nerve impulses to muscles, causing further weakness. Administration of other drugs, including some antibiotics, can also markedly increase the symptoms of myasthenia gravis. If your symptoms suddenly worsen, consult your doctor.


Azathioprine,Corticosteroids, Distigmine, Edrophonium, Neostigmine, Pyridostigmine

Drugs for bone disorders

Bone is a living structure. Its hard, mineral quality is created by the action of the bone cells. These cells continuously deposit and remove phosphorus and calcium, which are stored in a honeycombed protein framework called the matrix. Because the rates of deposit and removal (the bone metabolism) are about equal in adults, the bone mass remains fairly constant.

Removal and renewal is regulated by hormones and influenced by a number of factors, notably the level of calcium in the blood, which depends on the intake of calcium and vitamin D from the diet, the actions of various hormones, plus everyday movement and weight-bearing stress. When normal bone metabolism is altered, various bone disorders result.


In osteoporosis, the strength and density of bone are reduced. Such wasting occurs when the rate of removal of mineralized bone exceeds the rate of deposit. In most people, bone density decreases very gradually from the age of 30. But bone loss can dramatically increase when a person is immobilized for a period, and this is an important cause of osteoporosis in elderly people. Hormone deficiency is another important cause, commonly occurring in women with lowered oestrogen levels after the menopause or removal of the ovaries. Osteoporosis also occurs in disorders in which there is excess production of adrenal or thyroid hormones. Osteoporosis can result from long-term treatment with corticosteroid drugs.

People with osteoporosis often have no symptoms, but, if the vertebrae become so weakened that they are unable to bear the body’s weight, they may collapse spontaneously or after a minor accident. Subsequently, the individual suffers from back pain, reduced height, and a round-shouldered appearance. Osteoporosis also makes a fracture of an arm, leg, or hip more likely.

Most doctors emphasize the need to prevent the disorder by an adequate intake of protein and calcium and by regular exercise throughout adult life. Oestrogen supplements are no longer usually recommended to prevent osteoporosis.

The condition of bones damaged by osteoporosis cannot usually be improved, but drug treatment can help to prevent further deterioration and help fractures to heal. For people whose diet is deficient in calcium or vitamin D, supplements may be prescribed. However, these are of limited value and are often less useful than drugs that inhibit removal of calcium from the bones. In the past, the hormone calcitonin was used, but it has now been largely superseded by drugs such as etidronate and alendronate. These drugs, known as bisphosphonates, bind very tightly to bone matrix, preventing its removal by bone cells.


In osteomalacia (called rickets when it affects children), a lack of vitamin D leads to loss of calcium, resulting in softening of the bones. There is pain and tenderness and a risk of fracture and bone deformity. In children, growth is retarded.

Osteomalacia is most commonly caused by a lack of vitamin D. This can result from an inadequate diet, inability to absorb the vitamin, or insufficient exposure of the skin to sunlight (the action of the sun on the skin produces vitamin D inside the body). Individuals who are at special risk include those whose absorption of vitamin D is impaired by an intestinal disorder, like Crohn’s disease or coeliac disease. People with dark skin living in Northern Europe are also susceptible. Chronic kidney disease is an important cause of rickets in children and of osteomalacia in adults, since healthy kidneys play an essential role in the body’s metabolism of vitamin D.

Long-term relief depends on treating the underlying disorder where possible. In rare cases, treatment may be lifelong.


A number of substances that are related to vitamin D may be used in the treatment of bone disorders. These drugs include alfacalcidol, calcitriol, and ergocalciferol. The substance that is prescribed depends on the underlying problem.


Alendronic acid, Alfacalcidol, Calcitonin, Calcitriol, Calcium carbonate, Conjugated oestrogens, Ergocalciferol, Etidronate, Fluoride, Pamidronate, Risedronate, Salcatonin (calcitonin (salmon), Strontium ranelate, Teriparatide, Vitamin D