An anticancer drug used in the treatment of Hodgkin’s disease and leukaemia.
It is also used as an immunosuppressant drug and occasionally to treat connective tissue diseases such as systemic lupus erythematosus.
It is also used as an immunosuppressant drug and occasionally to treat connective tissue diseases such as systemic lupus erythematosus.
Alkylating agents are important because they interfere with the growth and reproduction of cells, disrupting their replication. This CYTOTOXIC property is used to retard the division and growth of cancer cells, and alkylating drugs are widely used in the chemotherapy of malignant tumours – often in conjunction with surgery and sometimes with radiotherapy. Unfortunately, troublesome side-effects occur, such as: damage to veins when the drug is given intravenously, with resultant leakage into adjacent tissues; impaired kidney function due to the formation of URIC ACID crystals; nausea and vomiting; ALOPECIA (hair loss); suppression of BONE MARROW activity (production of blood cells); and adverse effects on reproductive function, including TERATOGENESIS. Indeed, cytotoxic drugs must not be given in pregnancy, especially during the ?rst three months. Prolonged use of alkylating drugs, especially when accompanying radiotherapy, is also associated with a sign?cant rise in the incidence of acute non-lymphocytic LEUKAEMIA. Among the dozen or so alkylating drugs in use are CYCLOPHOSPHAMIDE, CHLORAMBUCIL, MELPHALAN, BUSULFAN and THIOTEPA. (See also CHEMOTHERAPY.)... alkylating agents
Treatment Any major de?ciencies, such as thyroxin or insulin lack, should be corrected. The activity of the immune system should then be reduced. CORTICOSTEROIDS and, in more severe cases, strong immunosuppressant drugs – AZATHIOPRINE, CYCLOPHOSPHAMIDE or METHOTREXATE – should be administered. Treatment is di?cult because of the need to control the autoimmune condition without damaging the body’s ability to combat other diseases.... autoimmune disorders
Habitat: Native to West Indies and Central America; now cultivated in Uttar Pradesh, Punjab, Rajasthan, Gujarat, Maharashtra and South India.
English: Papaya, Papaw.Ayurvedic: Erand-karkati, Papitaa.Unani: Papitaa Desi.Siddha/Tamil: Pappaali, Pappayi.Action: Ripe fruit—stomachic, digestive, carminative, diuretic, galactagogue. Useful in bleeding piles, haemoptysis, dysentery and chronic diarrhoea. Seeds— emmengagogue, abortifacient, vermifuge. Juice of seeds is administered in enlarged liver and spleen, and in bleeding piles.
Key application: Papain, the enzyme mixture extracted from raw papain (latex of Carica papaya), has been included among unapproved herbs by German Commission E. Experiment-based as well as clinical research indicate that papain may be effective (in the treatment of inflammations) in high doses (daily dose 1500 mg corresponding to 2520 FIP units).Unripe fruit—emmengagogue and abortifacient. Latex—applied topically on eczema, ringworm, psoriasis, corns, warts, sloughing wounds, carbuncles and eschar of burns.Green parts of the plant and seed contain an alkaloid carpaine. Seeds also contain carpasemine.Latex contain enzymes—papain and chymopapain and alkaloids carpaine and pseudocarpaine. A proteinaceous material from latex showed anticoagulant activity; in higher doses it is heart depressant and as a spasmogen on smooth muscle of guinea pig ileum. An alkaloid solution showed depressant action on heart, blood pressure and intestine.The anthelmintic action of seeds against Ascaris lumbricoides is due to carpasemine.Papain, an enzyme mixture prepared from the fruit, seeds and leaf, hydrolyses polypeptides, amides and esters, particularly when used in an alkaline environment, and is used in digestive disorders.Papain inhibits platelet aggregation, which may further increase the risk of bleeding in patients also taking anticoagulants. Concurrent administration of cyclophosphamide with papain caused sever damage to lung tissues in rats. (Sharon M. Herr.)Chymopapin C is an immunosup- pressive enzyme from plant extract. Carpaine, extracted from the plant, exhibited anti-tubercular activity, also antitumour in vitro, and hypotensive.Dosage: Leaf—40-80 ml infusion; latex—3-6 g (CCRAS.)... carica papayaK
Diagram of glomerulus (Malpighian corpuscle).
Fortunately the body has two kidneys and, as most people can survive on one, there is a good ‘functional reserve’ of kidney tissue.
Symptoms Many patients with kidney disorders do not have any symptoms, even when the condition is quite advanced. However,
others experience loin pain associated with obstruction (renal colic) or due to infection; fevers; swelling (oedema), usually of the legs but occasionally including the face and arms; blood in the urine (haematuria); and excess quantities of urine (polyuria), including at night (nocturia), due to failure of normal mechanisms in the kidney for concentrating urine. Patients with chronic renal failure often have very di?use symptoms including nausea and vomiting, tiredness due to ANAEMIA, shortness of breath, skin irritation, pins and needles (paraesthesia) due to damage of the peripheral nerves (peripheral neuropathy), and eventually (rarely seen nowadays) clouding of consciousness and death.
Signs of kidney disease include loin tenderness, enlarged kidneys, signs of ?uid retention, high blood pressure and, in patients with end-stage renal failure, pallor, pigmentation and a variety of neurological signs including absent re?exes, reduced sensation, and a coarse ?apping tremor (asterixis) due to severe disturbance of the body’s normal metabolism.
Renal failure Serious kidney disease may lead to impairment or failure of the kidney’s ability to ?lter waste products from the blood and excrete them in the urine – a process that controls the body’s water and salt balance and helps to maintain a stable blood pressure. Failure of this process causes URAEMIA – an increase in urea and other metabolic waste products – as well as other metabolic upsets in the blood and tissues, all of which produce varying symptoms. Failure can be sudden or develop more slowly (chronic). In the former, function usually returns to normal once the underlying cause has been treated. Chronic failure, however, usually irreparably reduces or stops normal function.
Acute failure commonly results from physiological shock following a bad injury or major illness. Serious bleeding or burns can reduce blood volume and pressure to the point where blood-supply to the kidney is greatly reduced. Acute myocardial infarction (see HEART, DISEASES OF) or pancreatitis (see PANCREAS, DISORDERS OF) may produce a similar result. A mismatched blood transfusion can produce acute failure. Obstruction to the urine-?ow by a stone (calculus) in the urinary tract, a bladder tumour or an enlarged prostate can also cause acute renal failure, as can glomerulonephritis (see below) and the haemolytic-uraemia syndrome.
HYPERTENSION, DIABETES MELLITUS, polycystic kidney disease (see below) or AMYLOIDOSIS are among conditions that cause chronic renal failure. Others include stone, tumour, prostatic enlargement and overuse of analgesic drugs. Chronic failure may eventually lead to end-stage renal failure, a life-threatening situation that will need DIALYSIS or a renal transplant (see TRANSPLANTATION).
Familial renal disorders include autosomal dominant inherited polycystic kidney disease and sex-linked familial nephropathy. Polycystic kidney disease is an important cause of renal failure in the UK. Patients, usually aged 30–50, present with HAEMATURIA, loin or abdominal discomfort or, rarely, urinary-tract infection, hypertension and enlarged kidneys. Diagnosis is based on ultrasound examination of the abdomen. Complications include renal failure, hepatic cysts and, rarely, SUBARACHNOID HAEMORRHAGE. No speci?c treatment is available. Familial nephropathy occurs more often in boys than in girls and commonly presents as Alport’s syndrome (familial nephritis with nerve DEAFNESS) with PROTEINURIA, haematuria, progressing to renal failure and deafness. The cause of the disease lies in an absence of a speci?c ANTIGEN in a part of the glomerulus. The treatment is conservative, with most patients eventually requiring dialysis or transplantation.
Acute glomerulonephritis is an immune-complex disorder due to entrapment within glomerular capillaries of ANTIGEN (usually derived from B haemolytic streptococci – see STREPTOCOCCUS) antibody complexes initiating an acute in?ammatory response (see IMMUNITY). The disease affects children and young adults, and classically presents with a sore throat followed two weeks later by a fall in urine output (oliguria), haematuria, hypertension and mildly abnormal renal function. The disease is self-limiting with 90 per cent of patients spontaneously recovering. Treatment consists of control of blood pressure, reduced ?uid and salt intake, and occasional DIURETICS and ANTIBIOTICS.
Chronic glomerulonephritis is also due to immunological renal problems and is also classi?ed by taking a renal biopsy. It may be subdivided into various histological varieties as determined by renal biospy. Proteinuria of various degrees is present in all these conditions but the clinical presentations vary, as do their treatments. Some resolve spontaneously; others are treated with steroids or even the cytotoxic drug CYCLOPHOSPHAMIDE or the immunosuppressant cyclosporin. Prognoses are generally satisfactory but some patients may require renal dialysis or kidney transplantation – an operation with a good success rate.
Hydronephrosis A chronic disease in which the kidney becomes greatly distended with ?uid. It is caused by obstruction to the ?ow of urine at the pelvi-ureteric junction (see KIDNEYS – Structure). If the ureter is obstructed, the ureter proximal to the obstruction will dilate and pressure will be transmitted back to the kidney to cause hydronephrosis. Obstruction may occur at the bladder neck or in the urethra itself. Enlargement of the prostate is a common cause of bladder-neck obstruction; this would give rise to hypertrophy of the bladder muscle and both dilatation of the ureter and hydronephrosis. If the obstruction is not relieved, progressive destruction of renal tissue will occur. As a result of the stagnation of the urine, infection is probable and CYSTITIS and PYELONEPHRITIS may occur.
Impaired blood supply may be the outcome of diabetes mellitus and physiological shock, which lowers the blood pressure, also affecting the blood supply. The result can be acute tubular necrosis. POLYARTERITIS NODOSA and SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) may damage the large blood vessels in the kidney. Treatment is of the underlying condition.
Infection of the kidney is called pyelonephritis, a key predisposing factor being obstruction of urine ?ow through the urinary tract. This causes stagnation and provides a fertile ground for bacterial growth. Acute pyelonephritis is more common in women, especially during pregnancy when bladder infection (CYSTITIS) spreads up the ureters to the kidney. Symptoms are fever, malaise and backache. Antibiotics and high ?uid intake are the most e?ective treatment. Chronic pyelonephritis may start in childhood as a result of congenital deformities that permit urine to ?ow up from the bladder to the kidney (re?ux). Persistent re?ux leads to recurrent infections causing permanent damage to the kidney. Specialist investigations are usually required as possible complications include hypertension and kidney failure.
Tumours of the kidney are fortunately rare. Non-malignant ones commonly do not cause symptoms, and even malignant tumours (renal cell carcinoma) may be asymptomatic for many years. As soon as symptoms appear – haematuria, back pain, nausea, malaise, sometimes secondary growths in the lungs, bones or liver, and weight loss – urgent treatment including surgery, radiotherapy and chemotherapy is necessary. This cancer occurs mostly in adults over 40 and has a hereditary element. The prognosis is not good unless diagnosed early. In young children a rare cancer called nephroblastoma (Wilm’s tumour) can occur; treatment is with surgery, radiotherapy and chemotherapy. It may grow to a substantial size before being diagnosed.
Cystinuria is an inherited metabolic defect in the renal tubular reabsorption of cystine, ornithine, lysine and arginine. Cystine precipitates in an alkaline urine to form cystine stones. Triple phosphate stones are associated with infection and may develop into a very large branching calculi (staghorn calculi). Stones present as renal or ureteric pain, or as an infection. Treatment has undergone considerable change with the introduction of MINIMALLY INVASIVE SURGERY (MIS) and the destruction of stone by sound waves (LITHOTRIPSY).... kidneys, diseases of
The drugs work by suppressing the production and activity of white blood cells called lymphocytes. Side effects vary, but all the drugs increase the risk of infection and of the development of certain cancers.... immunosuppressant drugs
Cytotoxic drugs are used either singly or in combination, when an enhanced response is the aim. Chemotherapy of cancer is a complex process and should be supervised by an oncologist in co-operation with physicians, surgeons, radiotherapists and radiologists as appropriate.
The cytotoxic drugs include:
(1) The alkylating agents which act by damaging DNA, thus interfering with cell reproduction. Cyclophosphamide, ifosfamide, chlorambucil, kelphalan, busulphan, thiotepa and mustine are examples of alkylating agents.
(2) There are a number of cytotoxic antibiotics used in the treatment of cancer – doxorubicin, bleomycin, dactinomycin, mithramycin and amsacrine are examples. They are used primarily in the treatment of acute leukaemia and lymphomas.
(3) Antimetabolites – these drugs combine irreversibly with vital enzyme systems of the cell and hence prevent normal cell division. Methotrexate, cytarabine, ?uorouracil, mercaptopurine and azathioprine are examples.
(4) Another group of cytotoxic drugs are the vinca alkaloids such as vincristine, vinblastine and vindesima.
(5) Platinum compounds such as carboplatin, cisplatin and oxaliplatin are e?ective. All of them are given intravenously, but the latter two tend to have more unpleasant side-effects. Carboplatin and cisplatin are useful in the treatment of solid tumours. Carboplatin, a derivative of cisplatin, is given intravenously in ovarian cancer and in small-cell lung cancer. Better tolerated than cisplatin, the drug causes less nausea and vomiting, nephrotoxicity, neurotoxicity and ototoxicity. Where platinum-containing therapy has failed, intravenous treatment with paclitaxel may be tried. With only a limited success rate, it is relatively toxic and should be carefully supervised; responses, however, are sometimes prolonged.
Also of increasing importance in treating cancer are interferons. These are naturally occurring proteins with complex effects on immunity and cell function. Although toxic, with numerous adverse effects, they have shown some anti-tumour e?ect against certain lymphomas and solid tumours.... cytotoxic
The disease is rare under the age of 30, frequency increasing with age to peak between 60 and 70 years. There may be a long preclinical phase, sometimes as long as 25 years. When symptoms do occur, they tend to re?ect bone involvement, reduced immune function, renal failure, anaemia or hyperviscosity of the blood. Vertebral collapse is common, with nerve root pressure and reduced stature. The disease is eventually fatal, infection being a common cause of death. Local skeletal problems should be treated with RADIOTHERAPY, and the general disease with CHEMOTHERAPY
– chie?y the ALKYLATING AGENTS melphalan or cyclophosphamide. Red-blood-cell TRANSFUSION is usually required, together with plasmapheresis (see PLASMA EXCHANGE), and orthopaedic surgery may be necessary following fractures.... myelomatosis
Treatment is with immunosuppressant drugs, such as cyclophosphamide or azathioprine, combined with corticosteroids to alleviate symptoms and attempt to bring about a remission.
With prompt treatment, most people recover completely within about a year, although kidney failure occasionally develops.
Without treatment, complications may occur, including perforation of the nasal septum, causing deformity of the nose; inflammation of the eyes; a rash, nodules, or ulcers on the skin; and damage to the heart muscle, which may be fatal.... wegener’s granulomatosis
BURSITIS, TENDINITIS and non-speci?c back pain (see BACKACHE).
Osteoarthritis (OA) rarely starts before 40, but by the age of 80 affects 80 per cent of the population. There are structural and functional changes in the articular cartilage, as well as changes in the collagenous matrix of tendons and ligaments. OA is not purely ‘wear and tear’; various sub-groups have a genetic component. Early OA may be precipitated by localised alteration in anatomy, such as a fracture or infection of a joint. Reactive new bone growth typically occurs, causing sclerosis (hardening) beneath the joint, and osteophytes – outgrowths of bone – are characteristic at the margins of the joint. The most common sites are the ?rst metatarsal (great toe), spinal facet joints, the knee, the base of the thumb and the terminal ?nger joints (Heberden’s nodes).
OA has a slow but variable course, with periods of pain and low-grade in?ammation. Acute in?ammation, common in the knee, may result from release of pyrophosphate crystals, causing pseudo-gout.
Urate gout results from crystallisation of URIC ACID in joints, against a background of hyperuricaemia. This high concentration of uric acid in the blood may result from genetic and environmental factors, such as excess dietary purines, alcohol or diuretic drugs.
In?ammatory arthritis is less common than OA, but potentially much more serious. Several types exist, including: SPONDYLARTHRITIS This affects younger men, chie?y involving spinal and leg joints. This may lead to in?ammation and eventual ossi?cation of the enthesis – that is, where the ligaments and tendons are inserted into the bone around joints. This may be associated with disorders in other parts of the body: skin in?ammation (PSORIASIS), bowel and genito-urinary in?ammation, sometimes resulting in infection of the organs (such as dysentery). The syndromes most clearly delineated are ankylosing spondylitis (see SPINE AND SPINAL CORD, DISEASES AND INJURIES OF), psoriatic or colitic spondylitis, and REITER’S SYNDROME. The diagnosis is made clinically and radiologically; no association has been found with autoantibodies (see AUTOANTIBODY). A particularly clear gene locus, HLA B27, has been identi?ed in ankylosing spondylitis. Psoriasis can be associated with a characteristic peripheral arthritis.
Systemic autoimmune rheumatic diseases (see AUTOIMMUNE DISORDERS). RHEUMATOID ARTHRITIS (RA) – see also main entry. The most common of these diseases. Acute in?ammation causes lymphoid synovitis, leading to erosion of the cartilage, associated joints and soft tissues. Fibrosis follows, causing deformity. Autoantibodies are common, particularly Rheumatoid Factor. A common complication of RA is Sjögren’s syndrome, when in?ammation of the mucosal glands may result in a dry mouth and eyes. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) and various overlap syndromes occur, such as systemic sclerosis and dermatomyositis. Autoantibodies against nuclear proteins such as DNA lead to deposits of immune complexes and VASCULITIS in various tissues, such as kidney, brain, skin and lungs. This may lead to various symptoms, and sometimes even to organ failure.
Infective arthritis includes: SEPTIC ARTHRITIS An uncommon but potentially fatal disease if not diagnosed and treated early with approriate antibiotics. Common causes are TUBERCLE bacilli and staphylococci (see STAPHYLOCOCCUS). Particularly at risk are the elderly and the immunologically vulnerable, such as those under treatment for cancer, or on CORTICOSTEROIDS or IMMUNOSUPPRESSANT drugs. RHEUMATIC FEVER Now rare in western countries. Resulting from an immunological reaction to a streptococcal infection, it is characterised by migratory arthritis, rash and cardiac involvement.
Other infections which may be associated with arthritis include rubella (German measles), parvovirus and LYME DISEASE.
Treatment Septic arthritis is the only type that can be cured using antibiotics, while the principles of treatment for the others are similar: to reduce risk factors (such as hyperuricaemia); to suppress in?ammation; to improve function with physiotherapy; and, in the event of joint failure, to perform surgical arthroplasty. NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS) include aspirin, paracetamol and many recently developed ones, such as the proprionic acid derivatives IBUPROFEN and naproxen, along with other drugs that have similar properties such as PIROXICAM. They all carry a risk of toxicity, such as renal dysfunction, or gastrointestinal irritation with haemorrhage. Stronger suppression of in?ammation requires corticosteroids and CYTOTOXIC drugs such as azathioprine or cyclophosphamide. Recent research promises more speci?c and less toxic anti-in?ammatory drugs, such as the monoclonal antibodies like in?iximab. An important treatment for some osteoarthritic joints is surgical replacement of the joints.... joints, diseases of
According to the type of cells that predominate, leukaemia may be classi?ed as acute or chronic lymphoblastic leukaemia or myeloid leukaemia. Acute lymphoblastic leukaemia (ALL) is mostly a disease of childhood and is rare after the age of 25. Acute myeloid leukaemia is most common in children and young adults, but may occur at any age. Chronic lymphatic leukaemia occurs at any age between 35 and 80, most commonly in the 60s, and is twice as common in men as in women. Chronic myeloid leukaemia is rare before the age of 25, and most common between the ages of 30 and 65; men and women are equally affected. Around 2,500 patients with acute leukaemia are diagnosed in the United Kingdom, with a similar number annually diagnosed with chronic leukaemia.
Cause Both types of acute leukaemia seem to arise from a MUTATION in a single white cell. The genetically changed cell then goes through an uncontrolled succession of divisions resulting in many millions of abnormal white cells in the blood, bone marrow and other tissues. Possible causes are virus infection, chemical exposure, radiation and genetic background. The cause of chronic lymphocytic leukaemia is not known; the chronic myeloid version may have a genetic background.
Symptoms In acute cases the patient is pale due to anaemia, may have a purpuric rash due to lack of platelets, and may have enlarged lymphatic glands and spleen. The temperature is raised, and the condition may be mistaken for an acute infection (or may ?rst become apparent because the patient develops a severe infection due to a lack of normal white blood cells).
In the chronic type of the disease the onset is gradual, and the ?rst symptoms which occasion discomfort are either swelling of the abdomen and shortness of breath, due to painless enlargement of the spleen; or the enlargement of glands in the neck, armpits and elsewhere; or the pallor, palpitation, and other symptoms of anaemia which often accompany leukaemia. Occasional bleeding from the nose, stomach, gums or bowels may occur, and may be severe. Generally, there is a slight fever.
When the blood is examined microscopically, not only is there an enormous increase in the number of white cells, which may be multiplied 30- or 60-fold, but various immature forms are also found. In the lymphatic form of the disease, most white cells resemble lymphocytes, which, in healthy blood, are present only in small numbers. In the myeloid form, myelocytes, or large immature cells from the bone marrow, which are never present in healthy blood, appear in large numbers, and there may also be large numbers of immature, nucleated erythrocytes.
Treatment This varies according to the type of leukaemia and to the particular condition of the patient. Excellent results are being obtained in the control of ALL using blood transfusions, CHEMOTHERAPY, RADIOTHERAPY and bone-marrow TRANSPLANTATION. In the case of acute leukaemia, the drugs now being used include MERCAPTOPURINE, METHOTREXATE and CYCLOPHOSPHAMIDE. Blood transfusion and CORTICOSTEROIDS play an important part in controlling the condition during the period before a response to chemotherapy can be expected. Chemotherapy has almost completely replaced radiotherapy in the treatment of chronic leukaemia. For the myeloid form, BUSULFAN is the most widely used drug, replaced by hydroxyurea, mercaptopurine, or one of the nitrogen mustard (see NITROGEN MUSTARDS) derivatives in the later stages of the disease. For the lymphatic form, the drugs used are CHLORAMBUCIL, CYCLOPHOSPHAMIDE, and the nitrogen mustard derivatives.
Prognosis Although there is still no guaranteed cure, the outlook in both acute and chronic leukaemia has greatly improved – particularly for the acute form of the disease. Between 70 and 80 per cent of children with acute lymphoblastic leukaemia may be cured; between 20 and 50 per cent of those with acute myeloid leukaemia now have much-improved survival rates. Prognosis of patients with chronic lymphocytic leukaemia is often good, depending on early diagnosis.... leukaemia
Surgery may be most common, and is often the only treatment, for some gastrointestinal tumours, soft-tissue tumours, gynaecological tumours and advanced cancers of the head and neck.
Radiotherapy uses ionising radiation to kill tumour cells. Radiation is by naturally occurring isotopes (see ISOTOPE) or arti?cially produced X-RAYS. Germ-cell tumours (see SEMINOMA; TERATOMA) and malignant lymphomas (see LYMPHOMA) appear to be particularly sensitive to irradiation, and many head and neck tumours, gynaecological cancers, and localised cancers of the PROSTATE GLAND and URINARY BLADDER are curable with radiotherapy. It is also a valuable means of reducing pain from bone metastases (see METASTASIS). Unpleasant side-effects are common: chie?y lethargy, loss of appetite and dry, itchy skin symptoms.
Chemotherapy is also an important treatment in germ-cell tumours (see above); in some forms of LEUKAEMIA and lymphoma; in ovarian cancer (following surgery – see OVARIES, DISEASES OF); and in small-cell lung cancer (although most patients die within 18 months – see LUNGS, DISEASES OF). It is also used in some breast cancers (see BREASTS, DISEASES OF); advanced myeloma (see MYELOMATOSIS); sarcomas (see under CANCER); and some childhood cancers (such as WILMS’ TUMOUR).
More than 20 substances are in common use, the major classes being ALKYLATING AGENTS (e.g. cyclophosphamide, chlorambucil, busul fan); ANTIMETABOLITES (e.g. methotrexate); VINCA ALKALOIDS (e.g. vincristine, vinblastine); and antitumour ANTIBIOTICS (e.g. actinomycin D). Choice of agent and the appropriate regimen requires expert guidance. Common side-effects include nausea and vomiting, bone-marrow suppression and ALOPECIA, with each substance having its own spectrum of unwanted effects.
Good doctor-patient communication, with the sharing of information and bringing the patient into the decision-making process, is vital even if time-consuming and exhausting.
Equally imortant treatment is PALLIATIVE, for example to ensure e?ective pain or nausea control. Common sources of pain in cancer may involve bone, nerve compression, soft tissue, visceral, myofascial, constipation, muscle spasm, low-back pain, joint pain (e.g. capsulitis) and chronic post-operative pain. Patients may be suffering from more than one pain, all of which should be identi?ed. The aim should be to eliminate pain.
There are three rungs of the analgesic ladder; if one rung fails, the next one should be tried:
(1) non-opioid drugs – for example, aspirin, PARACETAMOL, NON-STEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDS); (2) weak opioids – for example, CODEINE, DIHYDROCODEINE, dextropropoxyphene; (3) strong opioids
– for example, MORPHINE, DIAMORPHINE, buprenorphine. Oral treatment is always preferable, unless prevented by severe vomiting. (See also CANCER; ONCOLOGIST; PAIN; PALLIATIVE CARE.)... oncology
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