Altered sensation in the skin that occurs without a stimulus (see pins-and-needles).
associated with numbness and, sometimes, a burning feeling. The medical term is paraesthesia. Transient pins-andneedles is due to a temporary disturbance in the conduction of nerve signals from the skin. Persistent pins-and-needles may be caused by neuropathy.... pins-and-needles
Symptoms These depend upon whether the anaemia is sudden in onset, as in severe haemorrhage, or gradual. In all cases, however, the striking sign is pallor, the depth of which depends upon the severity of the anaemia. The colour of the skin may be misleading, except in cases due to severe haemorrhage, as the skin of many Caucasian people is normally pale. The best guide is the colour of the internal lining of the eyelid. When the onset of the anaemia is sudden, the patient complains of weakness and giddiness, and loses consciousness if he or she tries to stand or sit up. The breathing is rapid and distressed, the pulse is rapid and the blood pressure is low. In chronic cases the tongue is often sore (GLOSSITIS), and the nails of the ?ngers may be brittle and concave instead of convex (koilonychia). In some cases, particularly in women, the Plummer-Vinson syndrome is present: this consists of di?culty in swallowing and may be accompanied by huskiness; in these cases glossitis is also present. There may be slight enlargement of the SPLEEN, and there is usually some diminution in gastric acidity.
CHANGES IN THE BLOOD The characteristic change is a diminution in both the haemoglobin and the red cell content of the blood. There is a relatively greater fall in the haemoglobin than in the red cell count. If the blood is examined under a microscope, the red cells are seen to be paler and smaller than normal. These small red cells are known as microcytes.
Treatment consists primarily of giving suf?cient iron by mouth to restore, and then maintain, a normal blood picture. The main iron preparation now used is ferrous sulphate, 200 mg, thrice daily after meals. When the blood picture has become normal, the dosage is gradually reduced. A preparation of iron is available which can be given intravenously, but this is only used in cases which do not respond to iron given by mouth, or in cases in which it is essential to obtain a quick response.
If, of course, there is haemorrhage, this must be arrested, and if the loss of blood has been severe it may be necessary to give a blood transfusion (see TRANSFUSION – Transfusion of blood). Care must be taken to ensure that the patient is having an adequate diet. If there is any underlying metabolic, oncological, toxic or infective condition, this, of course, must be adequately treated after appropriate investigations.
Megaloblastic hyperchromic anaemia There are various forms of anaemia of this type, such as those due to nutritional de?ciencies, but the most important is that known as pernicious anaemia.
PERNICIOUS ANAEMIA An autoimmune disease in which sensitised lymphocytes (see LYMPHOCYTE) destroy the PARIETAL cells of the stomach. These cells normally produce INTRINSIC FACTOR, the carrier protein for vitamin B12 (see APPENDIX 5: VITAMINS) that permits its absorption in the terminal part of the ILEUM. Lack of the factor prevents vitamin B12 absorption and this causes macrocytic (or megaloblastic) anaemia. The disorder can affect men and women, usually those over the age of 40; onset is insidious so it may be well advanced before medical advice is sought. The skin and MUCOSA become pale, the tongue is smooth and atrophic and is accompanied by CHEILOSIS. Peripheral NEUROPATHY is often present, resulting in PARAESTHESIA and numbness and sometimes ATAXIA. A rare complication is subacute combined degeneration of the SPINAL CORD.
In 1926 two Americans, G R Minot and W P Murphy, discovered that pernicious anaemia, a previously fatal condition, responded to treatment with liver which provides the absent intrinsic factor. Normal development requires a substance known as extrinsic factor, and this depends on the presence of intrinsic factor for its absorption from the gut. The disease is characterised in the blood by abnormally large red cells (macrocytes) which vary in shape and size, while the number of white cells (LEUCOCYTES) diminishes. A key diagnostic ?nd is the presence of cells in the BONE MARROW.
Treatment consists of injections of vitamin B12 in the form of hydroxocobalamin which must be continued for life.
Aplastic anaemia is a disease in which the red blood corpuscles are very greatly reduced, and in which no attempt appears to be made in the bone marrow towards their regeneration. It is more accurately called hypoplastic anaemia as the degree of impairment of bone-marrow function is rarely complete. The cause in many cases is not known, but in rather less than half the cases the condition is due to some toxic substance, such as benzol or certain drugs, or ionising radiations. The patient becomes very pale, with a tendency to haemorrhages under the skin and mucous membranes, and the temperature may at times be raised. The red blood corpuscles diminish steadily in numbers. Treatment consists primarily of regular blood transfusions. Although the disease is often fatal, the outlook has improved in recent years: around 25 per cent of patients recover when adequately treated, and others survive for several years. In severe cases promising results are being reported from the use of bone-marrow transplantation.
Haemolytic anaemia results from the excessive destruction, or HAEMOLYSIS, of the red blood cells. This may be the result of undue fragility of the red blood cells, when the condition is known as congenital haemolytic anaemia, or of acholuric JAUNDICE.
Sickle-cell anaemia A form of anaemia characteristically found in people of African descent, so-called because of the sickle shape of the red blood cells. It is caused by the presence of the abnormal HAEMOGLOBIN, haemoglobin S, due to AMINO ACID substitutions in their polypeptide chains, re?ecting a genetic mutation. Deoxygenation of haemoglobin S leads to sickling, which increases the blood viscosity and tends to obstruct ?ow, thereby increasing the sickling of other cells. THROMBOSIS and areas of tissue INFARCTION may follow, causing severe pain, swelling and tenderness. The resulting sickle cells are more fragile than normal red blood cells, and have a shorter life span, hence the anaemia. Advice is obtainable from the Sickle Cell Society.... inadequate intake of iron
K
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
Touch sense proper, by which we perceive a touch or stroke and estimate the size and shape of bodies with which we come into contact, but which we do not see.
Pressure sense, by which we judge the heaviness of weights laid upon the skin, or appreciate the hardness of objects by pressing against them.
Heat sense, by which we perceive that an object is warmer than the skin.
Cold sense, by which we perceive that an object touching the skin is cold.
Pain sense, by which we appreciate pricks, pinches and other painful impressions.
Muscular sensitiveness, by which the painfulness of a squeeze is perceived. It is produced probably by direct pressure upon the nerve-?bres in the muscles.
Muscular sense, by which we test the weight of an object held in the hand, or gauge the amount of energy expended on an e?ort.
Sense of locality, by which we can, without looking, tell the position and attitude of any part of the body.
Common sensation, which is a vague term used to mean composite sensations produced by several of the foregoing, like tickling, or creeping, and the vague sense of well-being or the reverse that the mind receives from internal organs. (See the entry on PAIN.)
The structure of the end-organs situated in the skin, which receive impressions from the outer world, and of the nerve-?bres which conduct these impressions to the central nervous system, have been described under NERVOUS SYSTEM. (See also SKIN.)
Touch affects the Meissner’s or touch corpuscles placed beneath the epidermis; as these di?er in closeness in di?erent parts of the skin, the delicacy of the sense of touch varies greatly. Thus the points of a pair of compasses can be felt as two on the tip of the tongue when separated by only 1 mm; on the tips of the ?ngers they must be separated to twice that distance, whilst on the arm or leg they cannot be felt as two points unless separated by over 25 mm, and on the back they must be separated by more than 50 mm. On the parts covered by hair, the nerves ending around the roots of the hairs also take up impressions of touch.
Pressure is estimated probably through the same nerve-endings and nerves that have to do with touch, but it depends upon a di?erence in the sensations of parts pressed on and those of surrounding parts. Heat-sense, cold-sense and pain-sense all depend upon di?erent nerve-endings in the skin; by using various tests, the skin may be mapped out into a mosaic of little areas where the di?erent kinds of impressions are registered. Whilst the tongue and ?nger-tips are the parts most sensitive to touch, they are comparatively insensitive to heat, and can easily bear temperatures which the cheek or elbow could not tolerate. The muscular sense depends upon the sensory organs known as muscle-spindles, which are scattered through the substance of the muscles, and the sense of locality is dependent partly upon these and partly upon the nerves which end in tendons, ligaments and joints.
Disorders of the sense of touch occur in various diseases. HYPERAESTHESIA is a condition in which there is excessive sensitiveness to any stimulus, such as touch. When this reaches the stage when a mere touch or gentle handling causes acute pain, it is known as hyperalgesia. It is found in various diseases of the SPINAL CORD immediately above the level of the disease, combined often with loss of sensation below the diseased part. It is also present in NEURALGIA, the skin of the neuralgic area becoming excessively tender to touch, heat or cold. Heightened sensibility to temperature is a common symptom of NEURITIS. ANAESTHESIA, or diminution of the sense of touch, causing often a feeling of numbness, is present in many diseases affecting the nerves of sensation or their continuations up the posterior part of the spinal cord. The condition of dissociated analgesia, in which a touch is quite well felt, although there is complete insensibility to pain, is present in the disease of the spinal cord known as SYRINGOMYELIA, and a?ords a proof that the nerve-?bres for pain and those for touch are quite separate. In tabes dorsalis (see SYPHILIS) there is sometimes loss of the sense of touch on feet or arms; but in other cases of this disease there is no loss of the sense of touch, although there is a complete loss of the sense of locality in the lower limbs, thus proving that these two senses are quite distinct. PARAESTHESIAE are abnormal sensations such as creeping, tingling, pricking or hot ?ushes.... touch
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