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By: Cristina Gasparetto, MD

  • Professor of Medicine
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Common causes of osteomyelitis Staphylococcus aureus Streptococci Enterococci Pseudomonas sp Enterobacter sp Proteus sp Escherichia coli Serrotia sp Anaerobic bacteria (Peptostreptococcus sp; Clostridium sp; Bacteroides fragilis) infections but many other bacteria have been isolated (see Table 6 heart attack prevention order generic olmesartan on-line. It is from such skin infections that spread to other organs blood pressure pulse generic 10mg olmesartan visa, including the skeleton heart attack grill locations cost of olmesartan, generally takes place blood pressure chart good and bad trusted 10mg olmesartan. Pyogenic osteomyelitis is most common in children andtheageofonsetismostoftenbetweentheagesof3 and 15 arrhythmia update 2010 order cheap olmesartan on-line. The proximal tibia is a favoured site because here the capillaries loop up to supply the growth plate6 and the bacteria settle out like silt at the bend of a meandering river pulse pressure 38 40mg olmesartan with mastercard. Once the bacteria gain access to the bone marrow, they find themselves in what is in effect a wonderful culture medium, where they rapidly multiply, stimulating a brisk immunological response. A good deal of pus is produced and the increased volume of material within the medullary cavity raises the intra-medullary pressure. The bone may increase in size, and drainage channels called cloacae are formed, through which the pus drains from the bone to the outside, through sinuses7 that are formed in the overlying soft tissues. In the meantime, the presence of organisms under the periosteum stimulates the formation of new bone which may be very exuberant, sometimes forming a thick sheath of new bone around the shaft of the infected bone which is known as an involucrum 6. Interruption of the blood supply to the cortex, or disruption of the supply from the main nutrient artery, may result in areas of necrosis with pieces 5 Saureusowes its name to the fact that it appears as grape-like clusters under the microscope and forms golden colonies when it is cultured. A microangiographic study in children and adults, Clinical Orthopaedics and Related Research, 1986, 208, 119125. The distal part of the bone is slightly swollen, there is periosteal new bone on the shaft and a large cloaca (arrowed) is clearly seen. Sequestra may remain hidden within an infected bone although they may sometimes be seen through a large cloaca, and they will also be evident on X-ray. This combination of an involucrum, cloacae and sequestra is pathognomonic of pyogenic osteomyelitis and although the most likely infectious agent is Saureus, it is impossible to be certain about this since other pyogenic organisms will produce similar effects. The shaft of the bone may undergo substantial osteolysis and pathological fractures occur through weakened areas of the shaft and there may be substantial damage to the growth plate. In particularly unfortunate individuals, malignant change may supervene in the tract of the sinus,10 andtherem aybedepositionofanunusual protein material called amyloid in the kidney. Common causes of osteomyelitis in open fractures Staphylococcus aureus fi-haemolytic streptococci Clostridium sp Bacillus sp Stenotrophomonas maltophilia Nocardia sp Aspergillosus sp Rhizopus sp Mucor sp Death may also ensue if the infection spreads to other organs. The majority of cases of osteomyelitis seen in skeletal assemblages are found in adults which presumably indicates that they had survived for several years with the condition. There was no cure for the disease until the advent of effective antibiotics but it became one of the indications for amputation when the operation passed from military into general surgical practice in the eighteenth century. Compound fracture osteomyelitis: A compound, or open, fracture presents an easy means of access to infectious organisms. The tibia is the most frequent site of infection in this case, mostly in young men who engage in sport or other hazardous pursuits. The infection may come from normal skin fiora, organisms in the soil or by those tending to the injury. The infection is often polymicrobial and staphylococci and gram-negative bacilli are most frequently implicated (Table 6. It is striking how few fractures in the past appear to have been infected, however, but this may simply be that relatively few are compound. Phosphorus particles in the air were taken into the mouth and gained entry to the bone through diseased teeth or gums. The effects could be horrible in the extreme and there was no cure except for surgical removal, the prospect of which could not have been much less feared than the disease itself. In England, the Salvation Army set up a factory in London that used non-toxic red phosphorus instead of white phosphorus and the disease eventually came to an end when it became uneconomic to use white phosphorus. Vertebral osteomyelitis: Vertebral osteomyelitis is more common in adults than in children and most infections are due to Saureus. Considerable destruction of the vertebral body may result, with vertebral collapse and kyphosis. The result may mimic malignant disease16 and in the skeleton the disease needs to be differentiated from other infectious causes of spinal collapse, including tuberculosis and brucellosis. Discitis: the intervertebral disc has a limited blood supply in children but the adult disc is avascular and infections spread to it from infected vertebrae above or below. In children, there is some evidence for haematogenous spread to the disc with erosion of the subchondral bone plate and sclerosis without concomitant osteomyelitis. There is often a tortuous channel connecting the lesion to the growth plate which may be important in making the diagnosis, and there may be overlying periosteal new bone, although this is often negligible. The radiographic appearances are of lytic lesions which become surrounded by a sclerotic margin as the condition progresses. There are no sequestra and no periosteal new bone and cultures of fiuid drawn from the lesions are invariably sterile. Septic arthritis: Infection may spread to a joint by any of the routes considered for osteomyelitis; however, as with osteomyelitis, haematogenous spread is the most common, and Saureusthe most common causative agent. The bacteria infiltrate the synovium and from there are presumably shed into the lumen of 23 the joint. The synovium becomes swollen and infiamed, the articular cartilage is destroyed, erosions form within the joint and if the infection is untreated as would have normally been the case in the past bony ankylosis is almost inevitable. Almost any joint is susceptible to infection by one route or the other but in children, the hip and the knee are common targets for haematogenous spread. Penetrating injuries may potentially affect any joints, while in conditions in which there is sensory loss, such as diabetes or leprosy, the joints of the foot are particularly susceptible, especially in those who walked barefoot or with fiimsy footwear. Treatment was unavailable unless the surgeon felt able to drain the joint, or advised amputation. Nevertheless, almost two million people a year die from tuberculosis, most of them in Africa. John Graunt, a London haberdasher, published an account of the London Bills of Mortality25 in which causes of death were examined for the years between 1629 and 1660 and found that consumption was by far the major cause of death in non-plague years. The high death rate persisted throughout the eighteenth century and for the first half of the nineteenth when, for reasons that are still poorly understood, it began to decline steeply. Infection is spread through the medium of infected droplets and the primary infection develops in the lungs. What follows then depends very largely on the individuals ability to mount an effective cell-mediated immune reaction to the bacteria. Once inhaled, the infective droplets are engulfed by macrophages in which the bacteria continue to multiply if they are not killed immediately. They were published weekly on a Thursday with a yearly compilation published on the Thursday before Christmas. The two other bacteria in the complex that may rarely cause tuberculosis are Mafricanumand Mmicroti. These are comprised of T-cells and macrophages, the latter of which fuse to form giant cells known as Langerhans32 giant cells, surrounded by lymphocytes and often with central necrosis. In those unable to mount an adequate immune response,36 the disease may spread unchecked. The bacteria can also be reactivated in those who have previously contained the infection, either because host immunity wanes or because the bacteria start to replicate again,37 and at this stage the disease is characterised by spreading, coalescing tubercles with necrotic centres containing a cheese-like material. Tuberculosis is par excellence a disease of poverty, overcrowding and malnutrition. From the lungs, the disease may spread through the blood stream to distant organs, including bone. They liberate hydrogen peroxide and toxic enzymes which not only kill the bacteria but also destroy host tissue. A study of 103 cases in a developed country, 19801994, Medicine (Baltimore), 1999, 92 palaeopathology Conversely, about a third of those with skeletal lesions have a history of pulmonary tuberculosis. The disease in cattle was probably never common before the start of herding but one assumes that it must have been a considerable cause of morbidity and mortality thereafter. Tuberculosis is a primary lung disease in cattle but the organism is excreted in milk and humans contract the disease by eating or drinking infected milk or milk products, although those who may spend a large amount of time in cattle sheds may also contract it from infected droplets spread by diseased cows. From the gut, the bacteria gain entry to the lymphatic system and infect lymph nodes which enlarge and may suppurate. Tuberculosis of the cervical lymph nodes gained a certain notoriety during the seventeenth century, particularly when it was known as scrofula, or the Kings evil. A touch by the King was thought to bring about a cure, no doubt to the great disappointment to the many who seem to have been stroaked by the monarch. An important question with public health implications, American Review of Respiratory and Critical Care Medicine, 1995, 151, 12671268. The central vertebral body has been almost completelydestroyedandthespinehascollapsedtoformthecharacteristicangularkyphosis. Irrespective of which organism causes the skeletal lesions, the morphology is exactly the same and there is no truth in the statement that the bovine form is more likely to affect bone than the human. The disease is largely confined to the vertebral bodies, with the posterior elements of the vertebrae usually, but not invariably, spared. Progression of the disease results in considerable loss of bone tissue with subsequent weakening of the affected vertebral bodies and, eventually, collapse and ankylosis. The result is to produce a marked angular kyphosis of the spine which is known as Potts disease48 which may be complicated by paraplegia or other neurological conditions. Occasionally, one may find vertebrae with lesions on the front of the body which have resulted from infection beneath the anterior longitudinal ligament. Outside the spine, the lesions are generally solitary but this is not always the case and in the tropics especially, extraspinal lesions are more likely to be multifocal. The term spina ventosa refers to the cyst-like swelling of the infected finger, often with cortical destruction but no periosteal new bone formation. Proliferation of new bone is not extensive and ankylosis is almost inevitable as the disease progresses unchecked by treatment. An operational definition for tuberculosis is shown in the Operational definition for tuberculosis box. Operational definition for tuberculosis Spinal: Lytic lesions predominantly affecting the vertebral bodies with sparing of the posterior elements With Virtually no new bone formation There may be ankylosis, vertebral collapse and angular kyphosis. Brucellosis: Brucellosis is a disease of animals that is readily passed to humans and it is considered here because it affects the skeleton and may easily be confused with tuberculosis. Four species of brucella are pathogenic to human, each with a different animal host; Brucella abortus is found in cattle, Br melitensis in goats, Br suis in pigs, and Br canis in dogs. In northern Europe most infections are contracted from cattle, especially from handling infected blood, or meat. While in warmer climates, where goats are herded, infection with Br melitensis is more common, with infection coming from drinking contaminated milk. Infection with Br suis occurs mainly in North America while infection with the canine species is rare and provokes only a mild reaction. The skeletal effects 62 include sacroiliitis and there is often a monoarticular arthritis. The spine is affected in up to a third of those with the infection, most commonly the lumbar 63 spine, although all areas may be involved. Destructive lesions are noted in the vertebrae on the superior and inferior surfaces but these may spread to involve deeper parts of the vertebral body. There is an attempt at repair early in the course of the disease and new bone formation is a feature of brucellosis while radiographs of affected vertebrae show dense sclerosis around and beneath lesions, an important point that may be used to differentiate brucellosis from tuberculosis. Like tuberculosis, it is of great antiquity; it is thought to have originated in Eastern Africa or the Near East and spread throughout Europe, reaching the Americas within the past 500 years. ThisauthorlaterexaminedsomecarbonizedcheesefromHerculaneumandfoundevidenceforthepresence of bacteria, some of which seemed morphologically like brucella (Bacteria in two-millennia-old cheese, and related epizoonoses in Roman populations, Journal of Infection, 2002, 45, 122127. Richards, for example, suggests that at its peak in the fourteenth century therewereatmost3,0004,000 people with the disease in Britain, in a population of about three million. Although, there were about 200 leper hospitals in Britain, they mostly catered to a tiny numbers of patients, often no more than ten with a staff of three to care for them. The disease was often confused with other skin diseases such as psoriasis, eczema, erysipelas, or pustular acne, while deforming joint diseases such as psoriatic arthropathy or rheumatoid might also have done their bit to muddy the diagnostic waters. Although it was suggested that the medieval physicians actually confused the disease with syphilis, a view propounded particularly by Holcomb71 and effectively demolished by Demaitre. For example, over three-quarters of those buried at the leper hospital at Naestved in Denmark had the characteristic lesions of the disease, indicating a high degree of diagnostic precision. There is a wide spectrum of effect and the disease has been classified into a number of clinical types76 (see Table 6. The organism is an obligate intracellular parasite, that is, it can survive only inside other cells, and it has a special predilection for skin macrophages 69 M Goodrich, Other middle ages. Witnesses at the margins of medieval society, Philadelphia, University of Pennsylvania Press, 1998,pp1011; 111. Classification of leprosy and main clinical featuresfi Classification Clinical features Tuberculoid Single, small skin lesions; solitary enlarged peripheral nerves Borderline tuberculoid Many skin lesions; asymmetric irregular enlargement of several large peripheral nerves Borderline lepromatous Multiple skin lesions, all sizes; symmetrical involvement of many peripheral nerves Borderline Many small skin lesions; diffuse thickening of the skin; asymmetrical thickening of peripheral nerves with loss of sensationofweakness Lepromatous Innumerable confiuent skin lesions; diffuse thickening of the skin; symmetrical peripheral neuropathy Note: this classification is not always used in the clinical literature, as some workers prefer a simplified classification in which patients are referred to as having a paucibacillary or a multibacillaryform;thesecorrespondtothetuberculoidandlepromatousforms,respectively. Additionally, it prefers to reside in the cooler parts of the body, such as the skin and the periphery. Conversely, in the lepromatous form, the immune response is poor, granulomas are poorly formed and huge numbers of bacteria are present. Leprosy is a predominantly a disease of the nervous system and the skin (as can be seen from Table 6. The effects of the skeleton are confined largely to those with lepromatous or long-standing tuberculoid leprosy78 and by no means all patients with 77 the bacterium cannot be grown in normal culture media and the nine banded armadillo (Dasypus novemcinctus) is the only other animal in which the disease occurs, although genetically altered mice can also be induced to grow the organism in the laboratory. While it has been estimated that up to 88%of patients may be affected79 much lower prevalences are generally quoted. The maximum prevalence is probably much lower, and certainly considerably less than half. Specific changes are due to the direct infection of bone with the bacterium, often the bones of the hands or the feet,81 whereas the secondary changes result from other effects which do not involve direct infection. The skeletal changes were described by Moller-Christensen who examined human remains from Aebelholt and Naestved in Denmark. Moller-Christensens publications on leprosy constitute one of the classics of palaeopathology and represent one of the few occasions on which the study of bones has aided modern understanding of a disease. The concentric loss of cortical bone in the hands and feet begins peripherally and proceeds proximally with great destruction of the hands and feet, although the metacarpals and metatarsals are generally spared.

Syndromes

  • Prematurity
  • Family history of the disease
  • There is numbing or tingling in the fingers
  • Use of epidural anesthesia
  • Infection
  • Botulism

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Inhalational 50% Nitrous Oxide/50% Oxygen this is used in the late first stage when delivery is expected within 1 hour heart attack survival rate purchase generic olmesartan. When it is given in the first stage its use extends through the second stage of labour arrhythmia beta blocker buy 40 mg olmesartan fast delivery. Usually 1% Lidocaine (Lignocaine) with or without adrenaline is used to infiltrate the perineum before an episiotomy is given blood pressure chart for tracking buy 40mg olmesartan amex. The same drug may be used for pudendal block anaesthesia which facilitates instrumental delivery blood pressure wrist cuff purchase olmesartan canada. Premature delivery is one that occurs before thirtyfiseven completed weeks of gestation hypertension 4 mg order 10mg olmesartan with visa. The immature foetus is at risk of cerebral haemorrhage because the fragile cranial bones provide insufficient protection for the brain and there is increased susceptibility to infection and impaired clotting mechanisms blood pressure stroke level cheap olmesartan uk. NonfiPharmacological Treatment Prefiterm labour may often be prevented by increased rest and it should be suggested that, from midfipregnancy onwards, the woman lies down in the middle of the day. Pharmacological Treatment (Evidence rating: A) Rehydration and Tocolytic agents, such as bfisympathomimetic drugs. Salbutamol and Magnesium Sulphate are often employed to prevent and treat preterm labour. Start infusion at 10 micrograms/minute (2 ml/minute) and increase rate gradually to 45 micrograms/minute (9 ml/minute) until contractions cease, then gradually reduce the rate. The two types are Preterm (before 37 completed weeks) and Term (fi37 weeks, but fi 1 hour before onset of labour. Infections Post streptococcal infections pharyngeal infection skin sepsis (impetigo) infected scabies Other bacterial Infections. Children: Restrict fluids to 400 ml/m2 of body surface area and previous days urine output. Associated with Systemic Diseases Diabetes mellitus Systemic Lupus Erythematosus Amyloidosis Vasculitides 4. Gynaecologic Cause Bilateral ligation of ureters following abdominal hysterectomy 3. Medical (Adult and Paediatric Causes) Acute Glomerulonephritis Haemolysis due to: Malaria Infection Herbal medicines Typhoid fever Diarrhoea, vomiting and dehydration 4. Chronic kidney disease includes conditions that affect the kidney with the potential for progressive loss of kidney function or for complications resulting from decreased kidney function. Women are affected 10 times more than men due to the shortness of their urethra compared to that of men. Other possible routes of infection include ascent from urethral reflux of infected urine into prostatic duct, spread from rectum and spread from bloodstream. Insert suprapubic catheter and do not pass urethral catheter for retention of urine. Specific Treatment (Evidence rating: C) Ciprofloxacin, oral, 750 mg twice daily plus Doxycycline, oral, 100 mg, twice daily for a minimum of 14 days and a maximum of 21 days. Obstructive Hesitancy fi delay in initiating urination Poor/weak urinary stream Straining Terminal dribbling Overflow incontinence Urinary retention Acute retention fi sudden, painful overfidistention of the bladder due to inability to void urine Chronic retention fi bladder distention which is painless, gradual in onset and associated with some inability of the patient to completely empty the bladder on voiding B. There may be associated uraemic signs the kidneys may also be palpable due to hydronephrosis 174 Rectally the prostate gland is enlarged (size assessed in grades or grams); firm in consistency, smooth surface, nonfitender and the median sulcus is palpable. Definitive Treatment (Evidence rating: A) Patients with very mild symptoms which are not bothersome may be put on a programme of monitoring (watchful waiting) through regular checkups. Patients with mild symptoms: Drug therapy Prostate smooth muscle relaxants (selective alphafiadrenergic blockers) these medications may have side effects such as lowering of blood pressure and dizziness. Initial start dose of 1 mg at night; this may be doubled at weekly intervals according to response up to a maximum of 10 mg or Tamsulosin 400 microgram once daily. Their use will cause shrinkage of the prostate and relief of the attendant obstruction. Treatment is indefinite Combined Drug Therapy A combination of a selective alpha blocker and androgen suppression may produce better response than either used alone. The main aetiological factors are ageing, presence of functional testes, family history of prostate cancer and an unknown genetic factor which makes blacks more affected than other races. The prostate gland is hard with an irregular surface and the edges may be irregular. Definitive treatment depends on the stage (extent of progression or spread) of the cancer. Advanced disease is at best kept in check by hormonal manipulation which inhibits growth of the tumour by depriving it of androgens. So long as a man can achieve a hard enough erection to permit vaginal penetration, with a long enough staying power to perform the sexual act till ejaculation is attained, he is judged to be potent. The condition may be classified as primary (never been able to attain and/or maintain an erection for satisfactory sexual intercourse) or secondary, where impotence occurs in men who have a past history of satisfactory sexual performance. Refer also for testosterone and prolactin test, intracavernosal injection test and other tests depending on clinical findings. About one third of cases of infertility result from pathologic factors in men, one third from factors in both men and women and one third from factors in females. Based on reported cases about 15% of all married couples experience reproductive difficulties. Such patients are quite often very apprehensive, frustrated and reluctant to undergo investigations. Examples of such substances are rifampicin and rhodamine B food colouring used in cakes, cookies and soft drinks. There are many endemic areas in Ghana along the lakes or slowfiflowing rivers and irrigation systems. Pharmacological Treatment (Evidence rating: A) Praziquantel, oral For both adults and children: 40 mg/kg body weight as single dose. Seventyfifive percent of full term infants with undescended testes and 90% of premature infants would have spontaneous descent of testes by the age of one year. Patients are usually shy and reluctant to come to the hospital due to stigmatisation. They obstruct urinary outflow from the bladder but permit easy urethral catheterisation. Because the condition is congenital, secondary changes in the bladder and upper urinary tract are advanced at birth. Some patients may be born with severe renal impairment or develop one soon after birth if recognition is delayed. Some of the common stonefitypes include calcium oxalate, calcium phosphate, magnesium ammonium phosphate and uric acid. Bladder/Urethra Suprapubic pain Suprapubic tenderness Frequency Palpable bladder (from Urgency retention or a large stone) Haematuria Hard urethral lump (impacted Strangury fi An uncontrollable and often painful stone) desire to pass urine which results in little or no urine Haematuria (may be blood fistained) being voided. Kidney/Ureteric stone (Evidence rating: C) Admit Give parenteral analgesic for pain. Confirmation of site of obstruction is still needed Manage associated complications first as follows Initial Treatment Acute retention of urine. Uretheral catheterisation will not be feasible Try suprapubic cystostomy or suprapubic needle puncture and aspiration fi try this procedure if facilities for suprapubic cystostomy are lacking. It is carried out by trained surgeons usually under local anaesthesia after careful counselling and informed consent. Involving males in reproductive health and family planning has several benefits and has a positive impact on society. A backfiup method of contraception until after at least 20 ejaculations or 3 months after the procedure or until examination of semen shows no sperm. Surgery should be avoided in elephantiasis of the limbs because it worsens the disease in the long run Gentle controlled exercises of affected limbs 189 Application of cold compresses during acute attacks Pharmacological Treatment (Evidence Level: A) Ivermectin, oral, 150 microgram/kg body weight plus Albendazole, oral, 400 mg given every 6fi12 months Antibiotics for infected skin lesions Flucloxacillin or Amoxicillin (Amoxycillin), oral, 500 mg 8 hourly for 5 days. They result in complications with sequelae such as infertility, ectopic pregnancy, urethral stricture, cervical cancer, congenital syphilis, foetal wastage, low birth weight, prematurity and ophthalmia neonatorum. Therefore, one must treat, on clinical grounds, the most common causes of the collection of symptoms and signs that are presented (syndromic management. All sexual partners of the patient within the last 3 months need to be seen and treated. In case of treatment failure, refer the patient to a facility where microbiology culture and antimicrobial susceptibility can be done on the discharge. The flow chart below may be applied in the management of a patient with urethral discharge. When there is a change in the colour, odour, consistency or an increase in the flow of this discharge, or when the discharge is accompanied by symptoms such as itching, dysuria (discomfort or pain on urinating), genital swelling, lower abdominal pain or back pain, then she needs to seek medical assistance. Patient has had a new sexual partner in the last 3 months the risk assessment is said to be positive if a. Therefore, if a woman has a vaginal discharge, and also a positive risk factor, she is treated for both vaginitis and cervicitis. If she has a vaginal discharge with no positive risk factor, she is offered treatment for vaginitis alone. It is caused by organisms which ascend from the lower genital tract and invade the endometrium, fallopian tubes, ovaries and the peritoneum. The patient often gives a history of past episodes of similar lesions Ulcers due to chancroid are painful and have undermined ragged edges. The base is covered with a dirty purulent exudate and easily bleeds on touch Painless, indurated lesions with regular edges are most often due to syphillis A red beefy looking ulcer with an offensive discharge may be granuloma inguinale However, because genital ulcers often do not correspond to classic descriptions, in the syndromic management, initial management should be directed at both syphilis and chancroid. Notification of partner(s) (Contact tracing) Tell the patient that the ailment they have was aquired through sex Tell the patient to inform his/her sexual partners in the last 3 months so that they may also be treated. Compliance Tell the patient how to take the medicine Tell the patient to refrain from sex until all symptoms are gone and treatment of patients and their partners have been completed Tell the patient to return to the clinic if treatment fails the patient should avoid self medication and traditional remedies 198 3. Major Signs Weight loss of more than 10% of body weight Chronic diarrhoea > 1 month Prolonged fever > 1 month (intermittent or constant) Minor Signs Persistent cough for > 1 month Generalized pruritic dermatitis Recurrent herpes zoster Orofipharyngeal candidiasis Chronic progressive and disseminated herpes simplex infection. In the same vein, even though the virus has been found in urine, tears, sweat and saliva, the infectiousness of these body fluids has not been determined. It is important that it is initiated as soon as possible after the exposure (preferably within 1fi2 hours. Fever above 38C in children and adults often need urgent attention especially if the patient is restless/delirious. Pharmacological Treatment Adults: Give Paracetamol, oral, 1 g 3 to 4 times daily Treat the cause of the fever appropriately (see appropriate section) Children: Give Paracetamol, oral, according to the dosage schedule below. A thorough history, physical examination and appropriate investigation would usually reveal the cause of the fever. Complaints Diagnosis* (See appropriate Action* (See appropriate section) section) Rigors, periodic fevers, sweating, general * Malaria * Take a blood film for malaise, joint pains malaria parasites and treat appropriately Rigors, fever, sweating, general malaise, altered * Cerebral Malaria * Take a blood film for sensorium malaria parasites and treat appropriately Headache, vomiting, drowsiness, stiff neck, * Meningitis * Do not delay treatment seizures while awaiting lumbar puncture. Children: Susceptibility to infection is increased with chronic illness or malnutrition. The patient must be told this so he/she does not stop taking the medication just because he/she feels well. The patient should eat well, especially foods with plenty of protein and vitamins, and must try to get enough rest. Prescribing Rifampicin alone must be discouraged During this phase the patient must swallow all the oral drugs preferably on an empty stomach under direct observation before the streptomycin injection. The patient needs to be under close supervision by a health worker or any responsible person or member of the community with support from health staff during the full duration of treatment. Standard Course: this is of 12 months duration for a) Smear negative pulmonary tuberculosis and b) Extrapulmonary tuberculosis. Retreatment Regimen: this is for: a) Relapse b) Treatment failure It consists of an initial intensive phase of five drugs fi Rifampicin, Isoniazid, Pyrazinamide and Ethambutol daily for at least 3 months, supplemented with Streptomycin for the first 2 months. The continuation phase is with Rifampicin and Isoniazid and Ethambutol 3 times weekly for a further 5 months. Sometimes meningitis may be caused by Mycobacterium tuberculosis; following spread from another site of the body. All treatment should be intravenous initially for a minimum of 7 days and should be started without delay. Typhoid fever can be a serious illness characterised by fever, abdominal symptoms, and may end fatally. However, typhoid fever is over diagnosed by many practitioners in Ghana based on only a Widal test, which is an unreliable indicator of typhoid infection. The indiscriminate use of antibiotics for this condition has resulted in the resistance of S. At the first sign of pain or inflammation, patients must discontinue treatment and alternative treatment (e. The malaria parasite is transmitted through the bite of an infected female anopheline mosquito. The commonest parasite responsible for malaria in this country is Plasmodium falciparum. Education of the public on personal protection against mosquito bites, maintenance of clean domestic surroundings and use of insecticide treated materials. Artesunate can, however, be used in the second and third trimesters if treatment is considered to be lifesaving for the mother and other antimalarials are considered to be unsuitable. The second dose of three tablets of sulphadoxinefipyrimethamine (500 mg/25 mg) is to be given one month after the first 3. The third and final dose of three tablets of sulphadoxinefipyrimethamine (500 mg/25 mg) should be taken one month after the second dose and before 36 weeks gestation. Treatment of Malaria in Pregnancy When a pregnant woman gets malaria, she should be given a full course of quinine oral, 600 mg 8 hourly for 7 days. It is a very serious disease, which may rapidly cause death or permanent brain damage. The presence of malaria parasites seen under the microscope confirms the diagnosis; however, its absence does not exclude the diagnosis. Parenteral treatment should be continued until patient can tolerate oral quinine which should then be given to complete the full 7fiday course. Additional measures for the management of severe or complicated malaria are listed on the table below. Additional measures for the management of severe or complicated malaria Complication Recognition Action 1.

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Diferentes programas tem sido propostos para varios tipos de situacao: exercicios em flexao hypertension 24 order olmesartan cheap online, extensao blood pressure chart 2015 order olmesartan canada, alongamento blood pressure medication replacement buy olmesartan overnight delivery, aerobico e fortalecimento muscular heart attack gun buy generic olmesartan 20mg online, podem ser utilizados hypertension 8 weeks pregnant generic 20mg olmesartan visa. Varios estudos demonstraram a utilidade destes exercicios para diminuir sintomas e prevenir novas crises(10 heart attack left arm cheap olmesartan 20mg on line,11. Modalidades fisicas Muito embora sejam muito utilizadas e uteis na melhora dos sintomas por curto periodo de tempo, nao existem estudos controlados confirmando sua eficacia. Seu verdadeiro papel e fififififififififi fififififififi fififi fifififififi fifififififififififi fifififififi fififi adjuvante na cinesioterapia. O gelo diminui o edema, dor e espasmo muscular nas lombalgias agudas; o calor e utilizado preferencialmente na fase cronica, produzindo analgesia e melhorando a rigidez muscular. O calor pode ser utilizado de forma superficial (infravermelho, compressas) ou profundo (ultra-som. Finalmente, a estimulacao eletrica transcutanea estimula as fibras a-A de baixo limiar, o que inibiria os impulsos nociceptivos das pequenas fibra C e a-D(12. Outras formas de tratamento muito empregadas, como acupuntura e tracao, carecem de evidencias cientificas que confirmem sua utilidade. Infiltracoes locais As injecoes locais de anestesicos e corticosteroides tem sido indicadas em casos de dor localizada em pontos de gatilho musculares ou ligamentares. As injecoes epidurais, utilizadas nos casos de radiculalgia dos membros inferiores nao tem utilidade em casos de lombalgia comum. Infiltracoes de facetas sob fluoroscopia tem sido amplamente utilizadas, apesar da existencia de estudos conflitantes(13. Escola de coluna Particularmente uteis no controle dos sintomas e na prevencao de novas crises, conforme evidencias cientificas publicadas. Ajudam os pacientes a conhecer melhor o seu problema e a relacao da lombalgia com os habitos da vida. Permitem ainda um melhor conhecimento de questoes ergonomicas da coluna e de exercicios praticos diarios(14. Cinesioterapia Varias modalidades de reabilitacao sao empregadas em larga escala no tratamento de dores da coluna. Existe consideravel evidencia do beneficio de exercicios de alongamento e fortalecimento muscular em casos cronicos. No entanto, nao ha estudos suficientes para recomendar um protocolo de exercicios especificos. A dor cronica, por sua vez, pode ser mais resistente ao tratamento, requerendo uma avaliacao especializada e multiprofissional. Ainda assim, e muito importante evitar a pressao por medidas muito invasivas ou tratamentos miraculosos. Borenstein D: Epidemiology, etiology, diagnostic evaluation, and treatment of low back pain. Waddell G: 1987 Volvo Award in clinical sciences A new clinical model for the treatment of low back pain. Abenheim L, et alii: the role of activity in the therapeutic management of back pain. In Wiesel S, et alii: the International Society for the study of the lumbar spine. Johannsen F, Remvig L, Kryger P, Beck P, Warming S, Lybeck K: Exercises for chronic low back pain:a clinical trial. Brousseau, et alii: Efficacy of the transcutaneous electrical nerve stimulation for the treatment of chronic low back pain: a meta-analysis. Revel M, et alii: Capacity of the clinical picture to characterize low back patients relieved by facet joint anestesia. Consulte Malformacao Adaptacoes 211 de Arnold-Chiari Adormecimento 61 Articulacao atlanto-occipital 43 Adson. Consulte Sindrome de achados laboratoriais 133 Bechterew Artrogripose 184 Biopsia jejunal 135 Artropatias das doencas Braco. Consulte Manobra de 110, 111, 113, 127 Bragard Artropatias de doencas inflamatorias Braquialgia 52 intestinais 125 Brucelose 216 achados clinicos 126 Bursite 131 achados de imagem 127 achados laboratoriais 127 Calcaneo 114, 120, 121, 125, 131, Artropatias enteropaticas 67 133 Artropatias inflamatorias 109 Calcio 98, 99, 102, 104 Artropatias microcristalinas 71 Calcitonina 103, 105 Artrose cervical 59, 61 Campylobacter 129, 131 Artrose facetaria 158, 218, 225 Canal. Consulte Sindrome da Atlas 21, 27, 29, 43, 45, 63, 65, 66, cauda equina 74, 138 Cefaleia 41, 49, 55, 57, 62 Avaliacao das articulacoes Cefaleia suboccipital 60, 61, 66 sacroiliacas 115, 116 Celecoxib 87 Axis 21, 29, 43, 45, 138 Celiaca. Consulte Dor cervical Bacilo de Calmette-Guerin 129 Cervicalgias 41, 42 Bacterias gram-negativas 128 causas de 71 Balanite 128 Cervicalgias mecanicas 54 Balanite circinada 131, 132 Cervicite 111, 132 fifififififi fififififififififi fififi Charcot. Consulte Sindrome do Condicionamento fisico 89, 210, 229 chicote Conjuntivite 124, 126, 127, 130-132 Chlamydia pneumoniae 129, 131 Conservacao de energia 209, 212 Chlamydia trachomatis 129, 131, 132 Corpo vertebral. Consulte Quadratura Ciatalgia 162 de corpo vertebral Ciclobenzaprina 88 Corticosteroides 64, 160, 197, 231 Cifose 39, 82, 97, 165, 168, 169, 176Corticosteroides por via intradural 181, 186, 204 161 Cintilografia ossea 168 Criterios de classificacao do Grupo Cisalhamento. Consulte Vertebras em 123, 124 cunha Claudicacao 49, 148, 180, 181, 193, 194, 221 Dactilite 123, 128, 131, 132 Clostridium difficile 129, 131, 143 Dano neurologico 136, 138 Cobb-Lippman. Consulte Distancia de Cobb-Lippman dedo-chao Coccix 18, 19, 24 Dedos em salsicha 123 Colete de Milwaukee 173, 175, 179, Densidade mineral ossea 96 203, 204, 206, 211 Densitometria 181 Coletes 174, 182 Densitometria ossea 86, 100, 101 Coletes abdominais 161 Dermatite herpetiforme 134 Colica renal 82 Dermatomos 31, 32, 82 Coluna cervical 9, 30, 41-46, 48, 52, Desconforto abdominal 134 55, 59, 62-64, 66, 68, 69, 71, Desfiladeiro toracico. Consulte Sindrome Doenca de Marie-Strumpell 113 de Ehlers-Danlos Doenca de Paget 52, 100, 193 Eletroneuromiografia 86, 228 Doenca de Whipple 79, 108, 110, Emagrecimento 81 134, 135 Endometriose 218 Doenca inflamatoria intestinal Endoscopia 69 118, 126 Energia. Consulte Conservacao de Dor abdominal 126, 135 energia Dor aguda 156, 220, 232 Entamoeba histolytica 129 Dor cervical 41, 47, 49, 52-54, 57, Enteropatia por gluten. Consulte 59, 63, 67, 69, 71, 136, 138 Doenca celiaca Dor cervical cronica 59 Entesis 111, 114, 117, 125, 131, 133 Dor cervical episodica 60 Entesites 112, 113, 124, 129, 132 Dor cronica 215, 220, 222, 230, 232 Entesopatias 68, 111, 121 Dor em gluteos 111, 126 Envolvimento cardiovascular Dor, intensidade da. Consulte 113, 117 Intensidade da dor Envolvimento pulmonar 113 Dor irradiada 49, 82, 221 Episclerite 126, 127 Dor lombar 57, 81, 88, 93, 123, 126, Equimose 136 131, 134, 148, 156, 194, 213, Eritema nodoso 127, 129, 132, 136 216, 218 Escherichia coli 129, 143, 150 Dor lombo-sacral 114 Escola de coluna 231 Dor no braco 57 Escoliose no adulto 180 fifififififi fififififififififi fififi Espinhoso. Consulte Processo Espondilolistese 63, 158, 159, 178, espinhoso 182, 184, 192, 193, 217 Espondilite anquilosante 67, 68, 79, Esporoes 133 83, 93, 108, 110, 111, 113, 115, Esporte 80, 210 119, 121, 127, 135, 178, 193, Espru nao tropical. Consulte Doenca 214 celiaca achados clinicos 114, 118 Esteatorreia 134, 135 criterios de Nova York 114 Estenose de canal 62, 83, 85, 182, criterios de Roma 114 214 diagnostico laboratorial 118 Estenose do canal lombar 191 diagnostico por imagem 120 Estradiol 105 forma juvenil 115 Estrogenio 105 manifestacoes clinicas 113, 124 Exercicios fisicos 230 manifestacoes extra-articulares Exercicios isocineticos 210 119 Exercicios isometricos 89, 203, 210 Espondilite deformante 113 Exercicios isotonicos 89, 210 Espondilite psoriasica 79 Expansibilidade toracica 116, 126 Espondilites infecciosas 178 Espondiliticas. Consulte Sindromes Facetas articulares 20, 33, 49, 79, 88 espondiliticas Fadiga 161, 210, 219 Espondiloartrite anquilopoietica 113 Fascia plantar 124, 131 Espondiloartropatias 10, 82, 108, Fator reumatoide 123, 124, 128, 136 110-112, 114, 125, 128, 130, Fator reumatoide da classe IgM 110 220 Febre 52, 126, 148, 220, 225 achados clinicos 110, 111 Febre reumatica 130 classificacao 112 Febricula 115, 135 tipos 113 Fibromialgia 71, 80 Espondiloartropatias indiferenciadas Fibrose pulmonar 119, 124 10, 108, 110, 111, 113, 128 Fisioterapia 161, 175, 179, 208 achados clinicos 131 Flatulencia 134 achados de imagem 132 Forame intervertebral 28, 31, 32, 33, Espondiloartropatias soronegativas 43 52, 71, 79, 110 Forame vertebral 20, 21 Espondiloartrose 56 Forcas de cisalhamento 37 Espondilodiscites 93, 113 Forcas de compressao 37 Espondilodiscites infecciosas 80 Forcas de tracao 37 fififi fifififififi fififififififififi Forestier. Consulte Doenca de Iliaco 83, 170, 202 Forestier Ilio 24, 29 Fosfatase alcalina 99, 118 Imagens telescopadas 125 Fosforo 99 Incontinencia esfincteriana 65, 66 Fraqueza muscular 49, 61, 229 Incontinencia vesical 57 Fraqueza nas pernas 57 Infeccoes 69, 97, 100, 129, 148, 150, Fratura osteoporotica 66 152, 218, 227, 228 Fratura vertebral 96, 97, 101-103, Infeccoes genito-urinarias 129 105, 113, 204, 216 Infertilidade 134 Fraturas 95-97, 99, 101, 105 Infiltracoes epidurais 88, 182 Fungos 150, 152 Inflamacoes oculares 124 Instabilidade do segmento C1-C2 Giardia lamblia 129 137 Glicocorticoide 87, 88, 98 Insuficiencia aortica 111, 117, 119, Glomerulonefrite 132 124, 128, 132 Gluten 134, 135 Insuficiencia vertebro-basilar Gota 71, 193 60, 65, 66 Grupo Europeu de Estudo das Intensidade da dor 55, 208, 222, 229 Espondiloartropatias 111, 114, International League of Associations 128 for Rheumatol 111 Invaginacao basilar 138, 139 Heparina 98 Hernia discal 47, 51, 54, 57, 58, 85, Klippel-Feil. Consulte Sindrome de 155, 159, 160, 161, 168, 214, Klippel-Feil 217, 221, 229 Hernia discal lombar 156 Herpes zoster 53, 72, 159, 217 L5, sacralizacao de 19, 83, 84, 221, Hiperceratose subungueal 122 225 Hipercifose 101 Laceracao esofagica 69 Hiperostose anquilosante 117 Laminas 20, 22, 27, 44, 47 Hiperostose esqueletica idiopatica Lasegue. Consulte Colete de 230 Milwaukee Lombalgia mecanica 92, 214, 221 Miorrelaxantes 160, 197, 229, 232 Lombalgias e lombociatalgias Moll e Wright, classificacao de 78, 82, 84, 216 123, 124 Lombociatalgia 77-80, 82, 84, 86-89 Morte subita 137 Lordose 39, 82, 97, 165, 166, 168, 177-179, 186, 197, 205, 222, Nefropatia por IgA 118, 119 223 Neisseria gonorrhoea 129, 132 Neoplasias 51, 98, 100, 218, 227 Mal de Pott 150, 216 Nervos espinhais 31, 32 Malformacao de Arnold-Chiari 55 Neuropatias 228 Manipulacao 92, 161 Neuropatias perifericas 53, 195 Manobra de Bragard 83 Nistagmo 65, 66 Manobra de Spurling 51, 61 Notocordio 18 Manobra de Valsalva 51, 83, 156 Nucleo pulposo 25, 26, 38, 43, 45, Marfan. Consulte Doenca Obesidade 135, 222 de Marie-Strumpell Occipital 27, 29, 64, 116, 118, 136, Massa ossea, pico da 96 138 Medicina ocupacional 41 Odontoide, processo 21, 29, 43, 45, Megaapofises 19 64, 65, 137, 138 Membrana tectoria 27 Oftalmoplegia 139 Menopausa 95, 96, 101, 103 Olho 111 Menopausa precoce 98 Oligoartrite assimetrica 129, 131, 132 Mergulhos 59 Onicolise 122 Metastases 87, 216 Orteses 105, 175, 201, 203, 204, 211 Metastases osseas 228 Orteses cervicais 202 Metotrexato 98 Osso esponjoso 20 Micro-hematuria 132 Ossos do tarso 114 Microfraturas 66, 97 Osteite 161, 219 Mieloma multiplo 228 Osteoartrose da coluna cervical 59 Mielomeningocele 184, 186 Osteoblastoma 52 fififi fifififififi fififififififififi Osteoblastos 95, 103 Processo espinhoso 20, 21 Osteocalcina 100 Processo odontoide. Consulte Envolvimento Perda de peso 52, 98, 115, 126, pulmonar 134, 135, 158, 220, 225 Pericardite 117 Quadratura de corpo vertebral 121 Pernas, fraqueza nas 57 Quadriplegia 117-119 Pico da massa ossea. Consulte Massa Quebec Task Force on Spinal ossea, pico da Diseases 217 Pioderma gangrenoso 127 Plexos nervosos 32 Raloxifeno 103, 105 Poliartralgia 135 Reabilitacao 88, 207, 208, 231 Poliartrite nao erosiva 134, 136 Reabsorcao ossea 102 Polimialgia reumatica 71, 216 Reposicao hormonal 103, 105 Poliomielite 184 Repouso 55, 71, 81, 86, 92, 97, 114, Ponta de lapis. Consulte Imagem em 197, 205, 208, 210, 220, 229 ponta de lapis Ressonancia magnetica nuclear 58, Pott. Consulte Mal de Pott 78, 85, 100, 120, 137, 149, 150, Pressao abdominal 201, 205 156, 168, 182, 196, 227 fifififififi fififififififififi fififi Retocolite ulcerativa 79, 125, 126, Sindrome de Klippel-Feil 55, 56 127 Sindrome de Marfan 167, 184 Risser. Consulte Sinal de Risser Sindrome de Reiter 67, 68, 79, 129, Ritmo da dor 220 130, 133 Rofecoxib 87 Sindrome de Stokes-Adams 117 Sindrome do chicote 42, 59 S1, lombarizacao de 19 Sindrome do desfiladeiro toracico Sacralizacao de L5. Consulte L5, 51, 52, 54 sacralizacao de Sindrome facetaria 214 Sacro 18, 19, 23, 24, 29 Sindrome miofascial 71, 80 Sacroileite 111, 113, 116, 120, 121, Sindromes espondiliticas 67, 68, 123, 127, 133 110 Sacroileite assimetrica 125 Sinfise pubica 120, 121 Salmonella 129, 131, 150 Siringomielia 51, 55, 184 Salpingite 132 Sono, disturbio do 229 Sangue nas fezes 126 Spurling, manobra de 51, 61 Schober. Consulte Sindrome Sedentarismo 98 de Stokes-Adams Shigella 129, 131 Strongyloides stercoralis 129 Sinais de alerta 49, 81, 82, 84, 85, Subluxacao atlanto-axial 51, 55, 63, 168, 220 64, 65, 67, 118, 119, 137, Sinal de Babinsky 136 138, 139 Sinal de Risser 169, 170, 202, 204 Subluxacao atlanto-occipital 66 Sincope 60, 65, 66 Subluxacao subaxial 66, 138, 139 Sindesmofitos 67, 68, 113, 121, 125, 133 Tabagismo 81, 98 Sindesmofitos assimetricos 125 Tecnica de Cobb-Lippman 170, Sindesmofitos marginais 127, 133 172, 175, 179, 180, 181 Sindesmofitos nao marginais 125 Tendao de Aquiles 124, 131 Sindrome artrite-dermatite 136 Tendinite 128 Sindrome da cauda equina 92, 113, Teste de Adson 51, 53 118-120, 156, 159, 225, 228 Teste de compressao 49 Sindrome de Bechterew 113 Teste de Lasegue 83, 84, 158, 195, Sindrome de cauda equina 161 224, 225 Sindrome de Ehlers-Danlos 184 Teste de Schober 115 Sindrome de Horner 53 Teste de tracao 50 fififi fifififififi fififififififififi Tomografia computadorizada 58, Vertebra proeminente 21 63, 78, 120, 150, 156, 168, 195, Vertebra tipica 19, 20 226 Vertebral, canal 20, 44, 51, 58, 61Tontura 104, 136 63, 66 Torcicolo 55 Vertebral, forame. Consulte Atividades da Ultra-som 88, 231 vida diaria Unha em dedal 122, 123 Virus 184 Uretrite 111, 130-132 Vitamina D 102 Urticaria 136 Uveite 117, 119, 124, 128, 131 Whiplash 42, 59 Uveite anterior 112, 117, 128, 131 Whipple. Consulte Doenca de Uveite anterior aguda 111, 113, 127, Whipple 128 Whiskering 121, 125 Valsalva. Consulte Manobra de Yersinia 129, 131, 132 Valsalva Variantes da artrite reumatoide 110 Zumbido 60, 136 fifififififi fififififififififi fififi. Vincent Road Kochi 682 018, Kerala Phones: +91-484-4036109, +91-484-2395739, +91-484-2395740 e-mail: kochi@jaypeebrothers. No part of this publication should be reproduced, stored in a retrieval system, or transmitted in any form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the author and the publisher. This book has been published in good faith that the material provided by author is original. Every effort is made to ensure accuracy of material, but the publisher, printer and author will not be held responsible for any inadvertent error(s. In case of any dispute, all legal matters are to be settled under Delhi jurisdiction only. For details and reasons why I liked Professor Mohans book and why I recommended it then, please refer to my previous foreword below. My positive reaction to the previous Edition probably gives some clues on why I accepted the second invitation, this time to introduce the Sixth Edition to new students of Pathology and other potential readers. Great French writer Andre Gide once said le probleme nest pas comment reussir mais comment durer, which in translation to English means: the problem is not how to succeed but how to last. The fact that Dr Mohans book has reached its Sixth Edition is the best sign that you are holding in your hands a very successful book, and probably one of the medical bestsellers published on the Indian subcontinent. Up to now, it has been used by thousands of students and I am sure that it will continue to be read and cherished in the new Edition as well. For the Sixth Edition, Dr Mohan has partially restructured the book, substantially revised it, and updated the text wherever it was necessary. Following the advances of basic sciences and clinical pathology, the revisions and addition are most evident in portions pertaining to molecular biology and genetics. Other aspects of modern pathology have not been neglected either and contain numerous novelties; even the seasoned specialists will learn something new from each and every chapter. Furthermore, the author has dramatically increased the number of illustrations, which are so essential for understanding Pathology. The distribution of illustrations has also been changed so that they are now much closer to the text to which they relate. For the new generation of modern students who have grown up next to the computers, the author has placed all the images and tables on the website with facility for downloading them. These images will serve the twin purpose of quick review and self-assessment for students and will appeal to Pathology teachers who could use them for their lectures, being assured that their students will have access to the same material for review and study. The Quick Review Book, the ever popular companion to the previous two Editions, was also updated, succinctly supplementing the main text. It will provide a helpful study material to many a student and help them review the subject for examinations. In summary, it is my distinct pleasure and honour to most enthusiastically endorse the new edition of an established textbook and salute its publication. Dr Mohan deserves kudos for the job well done and for providing the medical students with such an attractive, modern, up-to-date and useful Textbook of Pathology. These books are sent to my office from publishers, with a standard request for a potential review in the Journal. I acknowledged the receipt of the books by email, and also congratulated the Publisher on a job well done. A brief electronic exchange between Kansas City and New Delhi ensued, whereupon Mr Vij asked me to write a foreword for the Reprint of 5th Edition of the Textbook. Even though there were no specific instructions attached to the request, I assumed that I should address my notes primarily to undergraduate and graduate students of Pathology. Furthermore, I decided to write the Foreword in the form of answers to the questions that I would have had if I were a medical student entering the field of Pathology. I hope that these hypothetical questions and answers of mine will be of interest to the readers of this Textbook. This is a modern Textbook written by an expert who knows his pathology; an experienced teacher who knows what is important and what is not, and who has obviously taught pathology for many years; a well informed academician who is au courant with modern trends in medical education, and knows how to present pathology as a preparatory step for future clinical education of medical students. This Indian Textbook covers more or less the same topics as the equivalent Textbooks currently used in the Western Hemisphere. Like the Western textbooks it covers the traditional fields of General and Systemic Pathology: one-third of the book viii is devoted to General Pathology, whereas the remaining two-thirds cover Systemic Pathology. In that respect the Indian textbook resembles more the European than the American textbooks, which have become more clinically-oriented. In my opinion this approach gives excellent results, but only if the students have enough time to devote to Pathology. Histopathology has been deleted from most curricula, and most American medical students do not know to use efficiently the microscope, which is unfortunate. Answer: the material is presented in a systematic manner in the best tradition of classical British textbooks, a tradition that can be traced to the classical writers of ancient Greece and Rome. This time tested teaching will be most appreciated by students who are methodical and do not take shortcuts in their effort to acquire encyclopedic knowledge of pathology. There are no ideal books that would satisfy everybody in every respect, but there is no doubt that Professor Mohans book is close to ideal for a classical pathology course and I predict that it will be popular with many students. As we all know clear writing reflects clear thinking, and clear thinking in my opinion, is an absolute prerequisite for good teaching. Judging from the book at hand, Professor Mohan (whom I do not know personally) is not only a clear thinker, but he must be also an exceptionally talented teacher. Each chapter is subdivided into smaller entities, which are further divided into paragraphs, ideally suited for easy reading. Color coded headings and the added emphasis in form of words printed in bold or capital letters are additional attractions that facilitate learning. Unique to this Textbook are the numerous hand-drawn color illustrations, including many renditions of histopathologic slides. Students will most likely understand them much easier than the relatively impersonal original microphotographs of the same histopathologic lesions. Flow-charts are most efficiently used to explicate the pathogenesis of various lesions or the pathophysiology of disease processes.

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