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The disease usually occurs through introduction via the umbilical cord of tetanus spores during delivery through the use of an unclean instrument to cut the cord buy viagra professional 100mg low price impotence 60 years old, or after delivery by ‘dressing’ the umbilical stump with substances heavily contaminated with tetanus spores buy cheap viagra professional 50 mg erectile dysfunction premature ejaculation, frequently as part of natal rituals. Tetanus neonatorum is typified by a newborn infant who sucks and cries well for the first few days after birth but subsequently develops progres- sive difficulty and then inability to feed because of trismus, generalized stiffness with spasms or convulsions and opisthotonos. Overall, case-fatality rates for neonatal tetanus are very high, exceeding 80% among cases with short incubation periods. Neurological sequelae including mild retardation occur in 5% to over 20% of those children who survive. Prevention of tetanus neonatorum can be achieved through a combina- tion of 2 approaches: a) improving maternity care with emphasis on increasing the tetanus toxoid immunization coverage of women of child- bearing age (especially pregnant women), and b) increasing the propor- tion of deliveries attended by trained attendants. Important control measures include licensing of midwives; providing professional supervision and education as to methods, equipment and techniques of asepsis in childbirth; and educating mothers, relatives and attendants in the practice of strict asepsis of the umbilical stump of newborn infants. The latter is especially important in many areas where strips of bamboo are used to sever the umbilical cord or where ashes, cow dung poultices or other contaminated substances are traditionally applied to the umbilicus. In those areas, any woman of childbearing age visiting a health facility should be screened and offered immunization, no matter what the reason for the visit. Nonimmunized women should receive at least 2 doses of tetanus toxoid according to the following schedule: the first dose at initial contact or as early as possible during pregnancy, the second dose 4 weeks after the first and preferably at least 2 weeks before delivery. A third dose could be given 6–12 months after the second, or during the next pregnancy. A total of 5 doses protects the previously unimmunized woman through- out the entire childbearing period. Identification—A chronic infection and usually mild disease, pre- dominantly of young children but increasingly recognized in adults, caused by migration of larval forms of toxocara species in the organs and tissues. It is characterized by eosinophilia of variable duration, hepatomeg- aly, hyperglobulinaemia, pulmonary symptoms and fever. Symptoms may persist for a year or longer; symptomatology is related to total parasite load. Pneumonitis, chronic abdominal pain, a generalized rash and focal neurological disturbances may occur, as may endophthalmitis (caused by larvae entering the eye), usually in older children; this can result in loss of vision in the affected eye (ocular larva migrans). Retinal lesions must be differentiated from retinoblastoma and other retinal masses. Severe disease occurs sporadically and affects mainly children aged 14–40 months, but also in older age groups. Siblings often have eosinophilia or other evidence of light or residual infection. Serological studies in asymptomatic children have shown a wide range in different populations. Internationally, seroprevalence ranges from lows of 0%–4% in Germany and urban Spain (Madrid) to 83% in some Caribbean subpopulations. Puppies are infected by transplacental and transmammary migration of larvae and pass eggs in their stools by the time they are 3 weeks old. Infection among bitches may end or become dormant with sexual maturity; with pregnancy, however, T. Similar though less marked differences apply for cats; older animals are less susceptible than young. Mode of transmission—For most infections in children, by direct or indirect transmission of infective toxocara eggs from contaminated soil to the mouth, directly by contact with infected soil or indirectly by eating unwashed raw vegetables. Some infections may occur through ingestion of larvae in raw liver from infected chickens, cattle and sheep. Eggs require 1–3 weeks’ incubation to become infective, but remain viable and infective in soil for many months; they are adversely affected by desiccation. After ingestion, embryonated eggs hatch in the intestine; larvae pene- trate the wall and migrate to the liver and other tissues via the lymphatic and circulatory systems. From the liver, larvae spread to other tissues, particularly the lungs and abdominal organs (visceral larva migrans) or the eyes (ocular larva migrans), and induce granulomatous lesions. The parasites cannot replicate in the human or other end-stage hosts; viable larvae may remain in tissues for years, usually in the absence of symptom- atic disease. When the tissues of end-stage hosts are eaten, the larvae may be infective for the new host. Incubation period—In children, weeks or months, depending on intensity of infection, reinfection and sensitivity of the patient. In infections through ingestion of raw liver, very short incubation periods (hours or days) have been reported. Susceptibility—Lower incidence in older children and adults relat- ing mainly to lesser exposure. Preventive measures: 1) Educate the public, especially pet owners, concerning sources and origin of the infection, particularly the danger of pica, of exposure to areas contaminated with feces of untreated puppies and of ingestion of raw or undercooked liver of animals exposed to dogs or cats. Parents of toddlers should be made aware of the risk associated with pets in the household and how to minimize them. Encourage cat and dog owners to practice responsible pet ownership, including prompt removal of pets’ feces from areas of public access. Children’s sandboxes offer an attractive site for defe- cating cats; cover when not in use. Dispose of feces passed as a result of treatment, as well as other stools, in a sanitary manner. Control of patient, contacts and the immediate environment: 1) Report to local health authority: Official report not ordinarily justifiable, Class 5 (see Reporting). Diethylcarbam- azine and thiabendazole have been used; effectiveness of anthelminthics is questionable at best. Following ingestion of undercooked fish and poultry containing third stage larvae, the parasites migrate through the tissue of humans or animals, forming transient inflammatory lesions or abscesses in various parts of the body. Larvae may invade the brain, producing focal cerebral lesions associated with eosinophilic pleocytosis. Anthelminthic drugs, including albendazole and mebendazole, are of ques- tionable value, and these drugs are considered investigational. The larvae enter the skin and migrate intracutaneously for long periods; eventually they may penetrate to deeper tissues. Each larva causes a serpiginous track, advancing several millimeters to a few centimeters a day, with intense itching especially at night. The cutaneous disease is self-limited, with spontaneous cure after weeks or months. Thiabendazole is effective as a topical ointment; albendazole or ivermectin is effective systemically. Identification—A systemic coccidian protozoan disease; infections are frequently asymptomatic, or present as acute disease with lymphade- nopathy only, or resemble infectious mononucleosis, with fever, lymph- adenopathy and lymphocytosis persisting for days or weeks. Development of an immune response decreases parasitaemia, but Toxoplasma cysts remaining in the tissues contain viable organisms. Later in pregnancy, maternal infection results in mild or subclinical fetal disease with delayed manifes- tations such as recurrent or chronic chorioretinitis. In immunosuppressed pregnant women who are Toxoplasma-seropositive, a reactivation of latent infection may rarely result in congenital toxoplasmosis.

The supraglottis includes the while on expiration these structures are forced epiglottis and false cords (vestibular folds) purchase generic viagra professional line impotence tcm. The When the obstruction lies below the vocal subglottis extends below the true cords to the cords order generic viagra professional on-line coffee causes erectile dysfunction, stridor is either heard both during inferior edge of the cricoid cartilage. The timing of stridor with respira- tory phase gives an idea about the site of Level of Physical findings obstruction obstruction. Stridor with Supraglottic Stridor is inspiratory and charac- terised by a lowpitched flutter. Glottic Stridor is inspiratory and expi- Stridor is produced by a number of condi- ratory and exhibits a phonatory tions which cause narrowing of the larynx or quality. Brassy, because the larynx is relatively small and barking cough is characteristic. Stridor is noisy breathing heard when Common Causes of Stridor there is obstruction to the free flow of air through the larynx or trachea. Acute laryngotracheobronchitis and acute lies mainly in the larynx, stridor is inspiratory laryngitis Stridor 325 3. Foreign bodies in the larynx and trachea Stridor gradually decreases in severity and 5. Sometimes other rare conditions like Reassurance is given to parents who are laryngeal webs, bifid epiglottis and laryn- told to avoid rough handling of the child, to geal cysts may be the aetiological factors. The and Haemophilus influenzae are secondary inva- condition manifests within a few weeks of ders. It is due to general flabbiness of the structures bounding Pathology the laryngeal aperture, particularly the flabbi- The inflammatory process is diffuse in the ness of the aryepiglottic folds. These get larynx and tracheobronchial tree but the main indrawn during inspiration thus producing area involved is the subglottic region of larynx. While on expiration, the folds are forced apart, The other characteristic feature is the stridor is inconstant and is sometimes production of tenacious, thick mucous which extremely marked. Stridor gets more the subglottic region and the thick secretions pronounced on crying and on exertion. Diagnosis is made on direct laryngoscopy, when indrawing of the aryepiglottic folds is Clinical Features evident and if the laryngoscope is passed The disease usually start as a mild upper between these folds, the stridor disappears. Dyspnoea with There occurs marked swelling of the recession of the intercostal supraclavicular and epiglottis which may extend to the supra- suprasternal spaces results. There is high fever, respiratory obstruction that can occur within toxaemia and restlessness. Oedema is the usual feature with semielliptical mounding of the subglottic The disease starts with a sore throat which tissues. Because of the inflamed Treatment supraglottic tissues, the patient finds it very difficult to swallow. The voice may be muffled Maintenance of the airway is of primary but is usually clear. Tracheostomy or endolaryngeal The degree of prostration and shock is intubation may be needed in severe cases. The patient looks anxious and Frequent suction of thick mucoid secretions frightened because of choking. Moist air should be provided to of the throat shows marked swelling of the such patients. This can be done by view shows what is termed as the ‘thumb sign; electrosonic nebulisers or by an oxygen tent erected over the bed and providing a boiling and this is due to the swollen epiglottis. These help to prevent Tracheostomy should be done to relieve complications by pathogenic organisms. Antibiotics, usually Corticosteroids help to reduce mucosal ampicillin, are the drugs of choice. The disease The term diphtheria is derived from the Greek is of bacterial origin and Haemophilus influenzae word diphtheria which means leather or type B is the most common causative organism. The disease is rare and is seen usually in the The disease affects children usually below age group of 3 to 6 years. The disease is still 328 Textbook of Ear, Nose and Throat Diseases prevalent in underdeveloping countries vessels into the systemic circulation including India. The degree of toxaemia depends Aetiology upon the causative strain of the Bacillus and Corynebacterium diphtheriae also known as Kleb the site of the infection. The disease is common in young children who These are classified as gravis, intermedius, and have not received proper immunisation. The membrane Pathology forms over the cords and laryngeal vestibule The faucial region is the most common site. The membrane is usually loosely to the larynx although primary laryngeal or attached to the ciliated columnar epithelium. The superficial layers of the epithelium get Direct laryngoscopy shows the membranous involved in a deposit of fibrin and leucocytes lesion of the larynx. The membrane is greyish white in is loosely attached to the mucosa, hence less appearance but may, sometimes, be brown or of toxins are absorbed than in faucial disease black due to haemorrhage in it. The membrane is firmly attached over the areas lined by The main local complication is airway obstruc- squamous epithelium and is loosely attached tion and asphyxia because of membrane over ciliated columnar epithelium. Toxae- The Bacillus produces a powerful exotoxin mia produces certain systemic complications which diffuses through lymphatics and blood which may be cardiac and neurological. Cardiovascular complications: These include induration of about 10 mm at about the fourth acute peripheral circulatory failure, toxic day indicates a positive test, i. Immunity can be provided appear during the second week of the passively by injecting diphtheria antitoxin or disease. Para- Treatment of Diphtheria lysis of the soft palate is the most common The main aim of treatment in such patients is complication which usually occurs during restoration of the airway, if it is in danger, and the third week of the disease. If respiratory sixth cranial nerves, and paralysis of the obstruction is impending, tracheostomy diaphragm. Sometimes acute tubular damage of the To neutralise the circulating toxins, anti- kidneys may occur besides areas of toxic diphtheritic serum is given parenterally after degeneration in the liver and spleen. The dose varies according to the and septicaemia are the other occasional severity of infection. Systemic steroids help to reduce the Schick test determines the susceptibility of a toxaemia and local inflammatory oedema. Arytenoids, aryepiglottic folds and vestibular bands may Predisposing Factors show varying degrees of oedema. Thick secre- tions appear on the surface of the laryngeal Excessive vocal use, smoking, sinusitis and tonsillitis predispose to laryngitis. Sometimes infection involves the perichondrium of the laryngeal cartilages producing perichondritis. Hence, the oedema occurs readily causing Rest to the voice is important for speedy obstruction of the airway. Steam inhalations are soothing to the inflamed mucosa and also provide humidi- Clinical Features fication.

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Viruses depend on the energy and metabolic machinery of the host cell to reproduce order viagra professional 50 mg with visa erectile dysfunction generics. A virus is an infectious agent found in virtually all life forms viagra professional 100 mg visa std that causes erectile dysfunction, including humans, animals, plants, fungi, and bacteria. Viruses are between 20 and 100 times smaller than bacteria and hence are too small to be seen by light microscopy. Viruses vary in size from the largest poxviruses of about 450 nanometers (about 0. Viruses are not considered free-living, since they cannot reproduce outside of a living cell; they have evolved to transmit their genetic information from one cell to another for the purpose of replication. Viruses often damage or kill the cells that they infect, causing disease in infected organisms. Although many infectious diseases, such as the common cold, are caused by viruses, there are no cures for these illnesses. The difficulty in developing antiviral therapies stems from the large number of variant viruses that can cause the same disease, as well as the inability of drugs to disable a virus without disabling healthy cells. However, the development of antiviral agents is a major focus of current research, and the study of viruses has led to many discoveries important to human health. Waterborne Diseases ©6/1/2018 37 (866) 557-1746 Virions Individual viruses, or virus particles, also called virions, contain genetic material, or genomes, in one of several forms. Capsids The viral protective shell, or capsid, can be either helical (spiral-shaped) or icosahedral (having 20 triangular sides). Viruses also carry genes for making proteins that are never incorporated into the virus particle and are found only in infected cells. These viral proteins are called nonstructural proteins; they include factors required for the replication of the viral genome and the production of the virus particle. Some virus particles consist only of nucleocapsids, while others contain additional structures. Some icosahedral and helical animal viruses are enclosed in a lipid envelope acquired when the virus buds through host-cell membranes. Inserted into this envelope are glycoproteins that the viral genome directs the cell to make; these molecules bind virus particles to susceptible host cells. Bacteriophages The most elaborate viruses are the bacteriophages, which use bacteria as their hosts. Some bacteriophages resemble an insect with an icosahedral head attached to a tubular sheath. Viroids and Prions Viroids and prions are smaller than viruses, but they are similarly associated with disease. Co-infection with hepatitis B and D can produce more severe disease than can infection with hepatitis B alone. Prions are mutated forms of a normal protein found on the surface of certain animal cells. Virus Classification Viruses are classified according to their type of genetic material, their strategy of replication, and their structure. Hundreds of other viruses remain unclassified because of the lack of sufficient information. Waterborne Diseases ©6/1/2018 38 (866) 557-1746 Waterborne Diseases ©6/1/2018 39 (866) 557-1746 Waterborne Diseases ©6/1/2018 40 (866) 557-1746 Replication The first contact between a virus particle and its host cell occurs when an outer viral structure docks with a specific molecule on the cell surface. Some viruses accomplish this goal by fusing their lipid envelope to the cell membrane, thus releasing the nucleocapsid into the cytoplasm of the cell. Other viruses must first be endocytosed (enveloped by a small section of the cell’s plasma membrane that pokes into the cell and pinches off to form a bubble-like vesicle called an endosome) before they can cross the cell membrane. Conditions in the endosome allow many viruses to change the shape of one or more of their proteins. These changes permit the virus either to fuse with the endosomal membrane or to lyse the endosome (cause it to break apart), allowing the nucleocapsid to enter the cell cytoplasm. The first viral proteins synthesized by some viruses are the enzymes required to copy the viral genome. Waterborne Diseases ©6/1/2018 41 (866) 557-1746 Using a combination of viral and cellular components, the viral genome can be replicated thousands of times. Late in the replication cycle for many viruses, proteins that make up the capsid are synthesized. These proteins package the viral genetic material to make newly formed nucleocapsids. Some viruses bud out of the cell’s plasma membrane by a process resembling reverse endocytosis. Other viruses cause the cell to lyse, thereby releasing newly formed virus particles ready to infect other cells. Still other viruses pass directly from one cell into an adjacent cell without being exposed to the extracellular environment. The virus replication cycle can be as short as a couple of hours for certain small viruses or as long as several days for some large viruses. Virus Battle Some viruses kill cells by inflicting severe damage resulting in cell lysis; other viruses cause the cell to kill itself in response to virus infection. This programmed cell suicide is thought to be a host defense mechanism to eliminate infected cells before the virus can complete its replication cycle and spread to other cells. Alternatively, cells may survive virus infection, and the virus can persist for the life of its host. Viral Infections Most viral infections cause no symptoms and do not result in disease. For example, only a small percentage of individuals who become infected with Epstein-Barr virus or western equine encephalomyelitis virus ever develop disease symptoms. In contrast, most people who are infected with measles, rabies, or influenza viruses develop the disease. A wide variety of viral and host factors determine the outcome of virus infections. A small genetic variation can produce a virus with increased capacity to cause disease. Herpes simplex virus and poxviruses enter through the skin by direct contact with virus-containing skin lesions on infected individuals. Hypodermic needles and animal and insect bites can transmit a variety of viruses through the skin. Viruses that infect through the respiratory tract are usually transmitted by airborne droplets of mucus or saliva from infected individuals who cough or sneeze. Waterborne Diseases ©6/1/2018 42 (866) 557-1746 Viruses that enter through the respiratory tract include orthomyxovirus (influenza), rhinovirus and adenovirus (common cold), and varicella-zoster virus (chicken pox). Viruses such as rotavirus, coronavirus, poliovirus, hepatitis A, and some adenoviruses enter the host through the gastrointestinal tract.

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There may be product discount 100 mg viagra professional with amex short term erectile dysfunction causes, and as a consequence amorphous calcium phos- antibodies to a number of endocrine glands as part of a phate is precipitated in organs and soft tissues [25] order viagra professional paypal impotent rage violet. At an early age epiphyseal dysplasia) and acquired (juvenile chronic of onset, the dentition is hypoplastic. Rarely, soft-tissue ossifi- A rare but recognized complication of hypoparathy- cation can occur in a periarticular distribution, usually in- roidism is an enthesopathy with extraskeletal ossification volving the hands and feet. In the spine this skeletal hyperostosis resembles most closely that de- Pseudo-pseudohypoparathyroidism (Pphp) scribed by Forestier as “senile” hyperostosis [28, 29]. The ab- pain and stiffness in the back with limitation of move- normalities of metacarpal and metatarsal shortening, cal- ment. Extraskeletal ossification may be present around varial thickening, exostoses, soft-tissue calcification, and the pelvis, hip, and in the interosseous membranes and ossification are best identified on radiographs. Metastatic calcification, bowing of long bones and phatase, and on a normal body pH. Clinical features include tetany, cy of any of these substances, or if there is severe sys- cataracts, and nail dystrophy. This results in a qualitative abnormality of bone, hereditary syndromes, including Turner’s syndrome, with a reduction in the mineral to osteoid ratio, resulting acrodysostosis, Prader-Willi syndrome, fibrodysplasia in rickets in children and osteomalacia in adults. This usually involves unresponsiveness of both mature skeleton, the radiographic abnormalities predom- bone and kidneys. At skeletal maturity, when the process of en- condition is referred to as pseudohypohyperparathy- chondral ossification has ceased, the defective mineral- roidism, and the histologic and radiological features re- ization of osteoid is evident radiographically as Looser’s semble those of azotemic osteodystrophy. Many different Radiographic Abnormalities conditions can cause the same radiological abnormalities of rickets and osteomalacia. In the past, there was much Abnormalities may not be evident at birth but subse- confusion between these conditions, which had similar quently there develops premature epiphyseal fusion, cal- clinical and radiological features but different patterns of varial thickening, bone exostoses, and calcification in the progression and responses to therapies of the day. Metacarpal shorten- of the causes of confusion have been clarified with the in- ing is present, particularly affecting the fourth and fifth creased understanding during the twentieth century of the digits. This may result in a positive metacarpal sign in structure and function of vitamin D and its metabolites. In the immature skeleton, the effect of vitamin D defi- ciency and the consequent defective mineralization of osteoid is seen principally at the growing ends of bones Vitamin D Deficiency [35, 36, 39] (Fig. In the early stage, there is apparent widening of the growth plate, which is the translucent Deficiency of vitamin D may occur as a consequence of “unmineralised” gap between the mineralized metaph- simple nutritional lack (diet, lack of sunlight), malab- ysis and epiphysis. More severe change produces “cup- sorption states (vitamin D is fat soluble and absorbed in ping” of the metaphysis, with irregular and poor miner- the small bowel), chronic liver disease (which affects hy- alization. Some expansion in width of the metaphysis re- droxylation at the 25 position), and chronic renal disease sults in swelling around the ends of the affected long (in which the active metabolite 1,25 di-hydroxy D is not bones. There may be a thin result in vitamin D deficiency; the radiological features ghost-like rim of mineralization at the periphery of the will be similar, being those of rickets or osteomalacia. The margin of the epiphysis appears in- response to treatment, contributed to some of the early distinct as enchondral ossification at this site is also de- confusion. If rickets is suspected it is these to the terms “refractory rickets” and “vitamin D resistant anatomical sites that are most likely to show radiograph- rickets” being used for these conditions. Adams at the insertion of the diaphragm (Harrison’s sulcus), pro- Osteomalacia trusio acetabuli, and triradiate deformity of the pelvis, which can cause problems with subsequent parturition. At skeletal maturity, the epiphysis fuses to the metaph- Involvement of the bones in the thorax and respiratory ysis with obliteration of the growth plate and cessation tract (larynx and trachea) rarely result in stridor and res- of longitudinal bone growth. In very severe rickets, when little skele- continues throughout life in order to maintain the tensile tal growth is taking place (i. Vitamin D deficiency in the vation or chronic ill health), radiological features of rick- adult skeleton results in osteomalacia, the pathognomon- ets may not be evident at the growth plate. In rickets of ic radiographic feature of which is Looser’s zone, named prematurity, little abnormality may be present at the after E. However, the bones are osteopenic and [44] are translucent areas in the bone that are composed prone to fractures. They are typically bi- diographic features of rickets may only become apparent lateral and symmetrical. Radiographically, they appear at puberty, during the growth spurt, with the metaphyseal as radiolucent lines that are perpendicular to the bone abnormalities predominating at the knee. Looser’s zones can occur in any bone, but most typ- provement in biochemical parameters (2 weeks) and clin- ically are found in the medial aspect of the femoral neck, ical symptoms. With treatment, the zone of provisional the pubic rami, the lateral border of the scapula, and the calcification will mineralize. They may involve the first and second ribs, in rated by translucent osteoid from the shaft of the bone which traumatic fractures are uncommon, being usually and may be mistaken for a metaphyseal fracture of child associated with severe trauma. Reduced bone density and poor definition of for Looser’s zones are the metatarsals and metacarpals, epiphyses are helpful distinguishing features for rickets. They may not The section of abnormal bone following healing of rick- always be visible on radiographs; radionuclide bone ets may be visible for a period of time, and give some in- scans are more sensitive in identifying radiographic oc- dication as to the age of onset and duration of the period cult Looser’s zones [45]. Eventually, this zone will become indistin- Looser’s zones must be differentiated from insuffi- guishable from normal bone with remodeling over a pe- ciency fractures that can occur in osteoporotic bone, riod of 3 to 4 months. The zone of provisional calcifica- particularly in the pubic rami, sacrum, and calcaneus. There will be evidence of retarded growth and development in rickets, but in my experience this tends to be more marked when the vitamin D deficiency is associated with chronic diseases that reduce calorie in- take, general well-being, and activity (i. Evidence of secondary hyperparathyroidism, with increased osteoclastic resorption, is always evident histologically, although not always radiographically. Metaphyseal chondrodysplasias encompass a variety of inherited bone dysplasias in which there are metaphy- seal abnormalities ranging from mild (Schmit Type) to severe (Jansen) [42]. Osteomalacia: to differentiate these dysplasias from other rachitic disor- Looser’s zone in the ders that the radiographic abnormalities at the metaphy- medial aspect of the ses may simulate. The other typical features of Paget’s disease serve as distinguishing radiological Glucose, inorganic phosphate, and amino acids are ab- features. However, as in rickets, osteomalacic bone is cose, or amino acids alone, or in combination, with addi- soft and bends. This is evident radiographically by pro- tional defects in urine acidification and concentration. There may be bowing of the long bones of the X-linked hypophosphatemia), or later in life (e. This may be proic acid), deposition of heavy metals or other sub- manifested radiographically as subperiosteal erosion, par- stances (multiple myeloma, cadmium, lead, mercury), in ticularly in the phalanges but other sites (sacroiliac joints, relation to immunological disorders (interstitial nephritis, symphysis pubis, proximal tibia, outer ends of the clavi- renal transplantation), or to the production of a humoral cle, skull vault – “pepperpot” skull) may be involved, de- substance in tumor-induced osteomalacia, also know as pending on the intensity of the hyperparathyroidism and “oncogenic rickets” [53, 54]. There may also be cortical ders, rickets or osteomalacia can be caused by multiple tunnelling and a hazy trabecular pattern. When serum concave endplates, due to deformation of the malacic calcium is generally normal, secondary hyperparathy- bone by the cartilaginous intervertebral disc (“cod fish” roidism does not occur. The bone disease associated with chronic renal impair- Sporadic cases also occur through spontaneous muta- ment is complex and multifactorial, and has changed over tions. The disease is characterised by phospha- ondary hyperparathyroidism (erosions, osteosclerosis, turia throughout life, hypophosphatemia, rickets and os- brown cysts) predominated, improvement in management teomalacia. Clinically affected individuals may be short and therapy have resulted in such radiographic features in stature, principally due to defective growth in the legs, being present in a minority of patients. New complications (amyloid depo- and large pharmacological doses of vitamin D (hence the sition, noninfective spondyloarthropathy, osteonecrosis) term “vitamin D-resistant rickets”) may heal the radio- are now seen in long-term hemodialysis and/or renal logical features of rickets, and also increase longitudinal transplantation.