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Fixed dose combination of oestrogen and progestin (other than oral contraceptive) containing per tablet oestrogen content of more than 50 mcg (equivalent to ethinyl oestradiol) treatment brachioradial pruritus purchase albenza once a day, and progestin content of more than 3 mg (equivalent to norethisterone acetate), and all fixed dose combination injectable preparations containing synthetic oestrogen and progesterone. Fixed dose combination of sedatives/ hypnotics/anxiolytics with analgesics-antipyretics. Fixed dose combination of rifampicin, isoniazid and pyrazinamide, except those which provide daily adult dose. Fixed dose combination of histamine H-2 receptor antagonists with antacids except for those combinations approved by Drugs Controller, India. The patent and proprietary medicines of fixed dose combinations of essential oils with alcohol having percentage higher than 20% proof, except preparations given in the Indian Pharmacopoeia. Fixed dose combination of any anthelmintic with cathartic/purgative except for piperazine/santonin. Fixed dose combination of salbutamol or any other drug having primarily bronchodilatory activity with centrally acting anti-tussive and/or antihistamine. Fixed dose combination of laxatives and/or anti-spasmodic drugs in enzyme preparations. Fixed dose combination of metoclopramide with systemically absorbed drugs, except fixed dose combination of metoclopramide with aspirin/paracetamol. Fixed dose combination of centrally acting antitussive with antihistamine, having high atropine-like activity in expectorants. Preparations claiming to combat cough associated with asthma containing centrally acting anti-tussive and/or an antihistamine. Liquid oral tonic preparations containing glycerophosphates and/or other phosphates, and/or central nervous system stimulant, and such preparations containing alcohol more than 20% proof. Antidiarrhoeal formulations containing phthalyl sulphathiazole or sulphaguanidine or succinyl sulphathiazole. Antidiarrhoeal formulations containing neomycin or streptomycin or dihydrostreptomycin, including their respective salts or esters. Liquid oral antidiarrhoeals or any other dosage form for paediatric use containing diphenoxylate or loperamide or atropine or belladonna, including their salts or esters or metabolites, hyoscyamine or their extracts or their alkaloids. Liquid oral antidiarrhoeals or any other dosage form for paediatric use containing halogenated hydroxyquinolines. Patent and proprietary oral rehydration salts other than those conforming to specified guidelines. Mepacrine hydrochloride (quinacrine and its salts) in any dosage form for use for female sterilization or contraception. Parenteral preparations fixed dose combination of streptomycin with Jan 1,1998 penicillin 3. Fixed dose combination of vitamin B1, vitamin B6 and vitamin B12 for Jan 1,2001 human use 4. Fixed dose combination of haemoglobin in any form (natural or Sep 1,2000 synthetic) 5. Fixed dose combination of pancreatin or pancrelipase containing Sep 1,2000 amylase, protease and lipase with any other enzyme 6. Fixed dose combination of haloperidol with any anticholinergic agent including propantheline bromide Jan 1,2002 Jan 1,2002 Jan 1,2002 Jan 1,2002 Contd. Fixed dose combination of nalidixic acid with any anti-amoebic Jan 1,2002 including metronidazole 12. Fixed dose combination of loperamide hydrochloride with furazolidone Jan 1,2002 13. The main objective is to prevent adverse health effects in workers arising from their work environment. Occupational toxicology is a discipline that draws on occupational hygiene, epidemiology, occupational medicine and regulatory toxicology. Diseases and illnesses related to specific occupations are commonly encountered in general medical practice, though many of them may be misdiagnosed as to the cause. In fact, it is estimated that the proportion of occupation-related medical ailments in primary care may be 15­20% of outpatient cases, although this includes patients with complaints such as body aches (musculo-skeletal pain). However, approximately 5­10% of all symptomatic Poison Control Centre consultations are occupational in nature, suggesting a large number of chemical exposures. To make matters more difficult, there could be long latency, extending to years, between exposure and disease, making the establishment of cause and effect even more of a conundrum. For chemical and biological agents, exposure limits are expressed as acceptable ambient concentration levels (occupational exposure limits) or as concentrations of a toxicant, its metabolites, or a specific marker of its effects (biological exposure indices). These are generally applicable worldwide, including India, and are designed to apply the best scientific evidence to ensure that no employee will suffer material impairment of health or General Considerations the problem with occupational illness is that it is rarely pathognomonic. Often, the link between an ailment and the workplace is obscure, and a special effort is required to connect the exposure to the disease. A few cases may involve massive exposure leading to acute onset of symptoms, such as an irritant gas release. In most cases, functional capacity with regular exposure, for the period of his working life. Threshold limit Values (TlVs) And Biological exposure indices (Beis): these have been developed as guidelines which have been adopted by many industries as internal occupational exposure limits. These are generally applied to toxicants that exert their effect over long periods.

When mice were given lethal doses of lyophilised Amanita phalloides symptoms pink eye albenza 400 mg purchase mastercard, the protective effect of kutkin was comparable to that seen with silibinin. It has been shown to be protective against Amanita intoxication when tested in dogs. Treatment of infection-Some investigators are of the opinion that prophylactic antibiotic therapy is vital to the treatment of acute liver failure. Treatment of coagulopathy-Fresh frozen plasma is necessary if there is evidence of serious or persistent bleeding. It employs an albumin-impregnated highly permeable dialyser with albumin-containing dialysate recycled in a closed loop with a charcoal cartridge, an anion exchange resin absorber, and a conventional haemodialysis membrane. It has been used in a small number of patients with fulminant hepatic failure secondary to cyclopeptide mushroom ingestion. In the West, hallucinogenic mushrooms ("magic mushrooms") such as those of Psilocybe genus have become part of the drug culture. There are even mail-order kits of the spores of such mushrooms that can be employed to cultivate "magic mushrooms" at home. In conclusion, it must be emphasised that incidents of mushroom poisoning do not constitute a recent phenomenon, but have existed since ancient times. The most important of these mycotoxins include aflatoxins, ergot alkaloids, * and trichothecenes. Never eat wild mushrooms obtained by foraging in the countryside unless the identity can be confirmed by an experienced mycologist. Distinguishing edible from toxic mushrooms is extremely difficult, regardless of what some foragers may claim. Even careful examination may not help in conclusively identifying a mushroom as non-toxic. Susceptibility to the toxicity of a poisonous mushroom varies from individual to individual, some demonstrating evidence of severe poisoning, while others do not. There are a number of myths associated with mushrooms bandied about as facts by self-professed "experts", which must be disregarded. Some species of mushroom may be edible in a particular geographical area, while in another location they may be toxic ("Jekyll & Hyde mushrooms"). As a general rule, it must be remembered that the following kinds of mushrooms are potentially toxic: pure white mushrooms, little brown mushrooms, large brown mushrooms, and red or pink-pored boletes. Most cases result from consuming wild mushrooms obtained by rural folk and nomads foraging in woods and the countryside. They are composed of highly substituted coumarin compounds that contain a fused dihydrofurofuran configuration. A dozen or more of these compounds have been identified: Aflatoxin, Aflatoxin B1, Aflatoxin B2, Aflatoxin B2a, Aflatoxin B3, Aflatoxin G1, Aflatoxin G2, Aflatoxin G2a, Aflatoxin M1, Aflatoxin M2, Aflatoxin P, and Aflatoxin T2. The "B" refers to blue, the "G" signifies green fluorescence, while "M" aflatoxins are fungal metabolites present in milk, and "T" compounds are found in tobacco. Consumption of dietary aflatoxins varies from 10 to 200 ng/kg/day, though the recommended maximum daily intake should be less than 50 ng/kg/day. Aflatoxins are usually encountered in the context of chronic exposure, via food intake or secondary to the handling of foodstuffs. Aflatoxins accumulate in the presence of liver disease, and the association with hepatic cancer is confounded by the occurrence of hepatitis-B. Thus, it must be admitted that in these conditions it is not clear whether aflatoxin is a primary cause of the disease, is an incidental product which accumulates secondary to the disease process, or is a contributing cause in association with other factors. Elevation of serum alkaline phosphatase is a good indicator of aflatoxin toxicity. In one study, there was a significant correlation between urinary levels of aflatoxins and the presence of hepatitis B surface antigen in serum, with risk of an increased incidence of heptatocellular carcinoma. In one experimental study involving ducklings which were given 5 micrograms of aflatoxin and 50 mg of turmeric for 14 days, increased weight gain was seen compared to controls. Almost complete reversal of fatty changes, granular degeneration, and necrosis was observed. Other fungal genera that produce similar toxins include Myrothecium, Trichoderma, Cephalosporium, Verticimonosporium, and Stachybotrys. Contamination of corn, sorghum, barley, or wheat with these toxins, is not uncommon leading to outbreaks of poisoning characterised by abdominal pain, throat irritation, vomiting, diarrhoea, vertigo, and headache. Acute toxicity resembles the damage done by radiation, nitrogen mustard, or mitomycin C. But inhalation exposure to Stachybotrys chartarum and Aspergillus versicolor, in moisture affected office buildings, was associated with the development of cough, dyspnoea, wheezing, and chest tightness among employees. The mouldy vinyl wall covering was found to contain the trichothecene toxin, deoxynivalenol; however it is unclear if it really was the culprit. Similarly, exposure to Stachybotrys atra and a Trichoderma species, has been associated with the development of pulmonary haemorrhage and haemosiderosis in infants. Contributing risk factors included tobacco smoke, and living in water-damaged homes which may enhance fungal growth. Alimentary toxic aleukia, first identified in Siberia, has been associated, in humans, with the consumption of grain contaminated with T-2 toxin. In more severe cases, acute oesophagitis, gastritis, and gastroenteritis may occur. The second stage is characterised by the development of leukopenia, granulopenia, and progressive lymphocytosis.

The term was initially used to describe painless whitlows on the fingers but was subsequently applied to the progressive loss of pain sensation and its effects (such asulceration treatment using drugs albenza 400 mg purchase overnight delivery, resorption of the phalanges and loss of soft tissue) in both hands and feet (Gaaette Hebdomadaire Medicine et de Chirurgie 1883; 35: 580). Post-traumatic syringomyelia: surgery when the neurological deficit or pain is intolerable. Examination Absent ankle jerks (due to peripheral neuropathy and motor involvement). Proceed as follows: Examine the following: -Mucous membranes for anaemia (pernicious anaemia). There is degeneration of the axons in both the ascending tracts of the posterior columns and the descending pyramidal tracts (hence combined degeneration). I would avoid giving packed cells before replacing vitamin B12 as this may irreversibly exacerbate the neurological manifestations. Furthermore, blood trans-fusion is reported to precipitate incipient heart failure and death. Intrinsic factor antibodies are seen in about 50% of patients with pernicious anaemia. There are two types of antibody: Type 1 - the blocking antibody which prevents vitamin Bi2 from binding to intrinsic factor and occurs in 55% of patients. Type 2 - the binding or precipitating antibody, which reacts with intrinsic factor or with vitamin B12-intrinsic factor complex and is seen in 35% of patients. The incidence of gastric carcinoma in patients with pernicious anaemia is increased three-fold compared with that in the general population. What gastrointestinal investigations would you perform in an asymptomatic patient with pernicious anaemia In the absence of gastrointestinal symptoms, gastroscopy or barium meal is not indicated, although many physicians tend to perform one of these investigations. This refers to the combined demyelination of both pyramids (or lateral columns) and posterior columns of the spinal cord. What is the response of the neurological lesions to treatment with vitamin B127 the response to vitamin B12 therapy is variable: the lesions may improve, remain unchanged or even deteriorate. Sensory abnormalities improve more than motor abnormalities, and peripheral neuropathy responds better to treatment than myelopathy. Pernicious anaemia was usually fatal until 1926, when Whipple, Minot and Murphy described the beneficial effects of feeding liver. The 1934 Nobel Prize in Medicine was awarded jointly to George Whipple (1878-1976) of University of Rochester, New York, and to George Minot (1885-1950) and William I~ Murphy (1892-1987) of Harvard Medical School and Peter Brent Brigham Hospital, Boston, for their discoveries concerning liver therapy in cases of anaemia. Castle first found that oral administration of gastric juice (intrinsic factor) or beef (extrinsic factor, i. Castle worked with Francis Peabody at the Harvard Medical School Unit at Boston City Hospital before he became Professor of Medicine at Harvard. High-stepping gait - patient may only hear his or her feet slapping the ground and feels as if walking on cotton-wool (due to loss of joint position sense). Squeeze calf muscles and the Achilles tendon (evokes no pain as deep sensation is lost). Note, Remember that, as a rule, the lower limbs are affected before the upper limbs. There are five clinical patterns of neurosyphilis: Meningovascular disease, which occurs 3-4 years after primary infection. Tertiary syphilis of the nervous system never develops in those who have received appropriate therapy in the early stages. Mention a few conditions in which the Wassermann reaction may be falsely positive. An acute hypersensitivity reaction seen when a patient with syphilis is treated with penicillin. Herxheimer (1861-1944), a Jewish German dermatologist who died in a concentration camp. In the first half of the 19th century, three European physicians - namely Mortiz Romberg, Marshal[Hall and Bernadus Brach described the loss of postural control in darkness of patients with severely impaired proprioceptive sensation (Neurology 2000; 55: 1201-6). Patient may be immobilized in the orthopaedic ward and use elbows to shuffle in bed. History of fracture of the upper arm in childhood (supracondylar fracture of humerus in childhood has an insidious course and can result in acute ulnar nerve palsy 20-30 years later - tardy ulnar palsy). The ulnar nerve is derived from the eighth cervical and first thoracic spinal nerves. It gives no branches above the elbow and supplies: In the forearm: Flexor carpi ulnaris. In the hand: Movers of the little finger - abductor digiti minimi, flexor digiti minimi and opponens digiti minimi. How would you differentiate between a lesion above the cubital fossa and a lesion at the wrist Ask the patient to grip a folded newspaper between the thumb and index finger of each hand so that the thumbs are uppermost this causes the adductor to contract. When the muscle is paralysed, the thumb is incapable of adequate adduction and becomes flexed at the interphalangeal joint due to contraction of the flexor pollicis longus (innervated by the median nerve). A lesion at or above the elbow causes paralysis of the ulnar half of the flexor digitorum profundus, interossei and lumbricals. Thus, the action of the paralysed profundus is not unopposed by the interossei and lumbricals; as a result the ring and little fingers are not flexed and hence there is no claw, whereas a lesion at the wrist causes an ulnar claw hand. The little and ring fingers are flexed at the interphalangeal joints and hyperextended at the metacarpophalangeal joints.