Anna-Lena Hellstr?m, MD

• Urotherapist and Professor,
• Queen Silvia Children? Hospital,
• G?teborg, Sweden

This is because it has been applied to several different clinical concepts over the last few decades diabetes blood sugar chart forxiga 5 mg generic, and associated with various mixtures of characteristics such as acute onset diabetes definition example generic forxiga 5mg with mastercard, comparatively brief duration diabetes diet and exercise buy forxiga 10mg otc, atypical symptoms or mixtures of symptoms blood sugar fasting purchase cheap forxiga online, and a comparatively good outcome diabetic diet and weight loss generic 5mg forxiga. There is no evidence to suggest a preferred choice for its usage diabetes early pregnancy signs generic 10mg forxiga free shipping, so the case for its inclusion as a diagnostic term was considered to be weak. Moreover, the need for an intermediate category of this type is obviated by the use of F23. As guidance for those who do use schizophreniform as a diagnostic term, it has been inserted in several places as an inclusion term relevant to those disorders that have the most overlap with the meanings it has acquired. The criteria proposed for its differentiation highlight the problems of defining the mutual boundaries of this whole group of disorders in practical terms. The final decision to place it in F20-F29 was influenced by feedback from the field trials of the 1987 draft, and by comments resulting from the worldwide circulation of the same draft to member societies of the World Psychiatric Association. It is clear that widespread and strong clinical traditions exist that favour its retention among schizophrenia and delusional disorders. It is relevant to this discussion that, given a set of affective symptoms, the addition of only mood-incongruent delusions is not sufficient to change the diagnosis to a schizoaffective category. At least one typically schizophrenic -16 symptom must be present with the affective symptoms during the same episode of the disorder. Mood [affective] disorders (F30-F39) It seems likely that psychiatrists will continue to disagree about the classification of disorders of mood until methods of dividing the clinical syndromes are developed that rely at least in part upon physiological or biochemical measurement, rather than being limited as at present to clinical descriptions of emotions and behaviour. As long as this limitation persists, one of the major choices lies between a comparatively simple classification with only a few degrees of severity, and one with greater details and more subdivisions. However, feedback from many of the clinicians involved in the field trials, and other comments received from a variety of sources, indicated a widespread demand for opportunities to specify several grades of depression and the other features noted above. In addition, it is clear from the preliminary analysis of field trial data that in many centres the category of "mild depressive episode" often had a comparatively low inter-rater reliability. It has also become evident that the views of clinicians on the required number of subdivisions of depression are strongly influenced by the types of patient they encounter most frequently. Those working in primary care, outpatient clinics and liaison settings need ways of describing patients with mild but clinically significant states of depression, whereas those whose work is mainly with inpatients frequently need to use the more extreme categories. Further consultations with experts on affective disorders resulted in the present versions. Options for specifying several aspects of affective disorders have been included, which, although still some way from being scientifically respectable, are regarded by psychiatrists in many parts of the world as clinically useful. It is hoped that their inclusion will stimulate further discussion and research into their true clinical value. Unsolved problems remain about how best to define and make diagnostic use of the incongruence of delusions with mood. There would seem to be both enough evidence and sufficient clinical demand for the inclusion of provisions for mood-congruent or mood-incongruent delusions to be included, at least as an "optional extra". These recurrent states are of unclear nosological significance and the provision of a category for their recording -17 should encourage the collection of information that will lead to a better understanding of their frequency and long-term course. Agoraphobia and panic disorder There has been considerable debate recently as to which of agoraphobia and panic disorder should be regarded as primary. From an international and cross-cultural perspective, the amount and type of evidence available does not appear to justify rejection of the still widely accepted notion that the phobic disorder is best regarded as the prime disorder, with attacks of panic usually indicating its severity. Mixed categories of anxiety and depression Psychiatrists and others, especially in developing countries, who see patients in primary health care services should find particular use for F41. The purpose of these categories is to facilitate the description of disorders manifest by a mixture of symptoms for which a simpler and more traditional psychiatric label is not appropriate but which nevertheless represent significantly common, severe states of distress and interference with functioning. They also result in frequent referral to primary care, medical and psychiatric services. Difficulties in using these categories reliably may be encountered, but it is important to test them and if necessary improve their definition. Instead, "dissociative" has been preferred, to bring together disorders previously termed hysteria, of both dissociative and conversion types. This is largely because patients with the dissociative and conversion varieties often share a number of other characteristics, and in addition they frequently exhibit both varieties at the same or different times. It also seems reasonable to presume that the same (or very similar) psychological mechanisms are common to both types of symptoms. There appears to be widespread international acceptance of the usefulness of grouping together several disorders with a predominantly physical or somatic mode of presentation under the term "somatoform". For the reasons already given, however, this new concept was not considered to be an adequate reason for separating amnesias and fugues from dissociative sensory and motor loss. Research carried out in various settings has demonstrated that a significant proportion of cases diagnosed as neurasthenia can also be classified under depression or anxiety: there are, however, cases in which the clinical syndrome does not match the description of any other category but does meet all the criteria specified for a syndrome of neurasthenia. It is hoped that further research on neurasthenia will be stimulated by its inclusion as a separate category. Culture-specific disorders the need for a separate category for disorders such as latah, amok, koro, and a variety of other possibly culture-specific disorders has been expressed less often in recent years. Attempts to identify sound descriptive studies, preferably with an epidemiological basis, that would strengthen the case for these inclusions as disorders clinically distinguishable from others already in the classification have failed, so they have not been separately classified. Descriptions of these disorders currently available in the literature suggest that they may be regarded as local variants of anxiety, depression, somatoform disorder, or adjustment disorder; the nearest equivalent code should therefore be used if required, together with an additional note of which culture-specific disorder is involved. There may also be prominent elements of attention-seeking behaviour or adoption of the sick role akin to that described in F68. Its inclusion is a recognition of the very real practical problems in many developing countries that make the gathering of details about many cases of puerperal illness virtually impossible. However, even in the absence of sufficient information to allow a diagnosis of some variety of affective disorder (or, more rarely, schizophrenia), there will usually be enough known to allow diagnosis of a mild (F53. The inclusion of this category should not be taken to imply that, given adequate information, a significant proportion of cases of postpartum mental illness cannot be classified in other categories. Most experts in this field are of the opinion that a clinical picture of puerperal psychosis is so rarely (if ever) reliably distinguishable from affective disorder or schizophrenia that a special category is not justified. Any psychiatrist who is of the minority opinion that special postpartum psychoses do indeed exist may use this category, but should be aware of its real purpose. The difference between observations and interpretation becomes particularly troublesome when attempts are made to write detailed guidelines or diagnostic criteria for these disorders; and the number of criteria that must be fulfilled before a diagnosis is regarded as confirmed remains an unsolved problem in the light of present knowledge. Nevertheless, the attempts that have been made to specify guidelines and criteria for this category may help to demonstrate that a new approach to the description of personality disorders is required. After initial hesitation, a brief description of borderline personality disorder (F60. Since these are, strictly speaking, disorders of role or illness behaviour, it should be convenient for psychiatrists to have them grouped with other disorders of adult behaviour. The crucial difference between the first two and malingering is that the motivation for malingering is obvious and usually confined to situations where personal danger, criminal sentencing, or large sums of money are involved. Such a system needs to be developed separately, and work to produce appropriate proposals for international use is now in progress. While some uncertainty remains about their nosological status, it has been considered that sufficient information is now available to justify the inclusion of the syndromes of Rett and Asperger in this group as specified disorders. Overactive disorder associated with mental retardation and stereotyped movements (F84. The use of this diagnosis indicates that the criteria for both hyperkinetic disorder (F90. These few exceptions to the general rule were considered justified on the grounds of clinical convenience in view of the frequent coexistence of those disorders and the demonstrated later importance of the mixed syndrome. There is, however, a cautionary note recommending its use mainly for younger children. This is because of the continuing need for a differentiation between children and adults with respect to various forms of morbid anxiety and related emotions. The frequency with which emotional disorders in childhood are followed by no significant similar disorder in adult life, and the frequent onset of neurotic disorders in adults are clear indicators of this -21 need. In other words, these childhood disorders are significant exaggerations of emotional states and reactions that are regarded as normal for the age in question when occurring in only a mild form. If the content of the emotional state is unusual, or if it occurs at an unusual age, the general categories elsewhere in the classification should be used. A number of categories that will be used frequently by child psychiatrists, such as eating disorders (F50. Nevertheless, clinical features specific to childhood were thought to justify the additional categories of feeding disorder of infancy (F98. This contains syndromes with predominantly physical manifestations and clear "organic" etiology, of which the Kleine-Levin syndrome (G47. It was decided that the least unsatisfactory solution was to use the last category in the numerical order of the classification, i. Decisions on whether to accept or reject proposals were influenced by a number of factors. Some proposals, although reasonable when considered in isolation, could not be accepted because of the implications that even minor changes to one part of the classification would have for other parts. Some other proposals had clear merit, but more research would be necessary before they could be considered for international use. A number of these proposals included in early versions of the general classification were omitted from the final version, including "accentuation of personality traits" and "hazardous use of psychoactive substances". It is hoped that research into the status and usefulness of these and other innovative categories will continue. The dysfunction may be primary, as in diseases, injuries, and insults that affect the brain directly or with predilection; or secondary, as in systemic diseases and disorders that attack the brain only as one of the multiple organs or systems of the body involved. Alcohol and drug-caused brain disorders, though logically belonging to this group, are classified under F10-F19 because of practical advantages in keeping all disorders due to psychoactive substance use in a single block. Although the spectrum of psychopathological manifestations of the conditions included here is broad, the essential features of the disorders form two main clusters. On the one hand, there are syndromes in which the invariable and most prominent features are either disturbances of cognitive functions, such as memory, intellect, and learning, or disturbances of the sensorium, such as disorders of consciousness and attention. On the other hand, there are syndromes of which the most conspicuous manifestations are in the areas of perception (hallucinations), thought contents (delusions), or mood and emotion (depression, elation, anxiety), or in the overall pattern of personality and behaviour, while cognitive or sensory dysfunction is minimal or difficult to ascertain. The latter group of disorders has less secure footing in this block than the former because it contains many disorders that are symptomatically similar to conditions classified in other blocks (F20-F29, F30-F39, F40-F49, F60-F69) and are known to occur without gross cerebral pathological change or dysfunction. However, the growing evidence that a variety of cerebral and systemic diseases are causally related to the occurrence of such syndromes provides sufficient justification for their inclusion here in a clinically oriented classification. The majority of the disorders in this block can, at least theoretically, have their onset at any age, except perhaps early childhood. While some of these disorders are seemingly irreversible and progressive, others are transient or respond to currently available treatments. Use of the term "organic" does not imply that conditions elsewhere in this classification are "nonorganic" in the sense of having no cerebral substrate. In the present context, the term "organic" means simply that the syndrome so classified can be attributed to an independently diagnosable cerebral or systemic disease or disorder. The term "symptomatic" is used for those organic mental disorders in which cerebral involvement is secondary to a systemic extracerebral disease or disorder. It follows from the foregoing that, in the majority of cases, the recording of a diagnosis of any one of the disorders in this block will require the use of two codes: one for the psychopathological syndrome and another for the underlying disorder. Dementia -45 A general description of dementia is given here, to indicate the minimum requirement for the diagnosis of dementia of any type, and is followed by the criteria that govern the diagnosis of more specific types. Dementia is a syndrome due to disease of the brain, usually of a chronic or progressive nature, in which there is disturbance of multiple higher cortical functions, including memory, thinking, orientation, comprehension, calculation, learning capacity, language, and judgement. Impairments of cognitive function are commonly accompanied, and occasionally preceded, by deterioration in emotional control, social behaviour, or motivation. In assessing the presence or absence of a dementia, special care should be taken to avoid false-positive identification: motivational or emotional factors, particularly depression, in addition to motor slowness and general physical frailty, rather than loss of intellectual capacity, may account for failure to perform. Dementia produces an appreciable decline in intellectual functioning, and usually some interference with personal activities of daily living, such as washing, dressing, eating, personal hygiene, excretory and toilet activities. How such a decline manifests itself will depend largely on the social and cultural setting in which the patient lives. Changes in role performance, such as lowered ability to keep or find a job, should not be used as criteria of dementia because of the large cross-cultural differences that exist in what is appropriate, and because there may be frequent, externally imposed changes in the availability of work within a particular culture. The impairment of memory typically affects the registration, storage, and retrieval of new information, but previously learned and familiar material may also be lost, particularly in the later stages. Dementia is more than dysmnesia: there is also impairment of thinking and of reasoning capacity, and a reduction in the flow of ideas. The processing of incoming information is impaired, in that the individual finds it increasingly difficult to attend to more than one stimulus at a time, such as taking part in a conversation with several persons, and to shift the focus of attention from one topic to another. If dementia is the sole diagnosis, evidence of clear consciousness is -46 required. However, a double diagnosis of delirium superimposed upon dementia is common (F05. The above symptoms and impairments should have been evident for at least 6 months for a confident clinical diagnosis of dementia to be made. Consider: a depressive disorder (F30-F39), which may exhibit many of the features of an early dementia, especially memory impairment, slowed thinking, and lack of spontaneity; delirium (F05); mild or moderate mental retardation (F70-F71); states of subnormal cognitive functioning attributable to a severely impoverished social environment and limited education; iatrogenic mental disorders due to medication (F06. Dementia may follow any other organic mental disorder classified in this block, or coexist with some of them, notably delirium (see F05. It is usually insidious in onset and develops slowly but steadily over a period of years. This period can be as short as 2 or 3 years, but can occasionally be considerably longer. In cases with onset before the age of 65-70, there is the likelihood of a family history of a similar dementia, a more rapid course, and prominence of features of temporal and parietal lobe damage, including dysphasia or dyspraxia. In cases with a later onset, the course tends to be slower and to be characterized by more general impairment of higher cortical functions.

Efficacy of postexposure treatment of yellow fever with ribavirin in a hamster model of the disease metabolic disease quotes generic forxiga 10mg with amex. Experimental study of possible treat ment of Marburg hemorrhagic fever with desferal diabetes type 1 treatment guidelines order forxiga cheap online, ribavirin diabetes type 2 shopping list discount 10mg forxiga overnight delivery, and homologous interferon [in Russian] type 2 diabetes easy definition order 10mg forxiga free shipping. Evaluation of immune globulin and recombinant interferon-alpha2b for treatment of experimental Ebola virus infections diabetes test over the counter cheap forxiga master card. The use of interferon for emergency prophylaxis of Marburg hemorrhagic fever in monkeys diabetes prevention of complications generic forxiga 10 mg. Recombinant human interferon-gamma modulates Rift Valley fever virus infec tion in the rhesus monkey. Gene-specific countermeasures against Ebola virus based on antisense phosphorodiamidate morpholino oligomers. Importance of dose of neutralizing antibodies in treat ment of Argentine hemorrhagic fever with immune plasma. Treatment of Ebola hemorrhagic fever with blood transfusions from conva lescent patients. On an infectious disease transmitted by Cercopithecus aethiops (Green monkey disease) [in German]. Report of a labora tory-acquired infection treated with plasma from a person recently recovered from the disease. Efficacy of immune plasma in treatment of Argentine hemorrhagic fever and association between treatment and a late neurological syndrome. In vivo enhancement of dengue virus infection in rhesus monkeys by passively transferred antibody. Passive antibody therapy of Lassa fever in cynomolgus monkeys: importance of neutralizing antibody and Lassa virus strain. From a practical standpoint, this observa many similarities among severe diseases caused by tion indicates that a large panel of antibody probes will 4 S aureus and S pyogenes superantigens imply a com be required for proper identification of samples. Furthermore, cross-link t-cell antigen receptors and class ii mhc the cD44 molecule reportedly provides protection 10 molecules, mimicking the cD4 molecule, and hence from liver damage in mice caused by seb exposure stimulate large numbers of t cells. Vaccines of seb and sea with altered critical residues Given the complex pathophysiology of toxic shock, involved in binding class ii mhc molecules were also the understanding of the cellular receptors and signal used successfully to vaccinate mice and monkeys ing pathways used by staphylococcal superantigens, against seb-induced disease. Rabbits, endotoxin-primed mice, and ad 10 minutes in a modified henderson head-only aerosol 40 ditional animal models have been developed. Young and mature adult male and female rhesus consistent with the potent stimulatory effect of seb 314 Staphylococcal Enterotoxin B and Related Toxins on the rhesus monkey immune system, was appar eosinophilic beaded fibrillar strands (fibrin), or with ent. Replicate gastrointestinal signs, the monkeys had a variable microsections stained with Giemsa revealed scarce period of up to 40 hours of clinical improvement. Peribronchovas cular connective tissue spaces were distended by pale, homogeneous, eosinophilic, proteinaceous material (edema), variably accompanied by entrapped, beaded fibrillar strands (fibrin), extravasated erythrocytes, neutrophils, macrophages, and small and large lym phocytes. Perivascular lymphatics were generally b distended by similar eosinophilic material and inflam matory cells. Documentation of an accidental laboratory inhala the headaches ranged from severe to mild, but were tion exposure of nine laboratory workers to seb best usually mild by the second day of hospitalization. Gastrointestinal symptoms occurred in more than eight of the individuals experienced at least one half of the individuals, nausea and anorexia in six, shaking chill that heralded the onset of illness. Five had vidual demonstrated hepatomegaly and bile in the inspiratory rales with dyspnea. During recovery, discoid atelectasis all patients who experienced chest pain had nor was noted. Plasma strains is possible by using polymerase chain reaction concentrations of superantigens were measured in amplification and toxin gene-specific oligonucleotide septic patients of an intensive care unit using an en primers. Diarrhea was not observed sure cases described above seemed to provide adequate in human accidental exposure cases, but deposition care. For nausea, initial symptomatic therapy with cough sup vomiting, and anorexia, symptomatic therapy should pressants containing dextromethorphan or codeine be considered. Prolonged coughing and phenothiazine derivatives (eg, prochlorperazine) unrelieved by codeine might benefit from a semisyn have been used parenterally or as suppositories. Prior exposure to seb by inhala case of tss with elevated tsst-1 and sea levels, tion does not appear to protect against a subsequent complicated by life-threatening multiorgan dysfunc episode. Vaccines produced by site-specific mu consequential t-cell activation,7,9,37,38 without altering tagenesis of the toxins, delivered by intramuscular or the three-dimensional structure of the antigen. Vaccines staphylococcal and streptococcal superantigen toxins, currently under development may afford protection to but the limit of field detection is unknown. Staphylococcal Enterotoxin B Battlefield Challenge Modeling with Medical and Non-Medical Countermeasures. Dissemination of the superantigen encoding genes seel, seem, szel and szem in Streptococcus equi subsp. Zinc binding and dimerization of Streptococcus pyogenes pyrogenic exotoxin c are not essential for t-cell stimulation. Role of cD44 and its v7 isoform in staphylococcal enterotoxin b-induced toxic shock: cD44 deficiency on hepatic mononuclear cells leads to reduced activation-induced apoptosis that results in increased liver damage. Divergence of human and nonhuman primate lymphocyte responses to bacterial su perantigens. Production of enterotoxins and toxic shock syndrome toxin by bovine mammary isolates of Staphylococcus aureus. Production of a toxic shock syndrome toxin variant by Staphylococcus aureus strains associated with sheep, goats, and cows. Role of protein tyrosine phosphorylation in monokine induction by the staphylococcal superantigen toxic shock syndrome toxin-1. Reductions in levels of bacterial superantigens/canna binoids by plasma exchange in a patient with severe toxic shock syndrome. Like abrin (from in the manufacture of lubricants, inks, varnishes, and the seeds of the rosary pea, Abrus precatorius), ricin is a dyes. After oil extraction, the remaining seed cake lectin and a member of a group of ribosome-inactivat may be detoxified by heat treatment and used as an ing proteins that block protein synthesis in eukaryotic animal feed supplement. The castor bean is native to Africa, but it has been the toxicity of castor beans has been known since introduced and cultivated throughout the tropical ancient times, and more than 750 cases of intoxication 2 and subtropical world. Although consid temperature range, it grows best in elevated year erably less potent than botulinum neurotoxins and round temperatures and rapidly succumbs to sub staphylococcal enterotoxins, ricin represents a signifi freezing temperatures. However, it is often grown as cant potential biological weapon because of its stability an ornamental annual in temperate zones. The seeds and worldwide availability as a by-product of castor are commercially cultivated in many regions of the oil production. In addition, it has been associated world, predominantly in Brazil, Ecuador, Ethiopia, with several terrorist actions and therefore may be a Haiti, India, and Thailand. In addition, both the oil and whole with serum proteins, and could be transferred to the seeds have been used in various parts of the world for offspring through milk. During World War I, the excellent est in bacterial toxins, interest in plant toxins waned. These subsidies persisted strated that protein synthesis was strongly inhibited until the 1960s, when synthetic oils replaced castor oil in a cell-free rabbit reticulocyte system, and suggested in the aircraft industry. There is no commercial produc that the effects resulted from inhibited elongation of tion of castor oil in the United States today. They also determined the first toxinology work on ricin was performed by that ricin consisted of two dissimilar polypeptide Hermann Stillmark at the Dorpat University in Estonia subunits and that the A chain was responsible for the for his 1888 thesis. He purified ricin to few years revealed the 60S ribosomal subunit as the a very high degree (although not completely to homo enzymatic target and led to further characterization of 7 geneity) and found that it agglutinated erythrocytes the enzymatic action. The active subunit of ricin is specifically In 1891 Paul Ehrlich studied ricin and abrin in targeted to tumor cells by conjugation to tumor-spe pioneering research that is now recognized as the cific antibodies. Experiments is mediated by a discrete sequence moiety separate 324 Ricin from the region related to protein synthesis inhibi United States, ricin and abrin are both included in the tion. Testing in a mouse model demon that ricin was included in the biological warfare pro strated improved effectiveness, suggesting that ricin grams of the Soviet Union, Iraq, and possibly other immunotoxins may yet have a place in the anticancer nations as well. In recent years, ricin has drawn the interest of ex Because of its potency, worldwide availability, and tremist groups. Several individuals have been arrested involved methods of adhering ricin to shrapnel and under the 1989 Biological Weapons Anti-Terrorism the production of effective aerosol clouds. In the past few years alone, the war ended before the evolution of weaponry based various major news organizations have reported the upon this research. While none of these events resulted in any known In addition to its coverage under the 1975 conven human intoxications, they clearly demonstrate that tion, ricin and one other toxin (saxitoxin) were also ricin is well known, available to and recognized by specifically included under the 1993 Chemical Weap extremist groups, and should be seriously considered ons Convention, ratified by Congress in 1997. The disul up 1% to 5% of the dry weight of the castor bean, fide bond links residue 259 of the A chain with residue although the yield can be highly variable. The crystal structure demonstrates a form is a heterodimer consisting of a 32-kd A chain con putative active cleft in the A chain, which is believed nected to the 32-kd B chain through a single disulfide to be the site of enzymatic action. Recombinant A the B chain, and cellular toxicity is much less; uptake and B chains, as well as specific mutants, have been depends on endocytosis. Both chains are glycoproteins expressed and characterized in several expression containing multiple mannose residues on their surfaces; systems including Escherichia coli. Purification and characterization is not difficult, Toxicity and the crystal structure has been determined to . A lactose disaccharide moiety is considerable variation in potency exists among species. Low potency by the oral route likely reflects poor absorption and possibly partial degradation in Endoplasmic Reticulum the gut. The two-chain structure is key to failure of C G A 4324 cellular internalization and subsequent toxicity. Binding, internalization, and intracellular track to glycoside residues on glycoproteins and glycolip ing of ricin leading to enzymatic action at the 60S ribosome. Trafficking protein disulfide isomerase can subsequent ribosomal of the toxin within the cell from the initial binding inactivation take place in the cytosol. As with related site to the Golgi apparatus occurs via endosomal toxins, transport to the cytosol is the rate-limiting step 29 transport and is seemingly regulated by intracellu during the decline in protein synthesis. Ingestion causes gastrointestinal symptoms Exposure Surveillance System from 1983 to 2002 notes including hemorrhage and necrosis of liver, spleen, no reported fatalities from ricin poisoning. The authors note crosis, and moderate systemic symptoms; inhalation oropharyngeal irritation, vomiting, abdominal pain, results in respiratory distress with airway and pul and diarrhea beginning within a few hours of inges monary lesions. Local necrosis in the gastrointestinal tract may a constant feature in humans, whether intoxication is lead to hematemesis, hematochezia, and/or melena. Leukocyte counts 2 to the resultant loss of fluid and electrolytes may lead to 5-fold above normal are characteristic findings among hypotension, tachycardia, dehydration, and cyanosis. A portion of the toxin is absorbed Markov during his agonizing death after a successful through the gastrointestinal tract leading to systemic assassination attempt. In oral (and parenteral) intoxication, cells in the reticuloendothelial system, such as Kupffer cells Oral Intoxication and macrophages, are particularly susceptible, due to the mannose receptor present in macrophages. In animal models, a significant amount of In 1985 Rauber and Heard summarized the findings orally administered ricin is found in the large intestine from their study of 751 cases of castor bean ingestion. Twelve of the 14 cases resulting in death oc with the degree of mastication of the beans. The reported number 327 Medical Aspects of Biological Warfare of beans ingested by patients who died varied greatly. Early on the third day, he became anuric and began Of the two lethal cases involving oral intoxication vomiting blood. An electrocardiogram demonstrated documented since 1930, one involved a 24-year-old complete atrioventricular conduction block. Markov man who ate 15 to 20 beans, and the other involved a died shortly thereafter. A mild pulmonary ported serious, or fatal, cases of castor bean ingestion edema was thought to have been secondary to cardiac have the same general clinical history: rapid (less than failure. Death Although data on aerosol exposure to ricin in hu occurred on the 3rd day or later. The most common mans are not available, lesions induced by oral and autopsy findings in oral intoxication were multifocal parenteral exposure are consistent with those from ulcerations and hemorrhages of gastric and small-in animal studies, suggesting that the same would hold testinal mucosa. In humans, an allergic syn lymph nodes, gut-associated lymphoid tissue, and drome has been reported in workers exposed to castor spleen were also present, as were Kupffer cell and liver bean dust in or around castor oil-processing plants. The clinical picture is characterized by the sudden onset of congestion of the nose and throat, itchiness of Injection the eyes, urticaria, and tightness of the chest. In more severe cases, wheezing can last for several hours, and Intramuscular or subcutaneous injection of high may lead to bronchial asthma. Affected individuals doses of ricin in humans results in severe local lym respond to symptomatic therapy and removal from phoid necrosis, gastrointestinal hemorrhage, liver ne the exposure source. Injection castor bean-positive skin prick tests, possess specific of ricin leads to necrosis at the injection site, which may IgE against castor beans by the radioallergosorbent 36 predispose one to secondary infection. A case report test technique, and may also have responded to a na of a 20-year-old male who injected castor bean extract sal challenge test with castor bean pollen. This is followed revealed hypotension, anuria, metabolic acidosis, and by a decrease in detectable ricin in the lung and an in hematochezia.

The Archer Precision Mini-Hook Test Lead Set has a banana plug for the probe on one end and a mini hook on the other end for easy attachment to the circuit blood glucose positive or negative feedback proven forxiga 5 mg. Connect the Probe to middle post of the primary side of the transformer (it also connects to the negative battery post) metabolic disease 2013 purchase cheapest forxiga. Clip the Handhold to one end of an alligator clip test jumper yahoo diabetic diet soda cheap forxiga 10mg with mastercard, and clip the other end to the base (B) of the transistor used in the circuit diabetes mellitus quizlet order forxiga with paypal. Attach an alligator clip to the post of the transformer that connects to the two capacitors diabetes type 2 quotes buy 5mg forxiga. Turn the control knob on and keep turning the potentiometer to nearly the maximum diabetes mellitus nursing diagnosis forxiga 10mg with mastercard. If it does not, check that your alligator clips are not bending the spring terminals so much that other wires attached there are loose. The wiring in it is arranged so that you can test for a toxin in a product, as well as search in yourself. This means you can search for Salmonella in the milk or cheese you just ate, not just for Salmonella in your stomach. Only if the resonant frequency of an item on one plate is equal to the resonant frequency of an item on the other plate will the entire circuit oscillate or resonate! By putting a known pure sample on one plate you can reliably conclude the other sample contains it if the circuit resonates. You may build a test plate box into a cardboard box (such as a facial tissue box) or a plastic box. A plastic project box, about 7 x 4 x 1, makes a more durable product, but requires a drill, and you should discard any metal lid it comes with. Test Plates Assembly Cut two 3-1/2 inch squares out of stiff paper such as a milk carton. Cover them with 4inch squares of aluminum foil, smoothed evenly and tucked snugly under the edges. Turn the box upside down and draw squares where you will mount them at the ends of the box. The third bolt is used as a terminal where the current from the oscillator circuit will arrive. Make a hole on the side of the box, near the left hand plate and mount the bolt so it sticks half way inside and halfway outside the box. Pierce first with a pin; follow with a pencil until a round hole is made at the center. The left side connection (terminal) gets attached to the left plate (bolt) with an alligator clip. All these connections should be checked carefully to make sure they are not touching others accidentally. They are simply capacitors, letting current in and out momen tarily and at a rate that is set by the frequency of the oscillator circuit, about 1,000 hertz. This frequency goes up as the resis tance (of the circuit or your body) goes down. You will be comparing the sound of a standard control current with a test current. Cut paper strips about 1 inch wide from a piece of white, unfragranced, paper towel. Dampen a paper strip on the towel and wind it around the copper pipe handhold to completely cover it. The wetness improves conductivity and the paper towel keeps the metal off your skin. Dampen your other hand by making a fist and dunking your knuckles into the wet paper towel in the saucer. You will be using the area on top of the first knuckle of the middle finger or forefinger to learn the technique. Immediately after dunking your knuckles dry them on a paper towel folded in quarters and placed beside the saucer. The de gree of dampness of your skin affects the resistance in the circuit and is a very important variable that you must learn to keep constant. Make your probe as soon as your knuckles have been dried (within two seconds) since they begin to air dry further immediately. With the handhold and probe both in one hand press the probe against the knuckle of the other hand, keeping the knuckles bent. Repeat a half second later, with the second half of the probe at the same location. It takes most people at least twelve hours of practice in order to be so consistent with their probes that they can hear the slight difference when the circuit is resonant. The starting sound when you touch down on the skin should be F, an octave and a half above middle C. The sound rises to a C as you press to the knuckle bone, then slips back to B, then back up to C-sharp as you complete the second half of your first probe. If you have a multitester you can connect it in series with the handhold or probe: the current should rise to about 50 microamps. The more it is used, the redder it gets and the higher the sound goes when you probe. Move to a nearby location, such as the edge of the patch, when the sound is too high to begin with, rather than adjusting the potentiometer. If you are getting strangely higher sounds for identical probes, stop and only probe every five minutes until you think the sound has gone down to stan dard. You may also find times when it is impossible to reach the necessary sound without pressing so hard it causes pain. It is tempting to hold the probe to your skin and just listen to the sound go up and down, but if you prolong the test you must let your body rest ten minutes, each time, before resuming probe practice! Resonance the information you are seeking is whether or not there is resonance, or feedback oscillation, in the circuit. You can never hear resonance on the first probe, for reasons that are technical and beyond the scope of this book. During resonance a higher pitch is reached faster; it seems to want to go infinitely high. Remember that more electricity flows, and the pitch gets higher, as your skin reddens or your body changes cycle. Your body needs a short recovery time (10 to 20 seconds) after every resonant probe. The longer the resonant probe, the longer the recovery time to reach the standard level again. In between the first and second probe a test substance will be switched in as described in lessons below. To avoid confusion it is important to practice making probes of the same pressure. Purchase a filter pitcher made of hard, opaque plastic, not the clear or flexible variety (see Sources). Fill the pitcher with cold tap water, only, not reverse osmosis, distilled, or any other water, since solvents do not filter out as easily as heavy metals. If your water has lead, copper or cadmium from corroded plumbing, the filter will clog in five days of normal use. So use this pitcher sparingly, just for making test substances and for operating the Syncrometer. Prepare these as follows: find three medium-sized vitamin bottles, glass or plastic, with non-metal lids. Next, pour about the same amount of filtered water into the second and third bottles. If the second probe sounds even a little higher you are not at the standard level. While you are learning, let your piano also help you to learn the standard level (starts exactly at F). If you do not rest and you resonate the circuit before returning to the standard level, the results will become aberrant and useless. The briefer you keep the resonant probe, the faster you return to the standard level. In later lessons we assume you checked for your standard level or are quite sure of it. White Blood Cells Checking for resonance between your white blood cells and a toxin is the single most important test you can make. In addition to making antibodies, interferon, inter leukins, and other attack chemicals, they also eat foreign sub stances in your body and eliminate them. Because no matter where the foreign substance is, chances are some white blood cells are working to remove it. They can be en cysted in a particular tissue which will test positive, while the white blood cells continue to test negative. Also, when bacteria and viruses are in their latent form, they do not show up in the white blood cells. Freon is an example of a toxin that is seldom found in the white blood cells; but typically, the white blood cells are excellent indicators of toxins. Making a White Blood Cell Specimen Obtain an empty vitamin bottle with a flat plastic lid and a roll of clear tape. The white blood cells are not going into the bottle, they are going on the bottle. Squeeze an oil gland on your face or body to obtain a ribbon of whitish matter (not mixed with blood). Spread it in a single, small streak across the lid of the bottle or the center of the glass slide. Stick a strip of clear tape over the streak on the bottle cap so that the ends hang over the edge and you can easily see where the specimen was put (see photo). The bottle type of white blood cell specimen is used by standing it on its lid (upside down) so that the specimen is next to the plate. If the circuit is now resonating, the junk food is already in your white blood cells. Take vitamin C and a B-50 complex to clear it rapidly; it may have had propyl alcohol or ben zene in it. Place your white blood cell specimen on one plate and the water sample on the other. If it appears in your white blood cells at any time you can conclude the water is not pure. Trouble shooting: a) If you repeat this experiment and you keep getting the same bottles wrong, start over. You may have accidentally contaminated or mislabeled the outside of the bottle, or switched bottle caps. However, I prefer to place a small amount (the size of a pea) of the substance into a ounce bottle of filtered water. There will be many chemical reactions between the substance and the water to produce a number of test substances all contained in one bottle. Within the body, where salt and water are abundant, similar reactions may occur between elements and water. Since the electronic properties of elemental copper are not the same as for copper compounds, we would miss many test results if we used only dry elemental copper as a test substance. For instance, a tire balancer made of lead can be easily obtained at an auto service station. The biggest repository of all toxic substances is the grocery store and your own home. You can make test substances out of your hand soap, water softener salt, and laundry detergent by putting a small amount (1/16 tsp. Here are some suggestions for finding sources of toxic products to make your own toxic element test. If the product is a solid, place a small amount in a plastic bag and add a tablespoon of filtered water to get a temporary test product. If the product is a liquid, pour a few drops into a glass bottle and add about 2 tsp. Small amber glass dropper bottles can be purchased by the dozen at drug stores (also see Sources). Copper: ask your hardware clerk to cut a small fragment off a copper pipe of the purest variety or a inch of pure copper wire. Gold: ask a jeweler for a crumb of the purest gold available or use a wedding ring. Lead: wheel balancers from a gas station, weights used on fishing lines, lead solder from electronics shop. Mercury: a mercury thermometer (there is no need to break it), piece of amalgam tooth filling. Radon: leave a glass jar with an inch of filtered water in it standing open in a basement that tested positive to radon using a kit. Vanadium: hold a piece of dampened paper towel over a gas stove burner as it is turned on. Zearalenone: combine leftover crumbs of three kinds of corn chips and three kinds of popcorn. Since few of these specimens are pure, there is a degree of logic that you must apply in most cases.

Syndromes

• Fuse the joint together to make the toe straight and no longer able to bend. 
• Nausea
• Do not eat or drink anything after midnight the night before your surgery.
• Be reluctant to become involved with people
• Slowly decrease the drug dose (if possible) under medical supervision.
• Sudden death
• Butyl acetate
• Give acetaminophen every 4 - 6 hours.

Identifications by exclusion can only be made when all casualities have been accounted for managing diabetes in dogs naturally buy 5 mg forxiga amex. Preexisting Disease the search for preexisting disease conditions is a routine part of any autopsy examination diabetes type 2 pictures forxiga 5mg with mastercard. Here the objective is not just to describe the health condition of the deceased signs of diabetes in young dogs buy forxiga without a prescription, but to search for conditions which might have caus ed incapacitation in flight or which might have led to a reduction in sensory or motor capacities diabetes symptoms gastroparesis order forxiga 10mg otc. Only three systems can cause immediate incapacitation: the central nervous system diabetic diet 2000 calories discount forxiga 5mg, the respiratory system mody diabetes gene test cheap forxiga 10mg on-line, and the cardiovascular system. Biliary colic, renal lithiasis, diarrhea, and in fections are important contributory factors, their presence often requires diligent searching. In looking for preexisting diseases, one of the classic questions is What role did ischemic heart disease play in postulated pilot incapacity The objective is to specify the extent of coronary occlusion and its morphological consequences and to indicate the likelihood that this might have resulted in either transient or permanent pathophysiological states. It is not reliable or useful to define a coronary lesion independently of a comprehensive analysis of the operational circumstances. Such a clinical history frequently provides evidence that clearly precludes the etiological relationship of established lesions. For example, a scenario in which the pilot of a troubled aircraft describes by radio the detailed progression of mechanical difficulties which preclude both continued flight and safe egress, makes it untenable that the acci dent was caused by sudden incapacitation, even in the presence of the most impressive morbid anatomy. Furthermore, it is useful to remember that a flight might be completed and indeed many have been completed, without accident, even when the pilot was incapacitated. The dif ferential diagnosis of the aberrant behavior related to an accident logically includes psychological and physiological considerations as well as organic disease. These are easily overlooked or misinterpreted by pathologists who do not have experience in aviation. Often a psychological autopsy is necessary to characterize potential behavioral factors. Description of Injuries All injuries sustained during the accident should be described in detail. This is true whether or not a specific injury might have contributed to the death of the subject. Obviously, the first order 25-6 Aircraft Accident Autopsies of business is to describe those injuries which could have been fatal. It is most important to iden tify, with as much certainty as possible, the exact cause of death. However, it also is quite impor tant to note all other injuries so that realistic assessments can be made of the safety design of the aircraft and of the effectiveness of specific items of protective equipment. This is sufficiently vague to be essentially meaningless for later use by investigators. It is more helpful to describe and interpret the injury as a transverse fracture of the ulna at a specific location mediated through blunt forces applied to the anterior aspect of the forearm. This can then be correlated to specific cockpit structures adjacent to the arm of the pilot, as he was observed in the cockpit following the impact. In short, the description of injuries must be as detailed as can reasonably be done and should include any observations and interpretations concerning the likely pathogenesis of the injuries. Full body radiographs with special emphasis on the head, neck and extremities are extremely useful in the clarification of injury mechanisms, particularly when correlated with photographs and diagrams. There are also patterns of injuries which may serve to define events and injury mechanisms. Knowledge of these patterns can be useful to a flight surgeon as he interprets and assists in the autopsy examination. For example, bilateral subconjunctival hemorrhage in the absence of other ocular injuries characteristically suggests premortem negative acceleration in the z-axis (-Gz). These patterns are best recognized when there is adequate documentation and timely discussion between the board flight surgeon and pathologist. Distribution of Injuries Certain injuries tend to occur frequently in aircraft accidents, simply because of the nature of the force environment and mechanisms found in such events. A flight surgeon should understand this distribution, but he should also recognize that the characteristics of these injuries may change as aviation missions change and as one deals with different types of aircraft. Unusual injuries representing a deviation from the expected may signal a previously unrecognized pathogenic mechanism or a peculiar event important to an understanding of the accident sequence. To monitor such events, the Naval Safety Center analyzes all aviation accident injuries as functions of anatomic site involved and aircraft type. This provides a means of comparing injuries that oc cur in one aircraft type with injuries occurring in a different type. Significant dif ferences invite attention to systematic failures that predispose to the subject injury. In a similar manner, it is possible to tabulate the kinds of injury reported and to identify the proportions of the total injury experience contributed by each diagnostic category (Table 25-1). The data tend to reflect injuries that are of major significance and readily and conclusively iden tifiable, but they do not consistently relate to the cause and mechanism of death. Table 25-1 Distribution of Navy and Marine Corps Aviation Accident Injuries by Diagnostic Categories Diagnosis Percent of Total Injuries Reported Fracture/Dislocation 22. The head and neck area is especially susceptible to injury from the forces of an aircraft accident, and the nature of head injuries is such that acute incapaci ty and fatal consequences can be anticipated. Twenty-four percent of all injuries affect the head and neck, even though their surface area and mass represent a lesser proportion of the body. A 25-8 Aircraft Accident Autopsies truly random distribution of injuries is not likely in an aircraft accident. Cockpit and cabin struc tural configuration, methods of restraint, common patterns of accident acceleration, and the nature of protective devices influence this injury distribution. The design of such devices, in cluding protective helmets, can logically derive from detailed observations of pathogenetic mechanisms of head and neck injury. The aviation accident experience is the medium through which one may make unique and valuable assessments of such mechanisms. One needs more information about the sequence of accident events, a better definition of the applied forces, and some indication of the order of magnitude of accident impact forces. Frequently, radiographs of the helmet will disclose otherwise missed fractures in the fiberglass which when correlated with the autopsy results will define cranio cervical injury mechanisms. Severe injuries can be sustained by the head and the cervical region which are not easily noted on routine examination. For example, a preliminary examination might indicate the cause of death was an impact force applied to the lower thoracic region, resulting in broken ribs, severe visceral lacerations, and extensive hemorrhaging. In fact, however, such injuries might well be survivable, with the actual cause of death being an unnoticed transection or laceration of the spinal cord at the base of the brain. When a number of injuries are sustained at the same time, it is very important to identify those which explain the mechanism of death. A posterior layerwise dissection of the neck must always be done to exclude such cervical trauma. The correct identification of head and neck injuries provides invaluable data for designers of aviation protective clothing and equipment. At this time, Navy research and development effort is being directed toward the development a new helmet for aircrewmen. The helmet is to allow better head movement during air-to-air combat and to provide even more protection than afford ed by current helmets. One of the best ways to answer these questions is with information developed through meticulous autopsy examination in which head and neck injuries are described in detail and carefully related to the crash circumstances. There are four mechanisms for head and neck injury which predominate in aviation accidents. When the body is moving at a given velocity and is suddenly decelerated, whether by impact or by ejection and dynamic ram air pressure, there can be an inertia of the head, neck, helmet, mask complex which can cause a severe differential deceleration of this com plex with respect to the rest of the body. There may be a flexion so that the head is moved forward or backward suddenly with consequent hyperextension of the neck and either injuries to the bone and muscle around the neck or a pulling of the central nervous axis. In order to demonstrate at autopsy that this has occurred, it is necessary to make a dissection of the central nervous system so that the brain stem, the medulla oblongata, and the cervical spinal cord are not altered in the dissection. A posterior dissection into the spine and occipital skull is recommended to expose the relevant tissues and to determine whether there are lacerations, hemorrhage, or other physical evidence of mechanical trauma at the site. In the aft-hyperextension case, hemorrhage may be noted in the para-spinal muscle system. With forward hyperflexion or hyperextension, fractures may be noted in the anterior vertebral bodies and in other muscle groups. If the brain stem is maintained intact, gross lacerations of that part of the brain stem or the vessels covering the brain stem may be seen on section. Under circumstances where the impact delivers sufficient energy to separate the helmet and then to disrupt the skull and brain beneath it, the cause of death is obvious. It is then apparent that the energy absorbing qualities of the helmet were exceeded. In such a case, the postmortem examination is largely a matter of documenting the injuries and attempting to estimate the magnitude of the force which caused the helmet to separate. Typical injuries to be noted include epidural, subdural, and subarachnoid hemorrhages, and avulsions, lacerations, and hemorrhage of the brain itself. A more elusive, and somewhat speculative, mechanism for head and neck injury can be used to account for cases in which the helmet remains intact, but a fatal injury is sustained nonetheless. In such an instance, the helmet has apparently distributed impact forces uniformly over the skull so as to keep tissue pressure per unit area, and consequent tissue damage, at a minimum. However, the fact that the accident was fatal would indicate that the actual distribution of impact forces did not provide adequate protection. The engineering principle behind the Roman arch was that force applied at the top was carried by the form of the curved structure to the pillar or base, where it could be supported better than at the top. It is comprised of the calvarium, the lateral temporal bone, and the petrous ridges of the temporal bone. This curved structure has as its base the part of the skull where the brain stem resides, the posterior part of the body of the sphenoid bone, and the basilar portion of the oc cipital bone. A characteristic finding in autopsies with head injuries in which helmets were worn is a fracture occurring just anterior to the petrous ridge a of the temporal bone and extending toward the brain stem. Frequently, the base of the skull at the juncture of the posterior and middle compartments becomes almost bivalved, so that one can actually move it as a bivalve structure, indicating the significance and depth of the fracture at the anterior limits of the petrous ridge. This section of bone is rather thin and apparently is more mechanically susceptible to discontinuity as forces are applied. It appears, then, that when energy is applied to an upper portion of the helmet it may simply be translated through the arch of the skull and delivered to the base of the brain, resulting in the fracture frequently seen at the anterior limits of the petrous bone. Energy applied there may become lethal immediately because vital centers for respiration and other autonomic functions are located in the brain stem. Hinge basilar skull fractures such as these have been noted in cases where the victim strikes his mandible on an object with such force as to transfer the force through the mandible to the temporomandibular joint and the skull base. The situation thus may exist where an autopsy shows a head that is completely intact externally and a helmet which has sustained some damage. The assumption may be made that the helmet was effective as designed because the damage is in the helmet and not in the exterior of the head. The translation of energy, imparted at the helmet and transmit ted through the arch of the skull, may have consequences in the brain stem which are quite lethal. This is an anomaly which can easily be overlooked during a routine postmortem ex amination. The analogy might be further extended to include the lesions made about the neck by the straps or the edge of the helmet, paralleling the abrasions and contusions that might be associated with a rope having encircled the same structures. Characteristically, the posterior arch is fractured and, interestingly enough, the odontoid process is not involved. One interesting and compelling aircraft accident investigated by the Naval Safety Center, Norfolk, Virginia, served to emphasize the practical application of this theoretical exercise (Colangelo, 1974). A Navy A-4 jet aircraft experienced difficulties in flight which caused the pilot to eject at an altitude, attitude, and airspeed that were within the operating envelope of the ejection seat. Supported by a fully blossomed, functioning parachute, however, the pilot reached the ground severely injured and died shortly after the accident as a result of a transverse laceration of the cervical spinal cord. The investigation established that the energy responsible for the fatal lesion was transmitted through the helmet and its inferior edge into the posterolateral neck, A vertebral dislocation of C-2 and C-3 resulted, which in turn severed the spinal cord. Similar observations had prompted an earlier modification of the helmet to incorporate a thicker protective edge roll. It is often tacitly assumed when a helmet which has been subjected to a large impact force exhibits only slight damage the head which is designed to protect should remain proportionally secure. The pathology itself was distinctive in that a dislocation without fracture occured at the C-2/C-3 level of the cervical spine. Histologic sections made through the C-2/C-3 vertebrae confirmed that no fracture was present, despite common observations in the literature that fracture is the usual, if not an in variable accompaniment, of such severe dislocations (American Academy of Orthopaedic Surgeons Symposium, 1969). The concept of the cervicocranium as an entity constituted by the cranium, the atlas, and the axis suggests that this functional segment above C-3 tends to move as a single unit, in dislocation as well as in flexion, extension, and rotation.

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