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The number of lifetime major depressive episodes is significantly associated with the probability of recurrence, such that the risk of recurrence increases by 16% with each successive episode (484). Maintenance therapy should be considered more strongly for patients with additional risk factors for recurrence, such as the presence of residual symptoms, ongoing psychosocial stressors, family history of mood disorders, and the severity of prior episodes (504) (see Table 10). Additional considerations that may play a role in the decision to use maintenance therapy include patient preference, the presence of side effects during continuation therapy, and the severity of prior depressive episodes, including factors such as psychosis or suicide risk. In general, the treatment that was effective in the acute and continuation phases should be used in the maintenance phase. Among the therapeutic options available for maintenance treatment, antidepressant medications have received Copyright 2010, American Psychiatric Association. In one study, maintenance cognitive therapy delivered over 2 years was as effective as maintenance medication for recurrent major depressive disorder (514). Some results suggest that the combination of antidepressant medications plus psychotherapy may be more effective in preventing relapse than treatment with single modalities (314, 365, 506, 515, 516). For patients receiving treatment with pharmacotherapy and/or psychotherapy, the frequency of visits during the maintenance phase should be set according to the clinical condition and the specific treatments being used. The frequency can range from as low as once every several months for stable patients who require only psychiatric management and medication monitoring to as high as once or twice per week for those receiving psychodynamic psychotherapy. The duration of the maintenance phase will vary depending on the frequency and severity of prior major depressive episodes, the tolerability of treatments, and patient preferences. For many patients, some form of maintenance treatment may be required indefinitely. Electroconvulsive therapy has also been used in the maintenance phase, although evidence for its benefits comes largely from case reports (239). Persistence of subthreshold depressive symptoms Prior history of multiple episodes of major depressive disorder Severity of initial and any subsequent episodes Earlier age at onset Presence of an additional nonaffective psychiatric diagnosis Presence of a chronic general medical disorder Family history of psychiatric illness, particularly mood disorder Ongoing psychosocial stressors or impairment Negative cognitive style Persistent sleep disturbances the most study. Lithium has also been used as maintenance treatment for major depressive disorder (441). Despite this, there is limited information on many of the clinical decisions involving medication use in the maintenance phase. Even though lower doses of medication are less likely to produce side effects, results from one study suggest that full doses are superior to lower doses in the maintenance phase (508). Particularly if medications are well-tolerated, it is generally advisable to prescribe the same antidepressant medication doses for maintenance therapy that were effective in prior phases of treatment. Even with adequate maintenance treatment, pharmacotherapy is not invariably successful in preventing relapse and return of symptoms, which still occur in as many as 25% of individuals (509, 510). It is unclear whether some relapses during maintenance therapy are loss of therapeutic efficacy, a phenomenon that has been referred to as tachyphylaxis, but many such relapses appear related to inadequate prophylactic effects of medication (511). When relapses occur, clinicians typically address them using the same approaches described to treat incomplete responses to treatment, such as increasing the dose of medication, changing to a different medication, or adding another medication or a depressionfocused psychotherapy to augment therapeutic response (510, 512). There have been fewer investigations of the effectiveness of psychotherapy in the maintenance phase. The precise timing and method of discontinuing psychotherapy and pharma- Copyright 2010, American Psychiatric Association. Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition cotherapy for major depressive disorder have not been systematically studied. The decision to discontinue treatment should be based on the same factors considered in the decision to initiate maintenance treatment (Table 10), including the probability of recurrence, the frequency and severity of past episodes, the persistence of depressive symptoms after recovery, the presence of co-occurring disorders, and patient preferences. In general, psychotherapy has a longer lasting treatment effect and carries a lower risk of relapse following discontinuation than pharmacotherapy. In terms of timing, patients should be advised not to discontinue medications before holidays, significant events. Patients should be carefully monitored during and immediately after treatment discontinuation to ensure that remission is stable. The highest risk for a relapse is seen in the first 2 months after discontinuation of treatment. Hence, it is important to schedule a follow-up visit during this period to ensure stability. When pharmacotherapy is being discontinued, it is best to taper the medication over the course of at least several weeks. Such tapering allows for the detection of recurring symptoms at a time when patients are still partially treated and therefore more easily returned to full therapeutic treatment if needed. In addition, such tapering can help minimize the incidence of antidepressant medication discontinuation syndromes, particularly with paroxetine and venlafaxine (98, 163, 164). Discontinuation syndromes are problematic because their symptoms include disturbances of mood, energy, sleep, and appetite and can therefore be mistaken for or mask signs of relapse (517). Consequently, patients should be advised not to stop medications abruptly and to take medications with them when they travel or are away from home. Discontinuation syndromes have been found to be more frequent after discontinuation of medications with shorter half-lives, and patients maintained on short-acting agents should 59 have their medications tapered gradually over a longer period (518, 519). For time-limited approaches, termination is usually broached from the initiation of treatment and periodically revisited, as the therapist-patient dyad notes which session they are in, how many remain, and how they have progressed toward defined goals. In dynamically oriented psychotherapy, the therapist typically raises termination as an issue well in advance of the final session, using the opportunity to explore remaining and unresolved issues in transference. Before the discontinuation of active treatment, patients should be informed of the potential for a depressive relapse. Early signs of major depressive disorder should be reviewed, often with a family member, and a plan established for seeking treatment in the event of recurrent symptoms. Patients should continue to be monitored over the next several months to identify early evidence of recurrent symptoms. Again, systematic assessment of symptoms, side effects, adherence, and functional status during this period of high vulnerability is strongly recommended. If a patient does suffer a recurrence after discontinuing medication, treatment should be promptly reinitiated. Usually, the previous treatment regimen to which the patient responded in the acute and continuation phases should be reinitiated (520). Patients who have a recurrence following discontinuation of antidepressant therapy should be considered to have experienced another major depressive disorder episode and should receive adequate acute-phase treatment followed by continuation-phase treatment and possibly maintenance-phase treatment. Psychiatrists should consider greater intensity of treatment for suicidal patients, including hospitalization when warranted and/or combined treatment with pharmacother- A. Patients with major depressive disorder who present to an emergency department with suicidal ideation, or who have made a suicide attempt, should be triaged to determine their level of safety and establish the appropriate level and setting of care. Upon entrance to the emergency department, they should be searched to permit removal of potentially dangerous items, such as weapons and personal belongings that could cause harm. Factors to consider in determining the nature and intensity of treatment include (but are not limited to) access to and lethality of suicide means, past and family history of suicidal behavior, co-occurring substance abuse, the availability and adequacy of social supports, and the nature of the doctor-patient alliance. To lower the risk of suicide, the psychiatrist should also treat modifiable risk factors, such as anxiety (especially panic attacks), insomnia, agitation, psychotic symptoms, and substance abuse (22), in addition to treating the major depressive episode. Family members can also play an important role in detecting and preventing suicidal behaviors. When permitted by the patient, the psychiatrist should educate those close to the patient concerning appropriate interventions and encourage communication. There has been a growing controversy about the risk of suicidal ideas and behaviors (sometimes referred to as "suicidality") after initiation of antidepressant treatment. Although information on such risk continues to evolve, a predictive relationship to suicide has never been demonstrated. Clinical experience has long suggested that patients may develop the energy and capacity to act on selfdestructive plans made earlier in the course of their illness if neurovegetative and psychomotor symptoms respond to antidepressant treatment before mood improves. More recently, meta-analyses of data from clinical trials have shown statistically significant increases in suicidal thoughts or behaviors in individuals age 25 years or younger who are treated with antidepressant medication, compared with placebo, with an approximately 1. For adults age 65 years or older, a review of the evidence from clinical trials showed a decrease in the risk of suicidal thinking or behaviors with antidepressant treatment, with no change in risk detected for other adults (age 25 to 64 years) (536). Many depressed patients report slowed thoughts, poor concentration, distractibility, and reduced capacity to process information.

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They lack sensation to heat, touch, and pain but othersis (loss of eyelashes or eyebrows) and other ocular problems. Although the nerve injury caused by leprosy is irreversible, early diagnosis and drug therapy can prevent sequelae. In the topathologic features of their lesions and organization of the underlying granuloma. The scale includes: (1) tuberculoid, (2) borderline tuberculoid, (3) borderline, and diagnosis is unavailable is based purely on clinical skin examination. Under this line tuberculoid) or multibacillary (>5 lesions, usually borderline, borderline lepromatous, or lepromatous). Patients in the tuberculoid spectrum have active cell-mediated immunity with low antibody responses to M leprae ing few bacilli. Lepromatous spectrum cases have high antibody responses with little cell mediated immunity to M leprae and several somewhat-diffuse lesions usually containing numerous bacilli. Serious consequences of leprosy occur from immune reactions and nerve involvement with resulting anesthesia, which can lead to repeated unrecognized trauma, ulcerations, Leprosy is a leading cause of permanent physical disability among communicable diseases worldwide. A diagnosis of leprosy should be considered in any patient with hypoesthetic or anesthetic skin rash, or skin patches, especially those that do not respond to ordinary therapies, and among those with a history of residence in areas with endemic leprosy or contact with armadillos. They are especially common during initial years of treatment but can occur in the absence of therapy. Acute tenderness and swelling at the site of cutaneous and neural lesions with development of new lesions are major manifestations. Several human genes M leprae, and fewer than 5% of people appear to be genetically susceptible to the infection. Accordingly, spouses of leprosy patients are not likely to develop leprosy, but biological parents, children, and siblings who are household contacts of untreated patients with leprosy are at increased risk. Transmission is thought to be most effective through long-term close contact with an infected individual, and it likely occurs through respiratory shedding of infectious armadillo (Dasypus novemcinctus) and 6-banded armadillo (Euphractus sexcinctus) are the only known nonhuman reservoirs of M leprae, and zoonotic transmission is reported in do not appear to be at increased risk of becoming infected with M leprae. There are approximately 6500 people with leprosy living in the United States; with of leprosy, with an average annual incidence rate of 0. The majority of leprosy cases reported in the United States occurred among residents of Texas, California, and Hawaii or among immigrants and other citizens who lived or worked in leprosy-endemic countries and likely acquired their disease while abroad. Other areas of high endemicity include Angola, Brazil, Central African Republic, Democratic Republic of Congo, Madagascar, Mozambique, the Republic of the Marshall Islands, South Sudan, the Federated States of Micronesia, and the United Republic of Tanzania. Younger patients (15 to 30 years of age) predominate in areas of high endemicity, and older average ages predominate in areas of low endemicity. The primary goal of therapy is prevention of per- manent nerve damage, which can be accomplished by early diagnosis and treatment. Combination antimicrobial multidrug therapy can be obtained free of charge from the tries. It is important to treat M leprae infections with more than 1 antimicrobial agent to minimize development of antimicrobial-resistant organisms. The infectivity of leprosy patients ceases within a few days of initiating standard multidrug therapy. This consideration is important to avoid monotherapy of active tuberculosis with rifampin while treating active leprosy. Leprosy reactions should be treated aggressively to prevent peripheral nerve damage. Rehabilitative measures, including surgery and physical therapy, may be necessary for some patients. All patients with leprosy should be educated about signs and symptoms of neuritis and cautioned to report signs and symptoms of neuritis immediately so that corticosteroid therapy can be instituted. Patients should receive counseling because of the social and psychological effects of this disease. Therapy for patients with leprosy should be undertaken in consultation with an expert as well as consultation on clinical and pathologic issues, and information about local Hansen disease clinics and clinicians who have experience with the disease. Prevention of disability is an important goal of treatment and care; a critical component of this is selfexamination for any patient with loss of sensitivity in the foot. Many patients suffer profound anxiety because of the stigma historically associated with leprosy. Household contacts should be examined initially, but long-term follow-up of asymptomatic contacts is not warranted. Newly diagnosed cases should be reported to state public health authorities, the Centers for Disease Control and Prevention, and the National Hansen Disease Program. The severity of disease ranges from asymptomatic or subclinical to selfjaundice, renal failure (oliguric or nonoliguric), myocarditis, hemorrhage (particularly pulmonary), and refractory shock. Regardless of its headache, nausea, and vomiting occasionally accompanied by rash or conjunctival sufof cases). Findings commonly associated with the immune-mediated phase include fever, aseptic meningitis, and uveitis; between 5% and 10% of Leptospira-infected patients are estimated to experience severe illness. Severe manifestations include any combination arrhythmias, and circulatory collapse. The estimated case-fatality rate is 5% to 15% with severe illness, although it can increase to >50% in patients with pulmonary hemorrhage syndrome. Asymptomatic or subclinical infection with seroconversion is frequent, especially in settings of endemic infection. The reservoirs for Leptospira species include a wide range of wild and domestic animals, primarily rats, dogs, and livestock (cattle, pigs) that may shed organisms asymptomatically for years. Leptospira organisms excreted in animal urine may remain viable in moist soil or water for weeks to months in warm climates. Humans usually become infected via entry of leptospires through contact of mucosal surfaces (especially conjunctivae) or abraded skin with contaminated environmental sources. Unusually, infection may be acquired through direct contact with infected animals or their tishurricanes and monsoons. Populations in regions of high endemicity in the tropics likely encounter Leptospira organisms commonly during routine activities of daily living. People who are predisposed by occupation include abattoir and sewer workers, miners, veterinarians, farmers, and military personnel. Recreational exposures and clusters of disease have been associated with adventure travel, sporting events including triathlons, and wading, heavy rainfall. Common history includes being submerged in or swallowing water during such activities. For these reasons, serum specimens always should be obtained to facilitate diagnosis. Antibodies can develop as early as 5 to 7 days after onset of illness, and can be measured by commercially available immunoassays, which are based on sonicates of the saprophyte these assays have variable sensitivity according to regional differences of the various Leptospira species; however, increases in antibody titer may not be detected until more than 10 days after onset, especially if antimicrobial therapy is initiated early. Further, in populations with high endemicity, background reactivity requires establishing regionally relevant diagnostic criteria and establishment of diagnostic versus background titers. Antibody increases can be transient, delayed, or absent in some patients, which may be related to antibiotic use, bacterial virulence, immunogenetics of the individual, or other unknown factors. Microscopic agglutination, the gold standard serologic test, is performed only in reference laboratories and requires seroconversion demonstrated between acute and convalescent specimens obtained at least 10 days apart. Intravenous penicillin is the drug of choice for patients with severe infection requiring hospitalization; penicillin has been shown to be effective in shortening duration of temic symptoms and persistence of associated laboratory abnormalities and may prevent reaction (an acute febrile reaction accompanied by headache, myalgia, and an aggravated clinical picture lasting less than 24 hours) can develop after initiation of penicillin therapy. Parenteral cefotaxime, ceftriaxone, and doxycycline have been demonstrated in randomdrome require prompt dialysis and mechanical ventilation, respectively, to improve clinical outcome. For patients with mild disease, oral doxycycline has been shown to shorten the course of illness and decrease occurrence of leptospiruria; ampicillin or amoxicillin can also be used to treat mild disease. Tetracycline-based antimicrobial agents, including if used for repeated treatment courses. However, doxycycline binds less readily to calcium compared with older tetracyclines, and in some studies, doxycycline was not associated been demonstrated in a clinical trial to be as effective as doxycycline and can be used as an alternative in patients for whom doxycycline is contraindicated. However, immunization may not prevent the shedding of leptospires in their urine, thus contaminating environments with which humans may come in contact. Swimmers should attempt to avoid immersion or swallowing water in potentially contaminated fresh water. Protective clothing, boots, and gloves should be worn by people with occupational exposure to decrease their risk. Doxycycline, 200 mg, administered orally once a week to adults, may provide effective prophylaxis against clinical disease and could be considered for high-risk groups (eg, triathletes) with short-term exposure, but infection may not be prevented. Indications for prophylactic doxycycline use for children have not been established. Transmission predominantly is foodborne, and illness occurs most frequently among pregnant women and their fetuses or newborn infants, older adults, and people with impaired cell-mediated immunity resulting from underlying illness or treatment (eg, organ transplant, hematologic malignancy, immunosuppression resulting from therapy with corticosteroid or anti-tumor necrosis factor agents, in spontaneous abortion, fetal death, preterm delivery, and neonatal illness or death.

Diseases

  • Inhalant abuse, aliphatic hydrocarbons
  • Marie type ataxia
  • Neurilemmomatosis
  • Osteochondrodysplasia thrombocytopenia hydrocephalus
  • Anophthalia pulmonary hypoplasia
  • Multiple carboxylase deficiency, biotin responsive

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Incubation Period Uncertain, but may be years since the virus stays dormant after the chickenpox virus. Infectious Period Skin lesions are infectious in the water vesicle (blister) stage until crusted over. Virus from the vesicle fluid of a person with herpes zoster can rarely cause chickenpox in a non-immune individual. Educate student about good personal hygiene, especially proper hand washing techniques. Students with herpes zoster are to be excluded from school if lesions are not or cannot be covered with a bandage or clothing. Dispose of bandages that have been in contact with the vesicles (blisters) in an appropriate bagged receptacle. These infections, which would not be a threat to people with normal immune systems, are called opportunistic infections. The virus also multiplies in the central nervous system, destroying brain cells, and may cause memory loss, personality changes, and dementia late in the course of the illness. Infants born to infected mothers may have maternal antibodies that disappear between 12 and 18 months after birth. If the baby is infected, it will not produce its own antibodies until its immune system is developed, at about 18 months. Estimates of possible incubation periods for symptoms range from a few months to several years for children infected at birth to over 10 years in adults who were infected through sexual intercourse. Tears and saliva contain very few, if any, viral particles and are not considered significant vectors of transmission. Children acquire the infection from their infected mothers before birth or, in rare cases, during a blood transfusion or during breastfeeding. Refer to district infection control program protocol and policy for infectious diseases. Inform parent/guardian to keep the immune-compromised student at home during outbreaks of diseases potentially serious for the student such as chickenpox, measles, and influenza. They should consult with their licensed health care provider and the licensed health care provider should determine whether the individual should stay home from school. Lesions may be found on the face, especially around the mouth and nose, but may be found on other areas of the body. Other streptococcal infections include sore throat, scarlet fever, and necrotizing fasciitis (flesheating bacteria). Any injury or break in the skin can permit the bacteria to invade the skin and cause infection. Infectious Period Lesions are considered infectious until treatment has been administered for 24 hours. The disease responds very quickly to systemic antibiotic treatment and/or prescription topical antibiotic ointments. Students should not participate in swimming, body contact sports, or food preparation activities until all lesions are healed. Antibiotics will decrease the spread of the disease and decrease the incidence of complications from the bacterial infection. Good personal hygiene and soap and water cleansing of minor skin breaks will help to prevent spread. Students should be discouraged from sharing towels, clothing, and other personal items. There may be a rash, more often in patients who have been treated with amoxicillin/ampicillin. In the adolescent in particular, there can be swelling and tenderness of the spleen. Students with a rash illness, especially if fever and/or other symptoms are present, should be referred to a health care provider for diagnosis. Future Prevention and Education Provide health education for students and their parent/guardian as to the usual mode of transmission and reinforce that Mono is not highly contagious. Complications are more severe for the very young, the very old, and pregnant women. Report to your local health jurisdiction significant increases in school absenteeism resulting from influenza-like illness or clusters of particularly severe infections. Refer to district infection control program protocols and policy for infectious diseases 3. Students with flu-like illness should be excluded from school until after the fever is gone (normally for 24 hours) and the child feels well enough to participate in normal activities. Persons 9 years and older only need 1 dose of seasonal influenza vaccine annually. Influenza season in the United States generally occurs sometime between December and April. The vaccine is made each year with the strains of influenza virus expected to cause the most infection. School closure is not generally recommended during an outbreak unless inadequate number of staff is available to carry on a program. Body lice can be found in bedding and clothing, particularly in the inner seams of clothing. The most common sites for lice bites are around the waist, groin and armpits-places where clothing seams are most likely to touch the skin. The main signs of body lice infestation are intense itching, scratch marks, and the detection of lice eggs or moving lice. Incubation Period Body lice eggs (nits) normally hatch in 1 to 2 weeks, depending on the temperature. Infectious Period Body lice can be spread as long as lice remain alive on the host or in clothing. Make referral to licensed health care provider for diagnosis if body lice are observed or suspected. Assess family situation and if necessary assist the family with community resources. Support the family in accessing showering or bathing facilities and regular changes of clean clothing and bedding. Because their bodies and claws resemble sea crabs, they are nicknamed "crab lice" or "crabs. An infestation of crab lice is usually detected in the pubic hair but may also be found less commonly in other places where there is coarse body hair, such as armpits, legs, mustaches, beards, eyebrows, or eyelashes. A person with crab lice may also have other sexuallytransmitted infections or diseases. However, a child may also become infested with crab lice if he or she shares a communal bed with adults who are infested. This is extremely unlikely because lice do not have feet designed to hold on to smooth surfaces such as toilet seats, and lice need a human blood source to survive. Consider child sexual abuse when crab lice are present in a student who is not sexually active. Individuals with crab lice should be examined by a licensed health care professional for other sexually transmitted infections or diseases. All potentially-affected persons (such as sexual partners or those sharing a bed) should be examined and treated simultaneously to avoid re-infestation. Head lice are parasitic insects less than 1/8 of an inch in length that feed on blood from the scalp. The information in this section reflects the current thinking of professional groups regarding head lice in schools. The American Academy of Pediatrics provides current clinical reports that clarify and update the protocols for diagnosis and treatment of head lice, and provide guidance for the management of infested children in the school setting. Head lice cannot survive away from the scalp for more than 2 days at room temperature.

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Thyroid weight was significantly increased (24%) in animals in the highest dose group, although significant alterations in thyroid hormones were not observed. Histological alterations of the thyroid gland, characterized by numerous vacuoles in the colloid of the thyroid follicles, were observed in all dosed animals. In the brain, minimal degeneration of Purkinje cells and loss of cerebellar white matter were reported. All 36 histologic lesions were reported by the authors to occur in a dose-related manner, although neither incidence nor statistical analysis of these findings was presented. A total of five females and seven males were used; each dose group contained both male and female animals (one dose group contained two females and one male while the others contained two males and one female). The solutions were administered once daily for 24 weeks, prior to feeding, in order to increase the gastrointestinal absorption of cyanide. Regularly measured serum thiocyanate levels were positively correlated with cyanide dose. Two categories of behavior were evaluated: performance measures, including innate behavior, and learning measures, including the acquisition and retention of new behaviors. Both T3 and T4 demonstrated a dose-related decrease (23 and 13%, respectively) that was statistically significant by week 18 of the study. A variety of behaviors were significantly altered in treated animals, including a decrease in dominance behavior (high-dose group), a decrease in fighting (mid- and high-dose group), an increase in flight response (all treated groups), a decrease in exploratory behaviors (all groups), and less aggressive feeding patterns (high-dose group). The authors concluded that the overall pattern of behavioral changes in the group administered 1. This study supports the large body of evidence demonstrating that the thyroid is a target organ for cyanide toxicity. Male rats from Woodlyn Laboratories (10/group, strain not specified) received diets (10% casein supplemented with 0. At 4 and 11 months, plasma T4 levels, T4 secretion rates, and urinary thiocyanate levels were measured in five animals per group. After sacrifice, brain, heart, liver, and thyroid weights were 2 Based on the average food intake across rat strains (U. Histopathologic evaluation was conducted on the brain, optic and sciatic nerves, spinal cord, and thyroid gland. This study design, although limited by the use of only one dose level, allowed for the comparison of effects mediated directly through cyanide versus the primary metabolite, thiocyanate. It also allowed for the comparison of cyanide and thiocyanate treatment in control rats compared to rats fed nutritionally restricted diets. Administration of cyanide altered serum T4 levels at 4 months but not at 11 months; thiocyanate altered serum T4 levels at both 4 and 11 months. After 4 months of treatment, rats in the cyanide-exposed groups had significantly decreased plasma T4 levels (53%) and decreased T4 secretion rates (68%) compared to controls; however, after 11 months of cyanide treatment, T4 levels no longer differed from those of controls, although T4 secretion rates were depressed 27%. In the nutritionally restricted control animals, levels and T4 secretion rates were lower compared to controls fed a standard diet. No histopathologic lesions were observed by light microscopy in the optic or sciatic nerves or thyroid gland of any group. No information on incidence or severity of the observed histologic lesions was reported by the authors. No measurable differences were reported in spinal cord pathology between cyanideand thiocyanate-treated rats. The authors indicated that 38 only rats surviving to the end of the study were analyzed histologically because the accuracy of necropsies performed on animals that died early were compromised by autolysis. It appears that seven, five, and nine males and six, seven, and six females were examined histologically in the 0, 4. From the data reported on food consumption and body weight, estimated doses were 0, 4. There were no treatment-related effects on growth rate, no gross signs of toxicity, no hematologic effects, and no histopathologic lesions in the tissues evaluated from an undisclosed subset of animals (heart, lungs, liver, kidneys, spleen, stomach, small and large intestines, adrenals, thyroid, testes or uterus and ovaries, cerebrum, and cerebellum). Howard and Hanzal (1955) also reported that there appeared to be no effect on relative organ weight of the liver, kidneys, spleen, brain, heart, adrenals, testes, or ovaries. Doses were lowered in the highest dose group at week 12 due to excessive toxicity/mortality. After 3 months of exposure, organ histology was performed on the kidney, heart, liver, testes, thyroid, and brain. Organ weights were measured for the following organs: adrenals, heart, kidneys, lungs, thymus, brain, liver, pituitary, testis, and thyroid (only the left lobe). Epididymis weight was not weighed independently, but was included as part of testicular weight. Statistically significant body weight decreases were observed in the highest two doses. Body weight was statistically significantly decreased 42% at the high dose and 15% in the mid-level dose. Average body weight decrease (4%) at the low dose was not statistically different than controls. Water consumption was decreased in all dose groups (17, 21, and 32% in the low, mid, and high dose, respectively) compared to controls. At the highest dose, absolute heart, liver, spleen, kidney, and brain weights were statistically significantly decreased compared to the controls. The number of animals included in each group was seven, six, six, and seven for the control, low-, mid-, and high-dose groups, respectively. Endpoints evaluated included clinical signs of toxicity, body weight, food consumption, serum cholesterol, glucose, T3, and T4. No treatment-related effects were reported for clinical signs of toxicity, body weight gain, food consumption, serum T3 and T4, or serum glucose. The test compound was administered twice daily in milk (one-half of the daily dose per treatment) for the first 3 months and in water for the remainder of the treatment period. Neuropathology, including congestion, hemorrhage, and gliosis in the cerebellum, spinal cord, and pons, as well as spheroids on the gray matter of the spinal cord, was observed at 40 0. Additional findings in the high-dose group included damage and loss of Purkinje cells in the cerebellum, spongiosis in the pons, and spheroids, axonal swelling, gliosis, spongiosis, and ghost cells in the medulla oblongata. Inhalation Studies No chronic or subchronic animal studies of cyanide inhalation exposure were located. Pathology evaluated for both monkeys and rats included gross and microscopic examination of heart, liver, kidney, cerebellum, lungs, thyroid, spleen, and bone marrow. Additionally, behavioral tests and electrocardiograms were administered to the monkeys. No significant changes were seen in monkeys other than decreased lung moisture content in both dose groups. The only effect noted in rats was significantly depressed body weight (13%) in the high-dose group. Sprague-Dawley rats (15/sex/group) were exposed by inhalation at average concentrations of 10. Endpoints analyzed included hematology, clinical chemistry (including T3 and T4 levels), and gross and microscopic histopathology on a wide range of organs and tissues. No effects on mortality, body weight, or behavior were observed in treated animals. Blood and urine levels of thiocyanate were elevated in a dosedependent manner, although no alterations in T3 or T4 were observed. No significant gross or microscopic histology was observed in treated animals compared with controls. Parameters examined included body weight, brain weight, cerebellar weight, maximum vermis length (length between cerebellar hemispheres), maximum side-to-side dimensions of the cerebellum, and maximum thickness (anteroposterior dimension) of the cerebellum. Aggressive and restless behavior was noted in the exposed dams but not in controls. No significant changes in body weight or brain weight were found at the additional five time points examined.

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Although bupropion is classified as a norepinephrine and dopamine reuptake inhibitor, the latter effect is relatively weak, and its mechanism of action remains unclear (106). There are three formulations of bupropion: immediate release, sustained release, and extended release. Bupropion is distinct from most antidepressants in not having an indication for the treatment of any primary anxiety disorder, and it may be less well tolerated than other antidepressants among patients with significant anxiety. Bupropion may be a good choice for patients who have a goal of quitting smoking as it has U. Patients typically experience minimal weight gain or even weight loss on bupropion (111), and for this reason it may be an appropriate antidepressant for patients who are overweight or obese. Mirtazapine is thought to work through noradrenergic and serotonergic mechanisms, although this tetracyclic compound is not a reuptake inhibitor (112). Although trazodone is an effective antidepressant, relative to placebo (105, 114, 115), in contemporary practice it is much more likely to be used in lower doses as a sedative-hypnotic than as an antidepressant. Despite widespread use of trazodone as a hypnotic, few data support its use for this indication. Nefazodone has an analogous structure to trazodone but somewhat different pharmacological properties. Side effects of antidepressant medications the severity of side effects from antidepressant medications in clinical trials has been assessed both through the frequency of reported side effects and through the frequency of treatment dropout. The likelihood of different side effects varies among classes of antidepressant medications, among subclasses, and among individual agents. When side effects occur during treatment with an antidepressant, an initial strategy is to lower the dose of the antidepressant or to change to an antidepressant that is not associated with that side effect. When lowering the dose or discontinuing the medication is not effective, additional strategies may be considered. These additional strategies are described in Table 7, which also lists prominent and clinically relevant side effects associated with particular medication classes. Serotonin syndrome, as the name implies, is presumed to result from high levels of serotonin in the brain. Because knowledge of potential drug-drug interactions is frequently changing, it is useful to consult a frequently updated drug information database before selecting an antidepressant in a patient taking other medications. These adverse events are generally dose dependent and tend to dissipate over the first few weeks of treatment. If akathisia does occur, a beta-blocker or benzodiazepine can be tried to reduce symptoms. The psychiatrist should ascertain whether the reported sexual dysfunction is a result of the antidepressant medication, the underlying major depressive disorder, a co-occurring medical disorder, a disturbance in a relationship, or a need for education about sexual functioning. If sexual dysfunction is determined to be a side effect of the antidepressant medication, a number of strategies are available, including Copyright 2010, American Psychiatric Association. Obtain dental consultation, if clinically indicated Add an 1-adrenergic antagonist. If clinically indicated, obtain bone density monitoring and add specific treatment to reduce bone loss. Specific pharmacological treatments that can be added for arousal difficulties, erectile dysfunction, or orgasm dysfunction include buspirone (131), bupropion (132), sildenafil (133), and tadalafil (134). Other phosphodiesterase inhibitors may be also useful in treating sexual side effects, and a variety of other medications have been used with anecdotal success (135, 136). Neurological effects Selective serotonin reuptake inhibitors can initially exacerbate both migraine headaches and tension headaches. These effects tend to be transient and improve within the first few weeks of treatment. Selective serotonin reuptake inhibitors have also been associated with extrapyramidal side effects, including akathisia, dystonia, parkinsonism, and tardive dyskinesia (139, 140). Falls Selective serotonin reuptake inhibitors, like other antidepressive agents, have been associated with an increased risk of falls. Meta-analyses have also documented an increased risk of falls in patients treated with antidepressive agents, in general (144, 145). Interaction with other drugs was higher for fluoxetine, fluvoxamine, and paroxetine than for sertraline, citalopram, and escitalopram (98, 160, 161). Inquiring about a history of falls in the past year and assessing for abnormalities in gait and balance can also help in identifying patients at particular risk for falling (153). Fluoxetine causes an initial reduction in weight, which tends to normalize with continued treatment (156). Features of serotonin syndrome include abdominal pain, diarrhea, flushing, sweating, hyperthermia, lethargy, mental status changes, tremor and myoclonus, rhabdomyolysis, renal failure, cardiovascular shock, and possibly death (157). Selective serotonin reuptake inhibitors have variable effects on hepatic microsomal enzymes and therefore cause both increases and decreases in the blood levels of other medications. Discontinuationemergent symptoms include both flu-like experiences such as nausea, headache, light-headedness, chills, and body aches, and neurological symptoms such as paresthesias, insomnia, and "electric shock-like" phenomena. However, some patients do experience more protracted discontinuation syndromes, particularly those treated with paroxetine, and may require a slower downward titration regimen. In the absence of a reduction in hypertension, a different antidepressant medication may be considered. Alternatively, in a patient with well-controlled depressive symptoms, it may be preferable to add an antihypertensive agent rather than risk a depressive relapse or recurrence with medication tapering. Discontinuation symptoms, which are sometimes protracted, are more likely to occur with venlafaxine (and, by implication, desvenlafaxine) than duloxetine (100) and may necessitate a slower downward titration regimen or change to fluoxetine. Bupropion Bupropion differs from other modern antidepressants by its lack of direct effects on serotonergic neurotransmission and, as a consequence, a virtual lack of sexual side effects (169). Neurologic side effects with bupropion include headaches, tremors, and seizures (106). Bupropion should also not be used in patients who have had anorexia nervosa or bulimia nervosa because of elevated risk of seizures (170). Bupropion has been associated with a low risk of psychotic symptoms, including delusions and hallucinations. Other side effects with bupropion include agitation, jitteriness, mild cognitive dysfunction, insomnia, and gastrointestinal upset. Mirtazapine the most common side effects of mirtazapine include dry mouth, sedation, and weight gain. For this reason, mirtazapine is often given at night and may be chosen for depressed patients with initial insomnia and weight loss. Although several patients treated with mirtazapine were observed to have agranulocytosis in early studies, subsequent clinical experience has not confirmed an elevated risk (172). Trazodone can also cause cardiovascular side effects, including orthostasis, particularly among elderly patients or those with preexisting heart disease. Use of trazodone has also been associated with life-threatening ventricular arrhythmias in several case reports (173). Trazodone also can cause sexual side effects, including erectile dysfunction in men; in rare instances, priapism occurs, which might require surgical correction (174, 175). Nefazodone Side effects with nefazodone include dry mouth, nausea, constipation, orthostasis, and visual alterations (176). However, in patients with insomnia, the sedating properties of nefazodone can be helpful in improving sleep (177). There appears to be a low incidence of treatment-emergent sexual dysfunction (178, 179) with nefazodone and, unlike trazodone, it has not been associated with priapism. Nefazodone has also been associated with rare but potentially fatal liver failure (180, 181), which has limited its use in recent years. Drug-drug interactions can also be problematic as nefazodone inhibits hepatic microsomal enzymes and can raise levels of concurrently administered medications such as certain antihistamines, benzodiazepines, and digoxin. Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition 4. Tricyclic antidepressants act similarly to class Ia antiarrhythmic agents such as quinidine, disopyramide, and procainamide, which increase the threshold for excitation by depressing fast sodium channels, prolong cardiac cell action potentials through actions on potassium channels, and prolong cardiac refractoriness through actions on both types of channels (183).

Syndromes

  • Is there anything you do to reduce or prevent accidents?
  • Paralysis or weakness on one side
  • Bowel obstruction
  • Feeling very hungry 1 to 3 hours after eating
  • Sexually transmitted diseases such as genital herpes, chlamydia, and gonorrhea
  • Tick-borne relapsing fever (TBRF) is transmitted by the Ornithodoros tick and occurs in Africa, Spain, Saudi Arabia, Asia, and certain areas in the western United States and Canada. The bacteria species associated with TBRF are Borrelia duttoni, Borrelia hermsii, and Borrelia parkerii.
  • Dry skin that is not springy
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This preparation contains 100 mg of standardised concentrated ginseng [probably Panax ginseng (Asian ginseng)] in each capsule. It was suggested that this might have been because he had begun using a ginseng product (not identified). The brand of ginseng used was Golden Glow, each capsule containing an extract equivalent to 0. Pharmacokinetics the oral bioavailability of glucosamine has been estimated to be about 25 to 50%, probably due to first-pass metabolism in the liver. Glucosamine is rapidly absorbed and distributed into numerous tissues, with a particular affinity for articular cartilage. Increased blood-glucose has been recorded in patients with diabetes, but no interaction was found in a controlled study. Glucosamine might modestly increase tetracycline or oxytetracycline levels, and very limited evidence suggests that glucosamine may possibly decrease the efficacy of paracetamol and some cytotoxic antineoplastics. Use and indications Glucosamine is a natural substance found in chitin, mucoproteins and mucopolysaccharides. It can be made by the body, and is found in relatively high concentrations in cartilage, tendons and ligaments. The primary use of supplemental glucosamine is for the treatment of osteoarthritis and other joint disorders. Glucosamine in supplements may be prepared synthetically, or extracted from chitin. G 226 Glucosamine 227 Glucosamine + Antidiabetics In a controlled study, glucosamine supplements with chondroitin had no effect on glycaemic control in patients taking oral antidiabetic drugs but one report notes that unexpected increases in blood-glucose levels have occurred. In one case, glucosamine also reduced hypoglycaemic episodes in a patient with metastatic insulinoma. However, it has been suggested that the results of this study may not be applicable to patients in the later stages of diabetes4 (i. Therefore it may be prudent to increase monitoring of blood-glucose in these patients if glucosamine supplements are taken. Also, if glucose control unexpectedly deteriorates, bear the possibility of self-medication with supplements such as glucosamine in mind. The effect of glucosamine-chondroitin supplementation on glycosylated hemoglobin levels in patients with type 2 diabetes mellitus: a placebo-controlled, double-blinded, randomized clinical trial. Can glucosamine supplements be applied for all patients with type 2 diabetes with osteoarthritis? However, the implication is that glucosamine could reduce the efficacy of these antineoplastics. Bear this possibility in mind should an unexpected response to treatment with topoisomerase inhibitors occur. Glucosamine + Diuretics Limited evidence from a large open study suggests that unnamed diuretics may slightly reduce the efficacy of glucosamine. Clinical evidence In a large open study, 1183 evaluable patients with osteoarthritis were given glucosamine 1. When response was analysed by concurrent treatment, in the 64 patients also taking diuretics (none specifically named), there was a slightly lower incidence of good efficacy (44%) and a slightly higher incidence of sufficient efficacy (52%), which reached statistical significance. Importance and management the concurrent use of glucosamine and diuretics is probably quite common, and the fact that this old study appears to be the only report in the literature of a possible interaction, and in itself inconclusive, suggests that any interaction is, in the main, unlikely to be clinically important. Oral glucosamine sulphate in the management of arthrosis: report on a multi-centre open investigation in Portugal. G Glucosamine + Antineoplastics the interaction between glucosamine and antineoplastics is based on experimental evidence only. Clinical evidence No interactions found Experimental evidence An in vitro study found that colon and ovary cancer cell lines showed resistance to doxorubicin and etoposide after exposure to glucosamine at a concentration of 10 mmol. Only a weak effect of glucosamine was found in the responsiveness of breast cancer cell lines to etoposide. Importance and management this possible interaction appears not to have been studied in vivo and, until more data are available, the clinical significance of the Glucosamine + Food No interactions found. Glucosamine + Paracetamol (Acetaminophen) Limited evidence suggests that glucosamine may reduce the efficacy of paracetamol (acetaminophen). Note that this would only occur with glucosamine sulfate salts and would not occur with glucosamine hydrochloride. The combined use of glucosamine and paracetamol to alleviate the symptoms of osteoarthritis is common, and the limited evidence here does not provide any reason to suggest any changes to this practice. Adverse interactions between herbal and dietary substances and prescription medications: a clinical survey. Importance and management Glucosamine is a widely used supplement, particularly in the middle-aged and elderly, who are also the group most likely to be using warfarin or similar anticoagulants. Even taking into account the possible cases reported to regulatory authorities, the interaction would seem to be quite rare. Clinical evidence A single-dose study in healthy subjects given tetracycline 250 mg alone or with glucosamine 250 mg found that the serum tetracycline levels were 105%, 50% and 25% higher at 2, 3 and 6 hours after administration, respectively, in those patients who had received the combined treatment. Similar results were found when oxytetracycline was given with glucosamine, with the corresponding increases being 36%, 44% and 30% at 2, 3 and 6 hours after administration, respectively. In contrast, in another single-dose study in 12 healthy subjects given tetracycline 250 mg alone, and then with glucosamine 125 mg and 250 mg at 1-week intervals, the addition of glucosamine slightly increased serum tetracycline levels at 2, 3, 6 and 8 hours, but this was not statistically significant. In the dogs, the increase in radioactivity was over twofold at 30 minutes, 1 hour and 24 hours after drug administration, whereas in the mice the increase was only greater than twofold at 15 minutes after drug administration. Importance and management these very early studies from the 1950s suggest that glucosamine might cause a modest increase in tetracycline levels. As a result of these studies, it appears that a preparation of oxytetracycline formulated with glucosamine was tried. A modest increase in tetracycline or oxytetracycline levels is unlikely to have adverse consequences, and, if anything, might be slightly beneficial. The effect of glucosamine on the absorption of tetracycline and oxytetracycline administered orally. Potential glucosamine-warfarin interaction resulting in increased international normalized ratio: case report and review of the literature and MedWatch database. Commission on Human Medicines/Medicines and Healthcare Products Regulatory Agency. Constituents the rhizome of goldenseal contains the isoquinoline alkaloids hydrastine and berberine, to which it may be standardised, and also berberastine, hydrastinine, canadine (tetrahydroberberine), canalidine and others. In addition, there is some in vitro evidence of P-glycoprotein inhibition,4 but no effect was seen on the levels of digoxin, page 232, which is used as a probe substrate of this transporter. For information on the pharmacokinetics of the constituent berberine, see under berberine, page 58. Interactions overview Goldenseal appears to modestly decrease the metabolism of midazolam, but has no significant effects on the pharmacokinetics of indinavir or digoxin. The interaction between goldenseal and diclofenac, paclitaxel or tolbutamide is based on experimental evidence only. For a possible interaction with ciclosporin, occurring as a result of the constituent berberine, see Berberine + Ciclosporin, page 59. Human cytochrome P450 inhibition and metabolicintermediate complex formation by goldenseal extract and its methylenedioxyphenyl components. Use and indications Used for inflammatory and infective conditions, such as amoebic dysentery and diarrhoea; gastric and liver disease. For details on the uses of berberine, a major constituent of goldenseal, see berberine, page 58. Clinical evidence A study in 12 healthy subjects investigated the effects of goldenseal 900 mg three times daily taken for 28 days on a single 8-mg dose of oral midazolam. The goldenseal product used gave an estimated daily dose of berberine of about 77 mg and of hydrastine of 132 mg. Importance and management Evidence for an interaction between goldenseal and midazolam is based on clinical studies in healthy subjects. They suggest that some caution might be appropriate if patients taking goldenseal supplements are given oral midazolam; however, the effects were modest. Nevertheless, the clinical effects of this interaction do not appear to have been studied and so it may be prudent to be aware of the small possibility of increased sedation if midazolam is given to patients taking goldenseal supplements.

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The term should not be used as a synonym for nuclide because isotopes refer specifically to different nuclei of the same element. It is equal to the work done by raising a mass of one newton through a distance of one meter (J = Nm), which corresponds to about 0. Kerma (k)-A measure of the kinetic energy transferred from gamma rays or neutrons to a unit mass of absorbing medium in the initial collision between the radiation and the absorber atoms. Labeled Compound-A compound containing one or more radioactive atoms intentionally added to its structure. By observations of radioactivity or isotopic composition, this compound or its fragments may be followed through physical, chemical, or biological processes. Late Effects (of radiation exposure)-Effects which appear 60 days or more following an acute exposure. Lung Clearance Class (fast, F; medium, M; slow, S)-A classification scheme for inhaled material according to its rate of clearance from the pulmonary region of the lungs to the blood and the gastrointestinal tract. Lymphoreticular Effects-Represent morphological effects involving lymphatic tissues such as the lymph nodes, spleen, and thymus. Malformations-Permanent structural changes that may adversely affect survival, development, or function. Mass Numbers (A)-The number of nucleons (protons and neutrons) in the nucleus of an atom. Minimal Risk Level-An estimate of daily human exposure to a substance that is likely to be without an appreciable risk of adverse noncancerous effects over a specified duration of exposure. Morbidity-State of being diseased; morbidity rate is the incidence or prevalence of disease in a specific population. Mutagen-A substance that causes changes (mutations) in the genetic material in a cell. Necropsy-The gross examination of the organs and tissues of a dead body to determine the cause of death or pathological conditions. Neurotoxicity-The occurrence of adverse effects on the nervous system following exposure to a substance. This particle accounts for conservation of energy in beta plus and beta minus decays. Nuclear Reactor-A power plant that heats the medium (typically water) by using the energy released from the nuclear fission of uranium or plutonium isotopes instead of burning coal, oil, or natural gas. All of these sources of energy simply heat water and use the steam which is produced to turn turbines that make electricity or propel a ship. The nuclear constitution is specified by the number of protons (Z), number of neutrons (N), and energy content; or, alternatively, by the atomic number (Z), mass number A(N+Z), and atomic mass. To be regarded as a distinct nuclide, the atom must be capable of existing for a measurable time. Thus, nuclear isomers are separate nuclides, whereas promptly decaying excited nuclear states and unstable intermediates in nuclear reactions are not so considered. Octanol-Water Partition Coefficient (Kow)-The equilibrium ratio of the concentrations of a chemical in n-octanol and water, in dilute solution. An odds ratio of greater than 1 is considered to indicate greater risk of disease in the exposed group compared to the unexposed. Pair Production-An absorption process for x- and gamma radiation in which the incident photon is absorbed in the vicinity of the nucleus of the absorbing atom, with subsequent production of an electron and positron pair (see annihilation). Parent-Any radionuclide nuclide which, upon disintegration, yields a new nuclide (termed the progeny or daughter), either directly or as a later member of a radioactive series. Pharmacokinetic Model-A set of equations that can be used to describe the time course of a parent chemical or metabolite in an animal system. There are two types of pharmacokinetic models: data-based and physiologically-based. A data-based model divides the animal system into a series of compartments which, in general, do not represent real, identifiable anatomic regions of the body whereas the physiologically-based model compartments represent real anatomic regions of the body. Utilizing computational techniques, it provides the means of studying the absorption, distribution, metabolism and excretion of chemicals by the body. These models advance the importance of physiologically based models in that they clearly describe the biological effect (response) produced by the system following exposure to an exogenous substance. These models require a variety of physiological information: tissue volumes, blood flow rates to tissues, cardiac output, alveolar ventilation rates and, possibly membrane permeabilities. The models also utilize biochemical information such as air/blood partition coefficients, and metabolic parameters. Photoelectric Effect-An attenuation process observed for x and gamma radiation in which an incident photon interacts with a tightly bound inner orbital electron of an atom delivering all of its energy to knock the electron out of the atom. Potential, Ionization-The energy expressed as electron volts (eV) necessary to separate one electron from an atom, resulting in the formation of an ion pair. Power, Stopping-A measure of the ability of a material to absorb energy from an ionizing particle passing through it; the greater the stopping power, the greater the energy absorbing ability (see Linear Energy Transfer). Progeny-The decay product or daughter products resulting after a radioactive decay or a series of radioactive decays. The progeny can also be radioactive, and the chain continues until a stable nuclide is formed. Proton-Elementary nuclear particle with a positive electric charge equal numerically to the charge of the electron and a rest mass of 1. Quality-A term describing the distribution of the energy deposited by a particle along its track; radiations that produce different densities of ionization per unit intensity are said to have different "qualities. Type of radiation X, gamma, or beta Alpha particles Neutrons of unknown energy High energy protons Quality Factor 1 20 10 10 Rad-The traditional unit of absorbed dose equal to 100 ergs per gram, or 0. Radiation-The emission and propagation of energy through space or through a material medium in the form of waves. The term radiation or radiant energy, when unqualified, usually refers to electromagnetic radiation. Such radiation commonly is classified according to frequency, as microwaves, infrared, visible (light), ultraviolet, and x and gamma rays (see Photon. However, radiation also occurs as corpuscular emission, such as alpha and beta radiation, neutrons, or rays of mixed or unknown type, such as cosmic radiation. Radiation, Annihilation-Photons produced when an electron and a positron unite and cease to exist. The annihilation of a positron-electron pair results in the production of two photons, each of 0. Radiation, Characteristic (Discrete)-Radiation originating from an excited atom after removal of an electron from an atom. The wavelength of the emitted radiation is specific, depending only on the element and particular energy levels involved. Radiation, Internal-Radiation from a source within the body (as a result of deposition of radionuclides in body tissues). Radiation, Ionizing-Any electromagnetic or particulate radiation capable of producing ions, directly or indirectly, in its passage through matter (see Radiation). Radiation, Monoenergetic-Radiation of a given type in which all particles or photons originate with and have the same energy. Radiation, Scattered-Radiation which during its passage through a substance, has been deviated in direction. Radiation, Secondary-A particle or ray that is produced when the primary radiation interacts with a material, and which has sufficient energy to produce its own ionization, such as bremsstrahlung or electrons knocked from atomic orbitals with enough energy to then produce ionization (see Delta Rays). Radioactivity-Spontaneous nuclear transformations that result in the formation of new elements. These transformations are accomplished by emission of alpha or beta particles from the nucleus or by the capture of an orbital electron. Radioactivity, Artificial-Man-made radioactivity produced by particle bombardment or nuclear fission, as opposed to naturally occurring radioactivity. Radioactivity, Induced-Radioactivity produced in a substance after bombardment with neutrons or other particles. The resulting activity is "natural radioactivity" if formed by nuclear reactions occurring in nature and "artificial radioactivity" if the reactions are caused by man. Radioactivity, Natural-The property of radioactivity exhibited by more than 50 naturally occurring radionuclides. Radioisotope-An unstable or radioactive isotope of an element that decays or disintegrates spontaneously, emitting radiation. Radiosensitivity-Relative susceptibility of cells, tissues, organs, organisms, or any living substance to the injurious action of radiation.

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Determining the precise cause and how to prevent thrombotic complications is an area of active investitreatment may be associated with severe headache, nuchal rigidity, fever, nausea, and Anaphylactic reactions induced by anti-IgA can occur rarely in patients with primary antibodies to IgA. These rare reactions have been reported only in patients with selecmay reduce the likelihood of further reactions. Headache, fever, chills, sinus tenderness, cough, mild hypotension Slow the infusion until symptoms resolve. After infusion Headache Myalgia/malaise a recipient, but the etiology of such reactions is uncertain. The most common systemic 2 weeks to minimize adverse effects and enhance adherence to the treatment regimen. Specific Immune Globulins may differ in number of donors whose plasma is included in the pool from which the product is prepared. These animal-derived immunoglobulin products are referred to here as "serum" for convenience. Some, but not all, products are subjected to an enzyme digestion process to decrease clinical reactions to administered foreign proteins. Antibody-containing products prepared from animal sera pose a special risk to the recipient, and the use of such products should be limited strictly to certain indications of asthma, allergic rhinitis, or urticaria after previous exposure to animals or injections of animal sera. Patients with a history of asthma or allergic symptoms, especially from products with the utmost caution. People who previously have received animal sera are at increased risk of developing acute allergic reactions and serum sickness after administration of sera from the same animal species. Emergency access to experts in diagnostics, decision making, serum procurement, testing for preexisting sensitivity, desensitization, and serum administration are availBotulism and Infant Botulism [p 294], Diphtheria [p 325]). Of these, only anaphylaxis is mediated by IgE antibodies, and thus, occurrence may be predicted by skin testing results. Anaphylaxis usually begins within minutes of exposure to the causative agent, and in general, the more rapid the onset, the more severe the overall course. Major Any symptom of an IgE-mediated reaction is reason to terminate administration of the serum and to reassess the need for and the method of administration of the animal antibody. If the antibody is needed, desensitization may be initiated once the patient has been stabilized. Severe febrile reactions should be treated with antipyretic agents or other safe, available methods to physically decrease temperature. Manifestations, which usually begin 7 to 10 days (occasionally as late as 3 weeks) after primary exposure to the foreign protein, consist of fever, urticaria, or a maculopapular rash (90% of cases); arthritis or arthralgia; and lymphadenopathy. However, serum sickness may be mild and may resolve spontaneously within a few days to 2 weeks. People who previously have received serum injections are at increased risk after readministration; manifestations in these patients usually occur shortly (from hours to 3 days) after administration of serum. Antihistamines can be helpful for management of serum sickness for alleviation of pruritus, edema, and urticaria. Fever, malaise, arthralgia, and arthritis can be controlled in controlled by other agents; prednisone or prednisolone in therapeutic dosages (1. Treatment of Anaphylactic Reactions Health care professionals administering biologic products or serum must be able to recogtent staff necessary to maintain the patency of the airway and to manage cardiovascular collapse must be available. Mild manifestations, such as skin reactions alone (eg, pruritus, erythema, urticaria, or angioedema), may be gerous and can be treated with antihistamines (Table 1. However, using clinical judgment, an injection of epinephrine may be given depending on the clinical situation (Table 1. Epinephrine should be injected promptly (eg, goal of <4 minutes) for anaphylaxis, which is likely (although not exclusively) occurring if the patient has 2 or swollen lips/tongue/uvula); (2) respiratory compromise (dyspnea, wheeze, bronchospasm, stridor, or hypoxemia); (3) low blood pressure; or (4) gastrointestinal tract involvement (eg, persistent crampy abdominal pain or vomiting). If a patient is known to have had a previous severe allergic reaction to the biologic product/serum, onset of skin, cardiovascular, or respiratory symptoms alone may warrant treatment with epinephrine. Use of readily available commercial epinephrine autoinjectors (available in 2 dosages by weight) and epinephrine is administered intramuscularly every 5 to 15 minutes, as necessary, to control symptoms and maintain blood pressure. If agent causing anaphylactic reaction was given by injection, epinephrine can be injected into the same site to slow absorption. Maintenance of the airway and administration of oxygen should be instituted promptly. Severe or potentially life-threatening systemic anaphylaxis involving severe bronchospasm, laryngeal edema, other airway compromise, shock, and cardiovascular collapse necessitates additional therapy. Administration of epinephrine intravenously can lead to lethal arrhythmia; cardiac monitoring is recommended. A slow, continuous, low-dose infusion is preferable to repeated bolus administration, because the dose can be titrated to the desired effect, and accidental administration of large boluses of epinephrine can be avoided. Corticosteroids should be used in all cases of anaphylaxis except cases that are mild and have responded promptly to initial therapy (see Table 1. However, no data support the usefulness of corticosteroids alone in treating anaphylaxis, and therefore they should not be administered in lieu of treatment with epinephrine and should be considered as adjunctive therapy. All patients showing signs and symptoms of systemic anaphylaxis, regardless of severity, should be observed for several hours in an appropriate facility, even after remission of immediate symptoms. Anaphylactic reactions can be uniphasic, biphasic, or protracted of observation has not been established, a reasonable period of observation would be 4 hours for a mild episode and as long as 24 hours for a severe episode. More aggressive therapy with epinephrine may override receptor blockade in some patients. Although studies have shown decreased immune responses to several vaccines given to neonates with very low birth weight (less than 1500 g) and neonates of very early gestational age (less than 29 weeks of gestation), most preterm infants, vaccine-induced immunity to prevent disease. Vaccine dosages given to term infants should not be reduced or divided when given to preterm or low birth weight infants. Preterm and low birth weight infants tolerate most childhood vaccines as well as do term infants. However, these postimmunization cardiorespiratory events do not appear to have a detrimental effect on the clinical course of immunized infants. Medically stable preterm infants who remain in the hospital at 2 months of chronologic age should be given all inactivated vaccines recommended at that age (see Recommended Immunization Schedule for Persons Aged 0 Through 18 Years [redbook. A medically stable infant bolic disease; or acute renal, cardiovascular, neurologic, or respiratory tract illness and who demonstrates a clinical course of sustained recovery and a pattern of steady growth. All or low birth weight infants, except for oral rotavirus vaccine, which should be deferred until the infant is being discharged from the hospital (see Rotavirus, p 684) to prevent the potential nosocomial spread of this live vaccine virus. The same volume of vaccine used for term infants is appropriate for medically stable preterm infants. The number of injections of other vaccines at 2 months of age can be minimized by using combination vaccines. When because of limited injection sites, the vaccines recommended at 2 months of age can be administered at different times. Because recommended parenteral vaccines are inactivated, any interval between doses of individual vaccines is acceptable. However, to avoid superimposing local reactions, 2-week intervals may be reasonable. The choice of needle lengths used for intramuscular vaccine administration is determined by available muscle mass of the preterm or low birth weight infant (see Table 1. Revalidation of the Score for Neonatal Acute Physiology in the Vermont Oxford Network. Only monovalent hepatitis B vaccine should be used for preterm or term infants younger than 6 weeks. Administration of a total of 4 doses of hepatitis B vaccine is permitted when a combination vaccine containing hepatitis B vaccine is administered after the birth dose. Tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis (Tdap) vaccine should be administered to all pregnant women (optimally between weeks 27 and 36 of gestation to yield high antibody levels in the infant) during every pregnancy.

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Therefore demonstrative studies have revealed a range of facets that allows the bacteria to cause oral manifestations. Conclusion Dental microbial communities are highly diverse and comprises of a range of microorganisms whose behavior depends on the oral ecosystem. Microbial communities affiliated with the dental biofilms are capable of exhibiting evolving features from the context of the microorganisms. In simple terms the microbial communities with the dental biofilms flaunts emergent aspects which is a consequence of a collaborative effort rather than individual organism. Hence is would not be appropriate to infer the characteristics of these microbial cities (biofilms) based on the characters of an individual organism. The extent of survival rates of the organism relies on its ability to interact which could also be a factor for the onset of oral manifestations. Sucrose has been disclosed as one of the main substrates for the organism to survive but lactose has also been highlighted by certain studies. However further analysis is required to have a deep seated comprehension on facets like microbial interaction within the biofilms and the prominence of molecular entities. University of South Carolina School of Medicine: Microbiology and Immunology; 2010. The Role of Streptococcus mutans & Oral Ecology in the Formation of Dental Caries. Will new generations of modified antimicrobial peptides improve their potential as pharmaceuticals? Molecular basis for the association of glucosyltransferases with the cell surface of oral streptococci. Sequence analysis of the gene for the glucan-binding protein of Streptococcus mutans Ingbritt. Role of the Streptococcus mutans gtf genes in caries induction in the specific-pathogen-free rat model. Microbial protection and virulence in periodontal tissue as a function of polymicrobial communities: symbiosis and dysbiosis. Differential response of Streptococcus mutans towards friend and foe in mixed-species cultures. Humoral immune responses in gingival crevice fluid: local and systemic implications. Cariogenicity of Streptococcus mutans V403 glucosyltransferase and fructosyltransferase mutants constructed by allelic exchange. Molecular analysis of a Streptococcus mutans strain exhibiting polymorphism in the tandem gtfB and gtfC genes. Fungal-bacterial interactions and their relevance to oral health: linking the clinic and the bench. Purpose for Submission: To obtain a Substantial Equivalence determination for the for the Xpert Xpress Strep A test performed on the GeneXpert Xpress System. Intended use(s): the Xpert Xpress Strep A test, performed on the GeneXpert Xpress Systems, is a rapid, qualitative in vitro diagnostic test for the detection of Streptococcus pyogenes (Group A b-hemolytic Streptococcus, Strep A) in throat swab specimens from patients with signs and symptoms of pharyngitis. The Xpert Xpress Strep A test can be used as an aid in the diagnosis of patients with signs and symptoms of pharyngitis. The performance of the Xpert Xpress Strep A test was evaluated using the procedures provided in this package insert only. The sample is mixed by shaking and 300ul of is added to the Xpert Xpress Strep A cartridge using a disposable transfer pipette. The Xpert Xpress Strep A results are interpreted by the GeneXpert Xpress software from measured fluorescent signals and are shown in the "Test Result" screen. The Xpert Xpress Strep A test can be used as an aid in the diagnosis of Group A Streptococcal pharyngitis. The assay is not intended to monitor treatment for Group A Streptococcus infections. Analyte Measurand Specimen Type Reagent Format Assay Format Process Control External Controls Detection Technique Assay Result Group A Streptococcus Conserved region of S. Same Same Same Same Same Same Same Same Same 4 Item Instrument System Differences Device (K173398) Xpert Xpress Strep A GeneXpert Xpress, GeneXpert Dx, GeneXpert Infinity-48s or GeneXpert Infinity-80 instrument systems Mechanical (sonication) ~24 minutes without early assay termination; ~18 minutes with early assay termination for positive samples Yes (for positive samples) Predicate (K141338) Liat Strep A Assay Liat Analyzer Bacterial Lysis Time-to-result Chaotrope and enzymatic digestion ~15 minutes Early Assay termination function No K. Each cartridge contains primers and probes for detection of the targeted region of the S. The operator then initiates the test from the operator interface and loads the cartridge into the GeneXpert instrument, after which all process steps are performed automatically. The Xpert Xpress Strep A Assay has an Early Termination Feature whereby results for samples that are strongly positive for S. Analytical performance: Analytical studies for the Xpert Xpress Strep A Assay were described in submission K172126 that was cleared on September 25, 2017. No changes have been made to the design of the Xpert Xpress Strep A Assay since the 510(k) clearance of K172126. For this submission the data from all analytical studies (except Reproducibility study) is identical to those conducted in support of K172126 clearance. Precision/Reproducibility: A multi-center study was conducted at three sites with three operators at each site. Each operator tested blinded panel twice per day over 5 testing days ( 3 operators x 2 times/day x 5 days x 3 sites=90 results). Three lots of Xpress Strep A Assay reagent were used in this study but only two lots of reagents were used at each testing site. All of the 13 initially indeterminate cases were retested (per the assay instruction) and yielded valid results upon repeat testing. Reproducibility Results Data Site 1 Sample Op 1 Neg Strep A Hig High Neg Strep A Low Pos 100% (10/10) 70% (7/10) 100% (10/10) Op 2 100% (10/10) 100% (10/10) 100% (10/10) Op 3 100% (10/10) 100% (10/10) 90. A total of 91% of high negative produced negative results (82/90) A total of 97% of the low positive produced positive results (87/90) A total of 100% of all moderate positive samples produced a positive result (90/90). Traceability, Stability, Expected values (controls, calibrators, or methods): No additional studies were performed. For studies and performance of the following, please refer to submission K172126: Traceability, Calibrator, Controls and Carry Over. Additional information was provided for Specimen Stability, Reagent Stability and Cartridge Hold Time Stability: Stability studies have been performed in K172126 to support the following claims: Specimen Stability: the following specimen stability claims are supported by study data from K172126. Detection limit: For detection limit and Analytical Reactivity/Inclusivity studies, please refer to submission K172126. Analytical specificity: For analytical specificity and Carry-over Contamination studies, please refer to submission K172126. Assay interference: For Interfering Substances Microbial Interference studies, please refer to submission K172126. Frozen Cell Stock Equivalency and Comparison of Performance of Natural versus Simulated Matrices studies, please refer to submission K172126. Clinical Sensitivity and Specificity: 9 the performance of the Xpert Xpress Strep A Assay was conducted at a total of nine (9) clinical sites in the U. The performance of the Xpert Xpress Strep A Assay was determined relative to the reference culture. Xpert Xpress Strep A Assay testing and the reference culture method were performed within 48 hours of specimen collection. Isolated colonies that exhibited b-hemolysis were typed by latex agglutination (Remel Streptex). Culture plates that did not exhibit b-hemolytic colonies after 48 hours were recorded as negative for Group A Streptococcus. A total of 666 specimens were collected from individual subjects initially enrolled in this clinical study. Of the 666 specimen, 43 specimen were excluded because of: lack of consent documents (10), previously enrolled subject (1), delay in shipment for reference culture testing (27), indeterminate culture results (4), and incorrect specimen type (1). A total of 618 specimens were therefore included in the final evaluable data for analysis of performance. The results were compared to culture and latex agglutination for Strep A typing (Table 5). Expert Xpress Strep A Assay Clinical Performance vs Reference Culture Reference Culture Positive Positive Xpert Xpress Strep A Sensitivity Specificity Positive Predictive Value Negative Predictive Value Prevalence Negative Total 157 13 158 Negative 27 1 Total 184 434 6182 433 460 99.

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During the acute phase, patients with major depressive disorder may be poorly motivated, unduly pessimistic about their chances of recovery with treatment, suffering from deficits in memory, or poorly caring for themselves. Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition maintenance phase, euthymic patients may undervalue the benefits of and focus on the burdens of treatment. The psychiatrist should recognize these possibilities, emphasize the importance of adherence for successful treatment and prophylaxis, and encourage the patient to articulate any concerns regarding adherence. Patient and family attitudes about depression and its treatment can also influence adherence. Family members can play an important role in promoting optimism about treatment, assisting patients with adherence and providing the psychiatrist with input on side effects or other treatment-related concerns that may influence adherence. For example, patients in psychotherapy may experience increased anxiety as they confront fearful or difficult topics. This anxiety, in turn, may decrease adherence to psychotherapy, and patients may begin to arrive late to or miss therapy sessions. In patients who are beginning treatment with a medication, common side effects of medication options should be discussed. Patients should be involved in treatment decisions and encouraged to convey input on side effects that they consider reasonable or unbearable. Side effects such as weight gain, cognitive dulling, sexual side effects, sedation or fatigue, and agitation may represent different burdens to different individuals. Emphasizing the following specific topics improves adherence: 1) explaining when and how often to take the medicine; 2) suggesting reminder systems, such as pill boxes, alarms, etc. Behavioral tailoring, which involves developing an individualized approach to incorporating medication into the daily routine and can also include simplifying the medication regimen, has demonstrated efficacy for individuals with schizophrenia and may also be applicable to individuals with other psychiatric illnesses (54). Adherence may also be improved by minimizing the cost and complexity of medication regimens. Most antidepressant medications are available in generic forms, which are generally less costly. For individuals who cannot afford needed medications, some pharmaceutical companies offer patient assistance programs. Information on such programs is available from pharmaceutical company Web sites, from the Web site of the Partnership for Prescription Assistance 29. Provide education to the patient and the family Education concerning major depressive disorder and its treatments should be provided to all patients. Specific topics to discuss may include that major depressive disorder is a medical illness and that effective treatments are both necessary and available. This information may be especially important for patients who attribute their illness to a moral defect, or for family members who are convinced that there is nothing wrong with the patient. Education regarding available treatment options will help patients make informed decisions, anticipate side effects, and adhere to treatments. Patients with depression can become easily discouraged in treatment, especially if there is less than a full initial response. The psychiatrist should encourage and educate patients to distinguish between the hopelessness that is a symptom of depression and the relatively hopeful actual prognosis. Given the chronic, episodic nature of major depressive disorder, exacerbations are common. Patients, as well as their families, if appropriate, should be instructed about the significant risk of relapse. They should be educated to identify early signs and symptoms of new episodes and the stressors that may precede them. Patients should also be instructed to seek adequate treatment as early in the course of the new episode as possible to decrease the likelihood of a full-blown exacerbation or complications. Patient and family education also includes general promotion of healthy behaviors such as good sleep hygiene and decreased use of caffeine, tobacco, alcohol, and other potentially deleterious substances. Regular exercise may also reduce the prevalence of depressive symptoms in the general population, with specific benefit found in older adults (64, 65) and individuals with co-occurring medical problems (57, 66). In addition, patients who have had a history of only partial response to adequate trials of single treatment modalities may benefit from combined treatment. Poor adherence with pharmacotherapy may also warrant combined treatment with medications and psychotherapy focused on treatment adherence. Electroconvulsive therapy should be considered as a potential treatment option for all patients with major depressive disorder who have psychotic features or catatonia and for those with an urgent need for response, such as patients who are suicidal or who are nutritionally compromised as a result of refusing food. Electroconvulsive therapy may also be the treatment modality of choice for patients with major depressive disorder who have a high degree of symptom severity. The dose of exercise and adherence to an exercise regimen may be particularly important to monitor in the assessment of whether an exercise intervention is useful for major depressive disorder (69, 70). If mood fails to improve after a few weeks with exercise alone, the psychiatrist should recommend medication or psychotherapy. For patients with depression of any severity and no medical contraindication to exercise, physical activity is a reasonable addition to a treatment plan for major depressive disorder. Psychiatrists should present patients with information concerning the evidence for a broad range of treatment options, including somatic therapies and psychosocial interventions. Antidepressant medications can be used as an initial treatment modality by patients with mild, moderate, or severe major depressive disorder. Clinical features that may suggest that medications are the preferred treatment modality include a history of prior positive response to antidepressant medications, the presence of moderate to severe symptoms, significant sleep or appetite disturbances, agitation, patient preference, and anticipation of the need for maintenance therapy. Psychotherapy may also be considered as monotherapy for patients with mild to moderate major depressive disorder. The availability of clinicians with appropriate training and expertise in specific psychotherapeutic approaches can be a factor in choosing a psychotherapy (67). Specifically, many severely depressed patients will require both a depression-focused psychotherapy and a somatic treatment such as pharmacotherapy. Given the lower occurrence of side effects and suggestion of enduring benefits associated with depression-focused psychotherapies (68), such treatments might be preferable alternatives to pharmacotherapy for some patients with mild to moderate depression. Recommended Modalities for Acute Phase Treatment of Major Depressive Disorder sexual effects, sedation, or weight gain. Therefore, the initial selection of an antidepressant medication will largely be based on the tolerability, safety, and cost of the medication, as well as patient preference and history of prior medication treatment (Table 3). Other factors include the medication half-life and potential for drug interactions related to properties such as plasma protein binding or metabolism through the cytochrome P450 system (Tables 4 and 5). Table 6 provides the starting and usual doses of medications that have been shown to be effective for treating major depressive disorder. Although some studies have suggested superiority of one mechanism of action over another, there are no replicable or robust findings to establish a clinically meaningful difference. For most patients, the effectiveness of antidepressant medications is generally comparable between classes and within classes of medications. Although remission rates are less robust and selective publication of positive studies could affect the apparent effectiveness of treatment (74, 75), these factors do not appear specific to particular medications or medication classes. Factors to Consider in Choosing an Antidepressant Medication Patient preference Nature of prior response to medication Relative efficacy and effectiveness Safety, tolerability, and anticipated side effects Co-occurring psychiatric or general medical conditions Potential drug interactions Half-life Cost Copyright 2010, American Psychiatric Association. The extent to which each medication is a substrate for a specific enzyme is indicated as follows: +++ = exclusive substrate, ++ = major substrate, + = minor substrate. The presence of co-occurring psychiatric or general medical conditions can be a significant factor influencing the choice of an antidepressant medication. Patients who are receiving tamoxifen for breast cancer or other indications should generally be treated with an antidepressant. Cytochrome P450 Enzyme Inhibition by Antidepressive Agents 1A2 Amitriptyline Bupropion Citalopram Desipramine Duloxetine Escitalopram Fluoxetine c Norfluoxetine Imipramine Mirtazapine Nortriptyline Paroxetine Selegiline Sertraline Desmethylsertralinec Venlafaxine d b 33 a 2A6 2B6 2C8 2C9 + 2C19 2D6 2E1 + 3A4 + + ++ + ++ +++ + + ++ + ++ + ++ ++ ++ + + + ++ + + + + ++ + + + +++ + + + + + + ++ + +++ + ++ + + + + ++ ++ ++ + + ++ + +++ ++ + + + + + ++ + + ++ + + Desvenlafaxine Sources: (82, 83). The extent to which each medication is a substrate for a specific enzyme is indicated as follows: +++ = strong inhibitor, ++ = moderate inhibitor, + = weak inhibitor. The information in this table can serve as a guide; however, the reader is encouraged to access regularly updated online sources of drug-drug interactions. Selective serotonin reuptake inhibitors Selective serotonin reuptake inhibitors currently available include fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, and escitalopram. Serotonin norepinephrine reuptake inhibitors the serotonin norepinephrine reuptake inhibitors currently available are venlafaxine, desvenlafaxine (the principal metabolite of venlafaxine), and duloxetine.

References:

  • http://www.dartmouth.edu/sport-trial/08022106.pdf
  • http://www.advocatedocs.com/wp-content/uploads/2018/04/Advances-in-Pediatrics-Managing-Anxiety-and-Depression-in-Children-Adolescents.pdf
  • https://feetmd.com/wp-content/uploads/2018/08/11.-Watson-2009-Proximal-First-Metatarsal-Opening-Wedge-Osteotomy-with-a-Low-Profile-Plate.pdf
  • https://www.ventegra.com/medpolicies/Medication%20Policy_Provigil.pdf