Treatment of internalizing disorder

The evaluation and treatment of internalizing disorders in children and adolescents has a long and rich tradition in the psychology and clinical psychiatry of the child. However, the use of longitudinal data to elucidate the evolution and outcome of these conditions, as well as their assessment and treatment, is less developed in the embryonic development stage.

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Table 111-3 Long-Term Treatment with Vitamin K Antagonists for Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE) Patient Categories Duration, months Comments First episode of DVT or PE secondary to a transient (reversible) risk factor 3 Recommendation applies to both proximal and calf vein thrombosis First episode of 6–12 Continuation of idiopathic DVT or PE anticoagulant therapy after 6–12 months may be considered First episode of DVT 6–12 Continuation of or PE with a documented thrombophilic abnormality anticoagulant therapy after 6–12 months may be considered ...

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Withholding further diagnostic testing and anticoagulant treatment in those patients with an unlikely clinical probability and a normal D-dimer level, which constitutes 30–50% of all referred patients, is safe. The remaining patients need to undergo (repeated) compression ultrasonography. An alternative approach is to perform a whole-leg imaging test on the day of referral. The advantage of this approach is that it eliminates the need for a repeat test (and may even obviate the probability assessment and D-dimer testing).

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Treatment with FFP is the most effective way to correct hemostasis in patients with liver failure. Infusion of FFP (5–10 mL/kg; each bag contains ~200 mL) is sufficient to ensure 10–20% of normal levels of clotting factors but not correction of PT or aPTT. Even high doses of FFP (20 mL/kg) do not correct the clotting times in all patients.

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Factor XI Deficiency: Treatment The treatment of FXI deficiency is based on the infusion of FFP at doses of 15–20 mL/kg to maintain trough levels ranging from 10 to 20%. Because FXI has a half-life of 40–70 h, the replacement therapy can be given on alternate days. The use of antifibrinolytic drugs is beneficial to control bleeds, with the exception of hematuria or bleeds in the bladder. The development of a FXI inhibitor was observed in 10% of severely FXI-deficient patients who received replacement therapy.

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Thrombotic Thrombocytopenic Purpura TTP and HUS were previously considered overlap syndromes. However, in the past few years the pathophysiology of inherited and idiopathic TTP has become better understood and clearly differs from HUS. TTP was first described in 1924 by Eli Moschcowitz and characterized by a pentad of findings that include microangiopathic hemolytic anemia, thrombocytopenia, renal failure, neurologic findings, and fever. The full-blown syndrome is less commonly seen now, probably due to earlier diagnosis.

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Immune Thrombocytopenic Purpura: Treatment The treatment of ITP utilizes drugs that decrease reticuloendothelial uptake of the antibody-bound platelet and/or decrease antibody production. However, the diagnosis of ITP does not necessarily mean that treatment must be instituted. Patients with platelet counts 30,000/µL appear not to have increased mortality related to the thrombocytopenia.

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Approach to the Patient: Thrombocytopenia The history and physical examination, results of the CBC, and review of the peripheral blood smear are all critical components in the initial evaluation of the thrombocytopenic patients (Fig. 109-2). The overall health of the patient and whether he/she is receiving drug treatment will influence the differential diagnosis. A healthy young adult with thrombocytopenia will have a much more limited differential diagnosis than an ill hospitalized patient who is receiving multiple medications.

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Pneumocystis jiroveci pneumonia, once seen in 5–10% of patients, can be prevented by treating patients with oral trimethoprim-sulfamethoxazole for 1 week pretransplant and resuming the treatment once patients have engrafted. The risk of infection diminishes considerably beyond 3 months after transplant unless chronic Most GVHD transplant develops, centers requiring recommend continuous continuing immunosuppression. trimethoprim-sulfamethoxazole prophylaxis while patients are receiving any immunosuppressive drugs and also recommend careful monitoring for late CMV reactivation.

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Anaplastic Large T/Null Cell Lymphoma: Treatment Treatment regimens appropriate for other aggressive lymphomas, such as diffuse large B cell lymphoma, should be utilized in patients with anaplastic large T/null cell lymphoma, with the exception that the B cell–specific antibody, rituximab, is omitted. Surprisingly, given the anaplastic appearance, this disorder has the best survival rate of any aggressive lymphoma. The 5-year survival is 75%.

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B Cell Chronic Lymphoid Leukemia/Small Lymphocytic Lymphoma: Treatment Patients whose presentation is typical B cell CLL with no manifestations of the disease other than bone marrow involvement and lymphocytosis (i.e., Rai stage O and Binet stage A; Table 105-7) can be followed without specific therapy for their malignancy. These patients have a median survival 10 years, and some will never require therapy for this disorder.

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Clinical Features, Treatment, and Prognosis of Specific Lymphoid Malignancies Precursor Cell B Cell Neoplasms Precursor B Cell Lymphoblastic Leukemia/Lymphoma The most common cancer in childhood is B cell ALL. Although this disorder can also present as a lymphoma in either adults or children, presentation as lymphoma is rare. The malignant cells in patients with precursor B cell lymphoblastic leukemia are most commonly of pre-B cell origin.

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Harrison's Internal Medicine Chapter 100. Megaloblastic Anemias Megaloblastic Anemias: Introduction The megaloblastic anemias are a group of disorders characterized by the presence of distinctive morphologic appearances of the developing red cells in the bone marrow. The cause is usually deficiency of either cobalamin (vitamin B 12) or folate, but megaloblastic anemia may arise because of genetic or acquired abnormalities affecting the metabolism of these vitamins or because of defects in DNA synthesis not related to cobalamin or folate (Table 100-1).

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Disease-Specific Nutritional Support SNS is basically a support therapy and is primary therapy only for the treatment or prevention of malnutrition. Certain conditions require modification of nutritional support because of organ or system impairment. For instance, in nitrogen accumulation disorders, protein intake may need to be reduced. However, in renal disease, except for brief periods of several days, protein intakes should approach requirement levels of at least 0.8 g/kg or higher up to 1.2 g/kg as long as the blood urea nitrogen does not exceed 100 mg/dL.

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Harrison's Internal Medicine Chapter 64. The Practice of Genetics in Clinical Medicine Implications of Molecular Genetics for Internal Medicine The field of medical genetics has traditionally focused on chromosomal abnormalities (Chap. 63) and Mendelian disorders (Chap. 62). However, there is genetic susceptibility to many common adult-onset diseases, including atherosclerosis, cardiac disorders, asthma, hypertension, autoimmune diseases, diabetes mellitus, macular degeneration, Alzheimer's disease, psychiatric disorders, and many forms of cancer.

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Most patients with trichotillomania, pressure-induced alopecia. The most common causes of nonscarring alopecia include telogen effluvium, androgenetic alopecia, alopecia areata, tinea capitis, and some cases of traumatic alopecia (Table 54-5). In women with androgenetic alopecia, an elevation in circulating levels of androgens may be seen as a result of ovarian or adrenal gland dysfunction. When there are signs of virilization, such as a deepened voice and enlarged clitoris, the possibility of an ovarian or adrenal gland tumor should be considered.

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Ecthyma is a variant of impetigo that causes punched-out ulcerative lesions. It may result from neglected or inadequately treated impetigo. Treatment of both ecthyma and impetigo involves gentle debridement of adherent crusts, which is facilitated by the use of soaks and topical antibiotics, in conjunction with appropriate oral antibiotics. Furunculosis is also caused by S. aureus, and this disorder has gained prominence in the last decade because of CA-MRSA. A furuncle, or boil, is a painful, erythematous, nodule that can occur on any cutaneous surface.

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The evidence implicating psoriasis as a T cell–mediated disorder has directed therapeutic efforts to immunoregulation. Cyclosporine and other immunosuppressive agents can be very effective in the treatment of psoriasis, and much attention is currently directed toward the development of biologic agents with more selective immunosuppressive properties and better safety profiles (Table 53-4). Experience with these agents is limited and information regarding combination therapy and adverse events continues to emerge.

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Lichen Simplex Chronicus Lichen simplex chronicus may represent the end stage of a variety of pruritic and eczematous disorders, including atopic dermatitis. It consists of a circumscribed plaque or plaques of lichenified skin (thickening of the skin and accentuation of normal skin markings) due to chronic scratching or rubbing. Common areas involved include the posterior nuchal region, dorsum of the feet, and ankles. Treatment of lichen simplex chronicus centers on breaking the cycle of chronic itching and scratching.

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Polycystic Ovarian Syndrome: Treatment The major abnormality in patients with PCOS is the failure of regular, predictable ovulation. Thus, these patients are at risk for the development of dysfunctional bleeding and endometrial hyperplasia associated with unopposed estrogen exposure. Endometrial protection can be achieved with the use of oral contraceptives or progestins (medroxyprogesterone acetate, 5–10 mg, or prometrium, 200 mg daily for 10–14 days of each month).

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