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Treatment of patients with multiple myeloma who have received at least two prior therapies managing gestational diabetes during labor buy generic repaglinide 1mg, including bortezomib and an immunomodulatory agent diabetes y sus complicaciones buy generic repaglinide 1mg line. Clinical benefit metabolic disease of the brain cheap 2mg repaglinide with amex, such as improvement in survival or symptoms diabetes mellitus type 2 diet buy repaglinide 0.5mg with visa, has not been verified. Premedication with dexamethasone may reduce the incidence and severity of reaction. Seek medical advice if dizziness, light-headedness, or fainting spells are experienced. Maternal/Child: Category D: can cause fetal harm when administered to a pregnant woman. Elderly: Differences in safety and efficacy between patients less than 65 years of age and patients 65 years of age and older have not been identified. Most commonly reported adverse reactions are anemia, diarrhea, dyspnea, fatigue, fever, nausea, and thrombocytopenia. The most common serious adverse reactions are acute renal failure, congestive heart failure, fever, and pneumonia. Other adverse reactions reported in at least 10% of patients include anorexia, arthralgia, asthenia, back pain, chest wall pain, chills, constipation, cough, dizziness, edema (peripheral), elevated aspartate aminotransferase, elevated serum creatinine, headache, hypercalcemia, hyperglycemia, hypertension, hypoesthesia, hypokalemia, hypomagnesemia, hyponatremia, hypophosphatemia, insomnia, leukopenia, lymphopenia, muscle spasm, neutropenia, pain, peripheral neuropathy, upper respiratory tract infection, and vomiting. May be given as a single dose, or one half of the calculated dose may be given initially and repeated the next day. Repeat course should not be administered until leukocytes are above 4,000/mm3 and platelets are above 100,000/mm3. Repeat doses adjusted according to hematologic response of previous dose (see Dose Adjustments). Dose adjustments must be considered based on the nadir blood counts from the prior dose according to the following chart. Carmustine Dose Adjustment Based on Bone Marrow Suppression Nadir After Prior Dose Leukocytes/mm3 $4,000 3,000-3,999 2,000-2,999,2,000 Platelets/mm3 $100,000 75,000-99,999 25,000-74,999,25,000 Percentage of Prior Dose to Be Given % 100% 100% 70% 50% Adjust doses accordingly when carmustine is used in combination with other myelosuppressive drugs or in patients with depleted bone marrow reserve. Initially dilute 100-mg vial with supplied sterile diluent (3 mL of dehydrated alcohol injection). Withdraw desired dose and further dilute in 100 mL or more of D5W and give as an infusion. Filters: No significant loss of potency with any size cellular ester membrane filter when reconstituted or diluted as recommended. Manufacturer lists as incompatible with polyvinyl chloride infusion bags; use only glass containers. One source suggests the following compatibilities: Y-site: Amifostine (Ethyol), aztreonam (Azactam), etoposide phosphate (Etopophos), filgrastim (Neupogen), fludarabine (Fludara), gemcitabine (Gemzar), granisetron (Kytril), melphalan (Alkeran), ondansetron (Zofran), piperacillin/tazobactam (Zosyn), sargramostim (Leukine), teniposide (Vumon), thiotepa, vinorelbine (Navelbine). Administration over fewer than 2 hours can lead to pain and burning at the injection site. Reduce rate for pain or burning at injection site, flushing of the skin, or suffusion of the conjunctiva. An alkylating agent of the nitrosourea group with anti-tumor activity, cell cycle phase nonspecific. Delayed-onset pulmonary fibrosis has occurred up to 17 years after treatment with injectable carmustine in patients who received it in childhood or early adolescence. Monitor: Determine absolute patency and quality of vein and adequate circulation of extremity. Maternal/Child: Category D: avoid pregnancy; embryotoxic and teratogenic in rats; has mutagenic potential. Risk versus benefit must be carefully considered due to a high risk of pulmonary toxicity occurring years after treatment and resulting in death. Bone marrow toxicity (especially leukopenia and thrombocytopenia) is most pronounced at 4 to 6 weeks; can be severe and cumulative with repeated dosage. Anemia, chest pain, elevated liver function test results, flushing of skin and suffusion of conjunctiva from too-rapid infusion rate, headache, hyperpigmentation and burning of skin (from actual contact with solution), hypersensitivity reactions, hypotension, nausea and vomiting, neuroretinitis, pulmonary infiltrates or fibrosis with long-term therapy, renal abnormalities, retinal hemorrhage, and tachycardia. Most will decrease in severity with reduced dosage, increased time span between doses, or symptomatic treatment. Duration of empiric therapy is based on clinical response and should continue at least until resolution of neutropenia.
Further diabetes symptoms in 6 month old generic repaglinide 0.5mg on line, the patient must avoid pregnancy during treatment and for at least 3 years after the treatment is over because of its long half life (about 120 days) treatment diabetes lady finger buy repaglinide 0.5mg fast delivery. Similarly anyone taking this drug should not diabetes history repaglinide 1 mg on-line, donate blood for 3 years after stopping it diabetes mellitus ziele cheap repaglinide 1 mg overnight delivery. Acitretin, a metabolite of etretinate, is now preferred to etretinate in therapy Its. It is preferred, in severe case with arthritis, where coal tar-U V therapy has failed. It should be used only in patients with normal hematological, renal and hepatic status. The important adverse effects are hypertension and renal toxicity which may be irreversible. The drug has also been used to treat pyoderma gangrenosum, pemphigus vulgaris and systemic vasculitis. Biological agents: Recently biological agents have been introduced in the treatment of, psoriasis (Table 71. Given parenterally they are effective in about 30-70% of patients with, moderate to severe psoriasis. It is indicatd in patients with moderate to severe plaque psoriasis who cannot take standard therapy. Hence, it should be reserved for acutely ill patients with erythrodermic psoriasis. Drug Therapy of Alopecia Alopecia is loss of hair in any region of the body the hair are of two types: vellus hair. At about the age of 8-10 years, the weak adrenal androgens cause a slight rise in the plasma testosterone level, and terminal hair appear on the forearms and legs in both boys and girls (ambisexual hair). At puberty, with the further rise in the plasma testosterone level into the adult female range, terminal hair appear in the pubic and axillary regions; these hair are also ambisexual. Boys with further advanced puberty and adult males develop terminal hair in other regions such as face and trunk (sexual hair). Further, it is responsible for the excessive loss of scalp hair in women with elevated plasma androgen levels. Hair growth is cyclic, with phases of growth (anagen), involution (catagen) and resting (telogen). In the scalp, about 80-88% of the hair are in anagen (for about 3 years), 1-2% are in catagen (for about 3 weeks) and the rest 10-20% are in telogen (for about 3 months), after which hair are shed. The growth of scalp hair is asynchronous, with hair in a given area in different phases; there is a balance among anagen, catagen and telogen hair in all regions of the scalp. A disruption of this balance causes many more hair to enter the telogen phase, and about 3 months later they are shed in bulk causing alopecia; this is called telogen effluvium. Severe stress can cause telogen effluvium; but as sudden severe hair loss occurs three months after the stressful event, the latter is likely to be forgotten. Alopecia of the scalp can be: I Scarring which is associated with inflammation, fibrosis and destruction of the hair follicles due to primary skin disorders such as lichen planus or systemic diseases such as lupus erythematosus. The other causes of non-scarring alopecia are: crash dieting, physical trauma, iron deficiency hypothyroidism, chronic malnutrition, chronic illness, androgen excess and, androgenetic alopecia. They may have other manifestations of hyperandrogenism such as menstrual abnormalities, hirsutism, acne and infertility the treatment is that of hyperandrogenism. The miniaturised hair of various lengths and diameters are the hallmark of this condition. In men, the alopecia ranges from bitemporal recession to thinning of the hair in the frontal and vertex regions to complete baldness except in the occipital and temporal regions. In women, the thinning is less severe but is maximum in the frontal and parietal regions. Endocrine testing is not required if the above described characteristic pattern of hair loss is present, and there is no evidence of hyperandrogenism. Treatment: this comprises of topical minoxidil (see below) in both sexes and oral finasteride in men (Chapter 69). The response to finasteride is better in the frontal region of the scalp, which has higher levels of 5-alpha reductase, than in the occipital region (which has higher levels of aromatase). It must be remembered that androgens cause: (a) the vellus-hair follicles to be replaced by terminal hair follicles in the region of ambosexual and sexual hair; and (b) Miniaturisation of the terminal hair follicles of the scalp.
Treatment of type 1 diabetes Typical mean blood glucose concentrations observed in insulindependent diabetics treated with: Normal mean Intensive [glucose] in insulin nondiabetic therapy individuals Percent Hemoblobin A1C 12 10 8 6 4 2 0 0 50 100 150 200 250 300 350 Mean blood [glucose] diabetes insipidus diagnostic test purchase repaglinide 0.5mg overnight delivery, mg/dl Standard insulin therapy Individuals with type 1 diabetes must rely on exogenous insulin injected subcutaneously to control the hyperglycemia and ketoacidosis diabetes type 1 breakfast ideas generic 2 mg repaglinide with amex. Two therapeutic regimens are currently in use-standard and intensive insulin treatment diabetes symptoms wikihow discount repaglinide 0.5mg without a prescription. Insulin may also be delivered by a pump diabetes type 2 vomiting 2 mg repaglinide with visa, which allows continuous subcutaneous infusion of insulin 24 hours a day at preset levels and the ability to program doses (a bolus) of insulin as needed at meal times. Many clinicians believe the increased risk of hypoglycemia that accompanies intensive therapy is justified by the substantial decrease in the incidence of long-term complications, such as diabetic retinopathy and nephropathy. Hypoglycemic episodes per 1000 patient months 100 Intensive therapy Conventional therapy ment typically consists of one or two daily injections of recombinant human insulin. Thus, HbA1C provides a measure of how well treatment has normalized blood glucose in the diabetic over that time. Mean blood glucose levels of 150 mg/dl can be achieved, with HbA1C approximately 7% of the total hemoglobin (red arrow: Figure 25. Nonetheless, patients on intensive therapy show a 50% or more reduction in the long-term microvascular complications of diabetes-retinopathy, nephropathy, and neuropathy-compared with patients receiving standard care. This confirms that the complications of diabetes are related to an elevation of plasma glucose. Hypoglycemia caused by excess insulin is the most common complication of insulin therapy, occurring in over 90% of patients. Recall that in normal individuals hypoglycemia triggers a compensatory secretion of counter-regulatory hormones, most notably glucagon and epinephrine, which promote hepatic production of glucose. However, patients with type 1 diabetes also develop a deficiency of glucagon secretion. This defect occurs early in the disease and is almost universally present 4 years after diagnosis. However, as the disease progresses, type 1 diabetes patients show diabetic autonomic neuropathy and impaired ability to secrete epinephrine in response to hypoglycemia. The combined deficiency of glucagon and epinephrine secretion creates a condition sometimes called "hypoglycemia unawareness. Exercise promotes glucose uptake into muscle and decreases the need for exogenous insulin. Patients are advised, therefore, to check blood glucose levels before or after intensive exercise to prevent or abort hypoglycemia. Elderly people typically do not go on tight control because hypoglycemia can cause strokes and heart attacks in this population. Also, the major goal of tight control is to prevent complications many years later. Tight control, then, is most worthwhile for otherwise healthy people who can expect to live at least ten more years. However, many individuals with type 2 diabetes have symptoms of polyuria and polydipsia of several weeks duration. Patients with type 2 diabetes have a combination of insulin resistance and dysfunctional cells (Figure 25. Diagnosis is based most commonly on the presence of hyperglycemia-that is, a fasting blood glucose concentration of equal to or greater than 126 mg/dl. Diabetes Mellitus Type 2 diabetes mellitus is characterized by hyperglycemia, insulin resistance, and relative impairment in insulin secretion. Insulin resistance Insulin resistance is the decreased ability of target tissues, such as liver, adipose, and muscle, to respond properly to normal (or elevated) circulating concentrations of insulin. For example, insulin resistance is characterized by uncontrolled hepatic glucose production, and decreased glucose uptake by muscle and adipose tissue. Insulin resistance and obesity: Obesity is the most common cause of insulin resistance; however, most people with obesity and insulin resistance do not become diabetic. In the absence of a defect in -cell function, nondiabetic, obese individuals can compensate for insulin resistance with elevated levels of insulin. This higher insulin concentration compensates for the diminished effect of the hormone (as a result of insulin resistance), and produces blood glucose levels similar to those observed in lean individuals (Figure 25. Insulin resistance and type 2 diabetes: Insulin resistance alone will not lead to type 2 diabetes. Rather, type 2 diabetes develops in insulin-resistant individuals who also show impaired -cell function.
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