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Precocious puberty: بلوغ زودرس: Precocious puberty is traditionally defined as the onset of secondary sexual development before the age of eight years in females and nine years in males. Because of trends towards earlier pubertal development, some healthy females will have breast or pubic hair development before this age, and extensive evaluation and treatment may not be required. If the evaluation leads to a diagnosis of progressive precocious puberty, treatment may be considered. Precocious puberty can be classified based upon the underlying pathologic process. ●Central precocious puberty – Central precocious puberty (CPP, also known as gonadotropin-dependent precocious puberty or true precocious puberty) is caused by early maturation of the hypothalamic-pituitary-gonadal axis. It is characterized by sequential maturation of breasts and pubic hair in females, and of maturation of the testes, penis, and pubic hair in males. The sexual characteristics are appropriate for the child's sex (isosexual). CPP is idiopathic in 80 to 90 percent of cases in females, whereas intracranial lesions are detected in 20 to 75 percent of males with CPP . ●Peripheral precocity – Peripheral precocity (also known as gonadotropin-independent precocious puberty or peripheral precocious puberty) is caused by excess secretion of sex hormones (estrogens or androgens) derived either from the gonads or adrenal glands, exogenous sources of sex steroids, or ectopic production of gonadotropins from a germ cell tumor (eg, human chorionic gonadotropin [hCG]) . We use the term precocity instead of puberty because puberty implies activation of the hypothalamic-pituitary-gonadal axis, as occurs in CPP, whereas precocity refers only to the secondary sexual characteristics. Peripheral precocity is most commonly either isosexual (concordant with the child's sex), or contrasexual (with virilization of females and feminization of males), but can also present with both virilizing and feminizing features in rare cases. Benign or nonprogressive pubertal variants – Benign pubertal variants include isolated breast development in females (premature thelarche) or isolated androgen-mediated sexual characteristics (such as pubic and/or axillary hair, acne, and apocrine odor) in males or females that result from early activation of the hypothalamic-pituitary-adrenal axis (premature adrenarche) . Both of these conditions can be a variant of normal puberty. However, repeat evaluations may be warranted in these children to be certain that the diagnosis is correct. اپتودیت #Precocious_puberty #بلوغ_زودرس تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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دختر ۱۴ ساله ساکن ناحيه سياهو بندرعباس با این عقرب گادیم که زرد رنگ است گزیده شده است. نکروز وسیع بیمار ۱۰ روز بعد گزش را مشاهده مینمایید! 🩻کانال تصاویر زیبایی پزشکی جهان JoIN➣ @Med_anatomy JoIN➣ @Med_anatomy
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Treatment of Hymenolepis nana Infection: Praziquantel Alternatively, nitazoxanide or, outside the United States, niclosamide The treatment of choice for H. nana infection is Praziquantel 25 mg/kg orally once Alternatives include nitazoxanide and niclosamide (not available in the United States). For nitazoxanide, dosage is For patients > 11 years: 500 mg orally 2 times a day for 3 days For children aged 4 to 11 years: 200 mg orally 2 times a day for 3 days For children aged 1 to 4 years: 100 mg orally 2 times a day for 3 days For niclosamide, dosage is For adults: 2 g orally once/day for 7 days For children > 34 kg: 1.5 g in a single dose on day 1, then 1 g once/day for 6 days For children 11 to 34 kg: 1 g in a single dose on day 1, then 500 mg once/day for 6 days A stool sample should be repeated one month after therapy is completed to verify cure. CDC تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Common conditions with abnormal liver biochemical tests. تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Common conditions with abnormal biochemical tests. تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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اپیزود بررسی بیمار، شماره‌ی دوم: بررسی بیمار با شکایات متعدد، با هم‌راهی دکتر مهدیه جعفری @emipcast
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Current Therapeutic Options for the Main Monogenic Autoinflammatory Diseases and PFAPA Syndrome: The most extensively studied and better pathogenically defined monogenic autoinflammatory conditions have been familial Mediterranean fever (FMF) , tumor necrosis factor (TNF) receptor–associated periodic fever syndrome (TRAPS), hyperimmunoglobulin D syndrome/mevalonate kinase deficiency (HIDS/MKD), and cryopyrin-associated periodic syndromes (CAPS), which comprise three disorders with the same genetic background, and different phenotypes and outcomes. The CAPS spectrum includes familial cold autoinflammatory syndrome (FCAS), the mildest form; Muckle-Wells syndrome (MWS), the intermediate presentation; and chronic infantile neurological, cutaneous, and articular syndrome (CINCA) or neonatal-onset multisystem inflammatory disorder (NOMID), the most severe disease . Until the late 1990s, traditional drugs, such as colchicine and glucocorticoids, had been used to treat autoinflammatory diseases. The pathogenic and therapeutic revolution started when NLRP3, one of the NOD-like receptors (NLRs) and part of the NLRP3 inflammasome, was discovered as the main actor in the activation of caspase 1 and the subsequent production of active interleukin 1β (IL-1β) . Mutations of genes involved in the inflammasome function or its related pathways were then identified as responsible for most of the monogenic autoinflammatory disorders recognized so far, also known as inflammasomopathies . The discovery of the aberrant production of IL-1β as the final cause of all inflammasomopathies led to the introduction of anti–IL-1 agents and other biologic drugs to the very limited therapeutic armamentarium available for such diseases until then . In addition, the more recent knowledge of other autoinflammatory mechanisms, such as the activation of nuclear factor κB (NF-κB) and type I interferon (IFN) pathways, also provided new therapeutic options, such as anti-TNF and Janu درs kinase (JAK) inhibitors agents, directed to the specific blockade of cytokines and molecules involved in these novel inflammatory mechanisms . Frontiers Front. Immunol., 03 June 2020 تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Precocious puberty: بلوغ زودرس: Precocious puberty is traditionally defined as the onset of secondary sexual development before the age of eight years in females and nine years in males. Because of trends towards earlier pubertal development, some healthy females will have breast or pubic hair development before this age, and extensive evaluation and treatment may not be required. If the evaluation leads to a diagnosis of progressive precocious puberty, treatment may be considered. Precocious puberty can be classified based upon the underlying pathologic process.Central precocious puberty – Central precocious puberty (CPP, also known as gonadotropin-dependent precocious puberty or true precocious puberty) is caused by early maturation of the hypothalamic-pituitary-gonadal axis. It is characterized by sequential maturation of breasts and pubic hair in females, and of maturation of the testes, penis, and pubic hair in males. The sexual characteristics are appropriate for the child's sex (isosexual). CPP is idiopathic in 80 to 90 percent of cases in females, whereas intracranial lesions are detected in 20 to 75 percent of males with CPP .Peripheral precocity – Peripheral precocity (also known as gonadotropin-independent precocious puberty or peripheral precocious puberty) is caused by excess secretion of sex hormones (estrogens or androgens) derived either from the gonads or adrenal glands, exogenous sources of sex steroids, or ectopic production of gonadotropins from a germ cell tumor (eg, human chorionic gonadotropin [hCG]) . We use the term precocity instead of puberty because puberty implies activation of the hypothalamic-pituitary-gonadal axis, as occurs in CPP, whereas precocity refers only to the secondary sexual characteristics. Peripheral precocity is most commonly either isosexual (concordant with the child's sex), or contrasexual (with virilization of females and feminization of males), but can also present with both virilizing and feminizing features in rare cases. Benign or nonprogressive pubertal variants – Benign pubertal variants include isolated breast development in females (premature thelarche) or isolated androgen-mediated sexual characteristics (such as pubic and/or axillary hair, acne, and apocrine odor) in males or females that result from early activation of the hypothalamic-pituitary-adrenal axis (premature adrenarche) . Both of these conditions can be a variant of normal puberty. However, repeat evaluations may be warranted in these children to be certain that the diagnosis is correct. اپتودیت #Precocious_puberty #بلوغ_زودرس تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
إظهار الكل...
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دختر ۱۴ ساله ساکن ناحيه سياهو بندرعباس با این عقرب گادیم که زرد رنگ است گزیده شده است. نکروز وسیع بیمار ۱۰ روز بعد گزش را مشاهده مینمایید! 🩻کانال تصاویر زیبایی پزشکی جهان JoIN➣ @Med_anatomy JoIN➣ @Med_anatomy
إظهار الكل...
Repost from N/a
Treatment of Hymenolepis nana Infection: Praziquantel Alternatively, nitazoxanide or, outside the United States, niclosamide The treatment of choice for H. nana infection is Praziquantel 25 mg/kg orally once Alternatives include nitazoxanide and niclosamide (not available in the United States). For nitazoxanide, dosage is For patients > 11 years: 500 mg orally 2 times a day for 3 days For children aged 4 to 11 years: 200 mg orally 2 times a day for 3 days For children aged 1 to 4 years: 100 mg orally 2 times a day for 3 days For niclosamide, dosage is For adults: 2 g orally once/day for 7 days For children > 34 kg: 1.5 g in a single dose on day 1, then 1 g once/day for 6 days For children 11 to 34 kg: 1 g in a single dose on day 1, then 500 mg once/day for 6 days A stool sample should be repeated one month after therapy is completed to verify cure. CDC تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
إظهار الكل...
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Common conditions with abnormal liver biochemical tests. تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
إظهار الكل...
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Common conditions with abnormal biochemical tests. تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
إظهار الكل...
اپیزود بررسی بیمار، شماره‌ی دوم: بررسی بیمار با شکایات متعدد، با هم‌راهی دکتر مهدیه جعفری @emipcast
إظهار الكل...
case review IR-1.mp329.12 MB
EMRaP Persian June 2024.m4a251.31 MB
Intro AMS hypoxia.mp321.35 MB
athletic cardiac arrest.mp314.45 MB
Status epilepticus (edited).m4a20.02 MB
Rural tox.m4a18.71 MB
Critical care alcohol withdrawal (edited).m4a11.93 MB
Repost from N/a
Current Therapeutic Options for the Main Monogenic Autoinflammatory Diseases and PFAPA Syndrome: The most extensively studied and better pathogenically defined monogenic autoinflammatory conditions have been familial Mediterranean fever (FMF) , tumor necrosis factor (TNF) receptor–associated periodic fever syndrome (TRAPS), hyperimmunoglobulin D syndrome/mevalonate kinase deficiency (HIDS/MKD), and cryopyrin-associated periodic syndromes (CAPS), which comprise three disorders with the same genetic background, and different phenotypes and outcomes. The CAPS spectrum includes familial cold autoinflammatory syndrome (FCAS), the mildest form; Muckle-Wells syndrome (MWS), the intermediate presentation; and chronic infantile neurological, cutaneous, and articular syndrome (CINCA) or neonatal-onset multisystem inflammatory disorder (NOMID), the most severe disease . Until the late 1990s, traditional drugs, such as colchicine and glucocorticoids, had been used to treat autoinflammatory diseases. The pathogenic and therapeutic revolution started when NLRP3, one of the NOD-like receptors (NLRs) and part of the NLRP3 inflammasome, was discovered as the main actor in the activation of caspase 1 and the subsequent production of active interleukin 1β (IL-1β) . Mutations of genes involved in the inflammasome function or its related pathways were then identified as responsible for most of the monogenic autoinflammatory disorders recognized so far, also known as inflammasomopathies . The discovery of the aberrant production of IL-1β as the final cause of all inflammasomopathies led to the introduction of anti–IL-1 agents and other biologic drugs to the very limited therapeutic armamentarium available for such diseases until then . In addition, the more recent knowledge of other autoinflammatory mechanisms, such as the activation of nuclear factor κB (NF-κB) and type I interferon (IFN) pathways, also provided new therapeutic options, such as anti-TNF and Janu درs kinase (JAK) inhibitors agents, directed to the specific blockade of cytokines and molecules involved in these novel inflammatory mechanisms . Frontiers Front. Immunol., 03 June 2020 تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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