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Brain tumor headache: سردرد ناشی از تومور های مغزی: MECHANISMS OF HEADACHE:  — Traction on the large blood vessels and dura as well as direct compression of cranial and cervical nerve fibers by the tumor itself are the likely mechanisms for headaches attributed to brain tumors . Peripheral and central sensitization may also contribute . Of note, the brain parenchyma is insensitive to pain. Structures that are sensitive to pain include the following : ●The large arteries at the base of the brain and the first few centimeters of their immediate branches ●The meningeal arteries ●The large venous channels of the brain and dura ●Parts of the dura, including the tentorium and the diaphragma sellae ●Cranial nerves that carry pain fibers (V, VII, IX, X) ●Skin and subcutaneous tissue, muscle, vessels, and periosteum of the skull Tumors and other mass lesions can cause headache by direct pressure on any of the above structures. Pain arising from the intracranial cavity is a form of visceral pain, and therefore referred to more superficial structures; it is not perceived as coming directly from the compressed region . In general, unilateral lesions refer pain ipsilaterally, supratentorial lesions refer pain to the frontal regions, and posterior fossa masses refer pain to the occiput . However, these associations have poor localizing value in clinical practice. As an example, in a study that evaluated 37 patients with infratentorial tumors, 73 percent of patients had headache in the frontal, temporal, and/or parietal regions, while nuchal and occipital pain occurred in only 27 percent . Acute or severe headache from a brain tumor can potentially be caused by elevated intracranial pressure resulting from hydrocephalus, mass effect of the tumor itself, or hemorrhage into or around the tumor . A tumor can distort or displace structures distant from its locale, resulting in referred pain that does not correspond with its location. In such cases of "distant traction," elevated intracranial pressure may be the cause of the headache . However, the relationship between elevated intracranial pressure and headache in brain tumor remains uncertain. #headache #سردرد #تومور_مغزی تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles

dermatophyte infections: عفونت قارچی پوست: The major clinical subtypes of dermatophyte infections include infections of the epidermis, hair, and nails. ●Epidermis •Tinea corporis – Infection of body surfaces other than the feet, groin, face, scalp hair, or beard hair •Tinea pedis – Infection of the foot •Tinea cruris – Infection of the groin, proximal inner thighs, or buttocks •Tinea faciei – Infection of the face •Tinea manuum – Infection of the hand ●Hair •Tinea capitis – Infection of scalp hair •Tinea barbae – Infection of beard hair ●Nails •Dermatophyte onychomycosis (tinea unguium) Majocchi's granuloma is an additional subtype of dermatophyte infection characterized by the spread of epidermal infection into deep portions of the hair follicle and dermis. In general, we do not use topical corticosteroids in the treatment of dermatophyte infections. Although combination antifungal and low-potency corticosteroid products can be effective and may accelerate resolution of the clinical manifestations of superficial dermatophyte infections , combination therapy is not necessary for achieving cure. In particular, use of products that include medium- or high-potency corticosteroids (eg, betamethasone-clotrimazole) is discouraged because use of a topical corticosteroid introduces risk for topical corticosteroid-induced skin atrophy. Treatment failures have also been reported , and some authors postulate that overuse of topical corticosteroids may contribute to the emergence of resistant dermatophyte infections. An infrequent exception to our avoidance of combination therapy is the addition of a low-potency topical corticosteroid (group 6 or 7) to antifungal therapy for patients with highly inflammatory lesions associated with severe pruritus . Some topical antifungal drugs (eg, allylamines and ciclopirox) have intrinsic anti-inflammatory properties that may also help to reduce inflammation . اپتودیت #tinea_corporis تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles

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

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

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

Common conditions with abnormal biochemical tests. تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles

اپیزود بررسی بیمار، شماره‌ی دوم: بررسی بیمار با شکایات متعدد، با هم‌راهی دکتر مهدیه جعفری @emipcast

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