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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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Emphysematous urinary tract infections: عفونت ادراری آمفیزماتو: Emphysematous urinary tract infections (UTIs) are infections of the lower or upper urinary tract associated with gas formation. They may involve the bladder (cystitis), renal pelvis (pyelitis), or kidney (pyelonephritis). Diabetes mellitus is a major risk factor for these infections .  — Emphysematous UTIs are usually due to Escherichia coli or Klebsiella pneumoniae. These two organisms account for 65 to 100 percent of the isolates described in various retrospective reports . Other reported causative organisms include Proteus, Enterococcus, Pseudomonas, Clostridium, and, rarely, Candida spp and Aspergillus . Some infections are polymicrobial. The pathogenesis of emphysematous UTIs is poorly understood. Among patients with diabetes mellitus, elevated tissue glucose levels may provide a more favorable microenvironment for gas-forming microbes. However, bacterial gas production does not fully explain the pathologic and clinical manifestations of emphysematous UTIs . Diabetes mellitus and urinary tract obstruction are the major risk factors for emphysematous UTIs. They occur more commonly in females. Emphysematous pyelonephritis has also been rarely reported in renal transplant recipients . The clinical features of emphysematous pyelonephritis and pyelitis are indistinguishable from those seen in severe, acute pyelonephritis. Most patients complain of fevers, chills, flank or abdominal pain, nausea, and vomiting. The onset of symptoms may be abrupt or evolve slowly over two to three weeks. CT is the preferred imaging modality as it is more sensitive than other modalities and can delineate the extent of gas formation and any obstructing lesions in the urinary tract . CT findings have also been used for prognostic classification of emphysematous pyelonephritis. Air associated with emphysematous UTI can also be detected on plain films of the abdomen, with a reported sensitivity ranging from 50 to 85 percent . #UTI #عفونت_ادراری تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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The American Thyroid Association recommends that levothyroxine be consistently taken 60 minutes before breakfast or at bedtime, at least three hours after dinner. در زمان ثابتی استفاده شود.
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anion gap: آنیون گپ: Using the results of the comprehensive metabolic panel (CMP), the anion gap is the difference between measured cations (positively charged ions like Na+ and K+) and measured anions (negatively charged ions like Cl- and HCO3-). There are three types: serum, plasma, and urine anion gaps. The most common application of the anion gap is classifying cases of metabolic acidosis, states of lower than normal blood pH. Specifically, classifying into either those that do and those that do not have unmeasured anions in the plasma. The human body is electrically neutral; therefore, in reality, does not have a true anion gap. The calculation then finds utility in exposing variations in that balance. However, changes in albumin and bicarbonate concentrations warrant specific attention.  anion gap formula: ([Na+] +[K+]) – ([Cl-] + [HCO3-]) = [UA] – [UC] Anion Gap = UA – UC From this manipulation, a health care practitioner or researcher can see that the 4 to 12 mmol/L range of the anion gap is precisely equal to the difference between the unmeasured anions and cations. نکات قابل توجه: Every 1 g/L decrease in albumin will decrease the anion gap by 0.25 mmol/L. A patient with hypoalbuminemia may present with a normal anion gap when in actuality, they have a high anion gap acidosis. Consider in ICU patients. Another ratio worth adding to your anion gap toolkit is every decrease in 10 g/L albumin = 2.3 mmol/L decrease in the anion gap. Interestingly, paraproteins such as IgG also cause a reduction in anion gap due to their positive charge. Thus, patients with monoclonal proliferation such as those suffering from IgG myeloma have significant increases in cation or positive ion concentration resulting in decreased and rarely increased anion gaps. Likewise, a polyclonal proliferation of IgG would have the same effect, which can present in a patient with HIV. Finally, patients prescribed lithium carbonate for bipolar disorder can have reduced anion gap. At therapeutic doses of 1.0 mmol/L, no change in the anion gap materializes. However, in lithium intoxication, a noticeable reduction is appreciated. Other causes of reduced ion gap include hypoalbuminemia, hypertriglyceridemia, decreased unmeasured anions such as phosphorus, and increased unmeasured cations such as magnesium. increased anion gap metabolic acidosis: Carbon monoxide/cyanide Aminoglycosides Theophylline Methanol Uremia Diabetic ketoacidosis Paracetamol/acetaminophen Iron/isoniazid Lactic acidosis Ethanol/ethylene glycol Salicylate/ASA normal anion gap metabolic acidosis: Ureterostomy Small bowel fistula Extra chloride Diarrhea Carbonic anhydrase inhibitor Adrenal insufficiency Rental tubular acidosis Pancreatic fistula. #anion_gap #acidosis #آنیون_گپ #اسیدوز تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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#pneumococcal_vaccine #PCV #PPSV23 #واکسن_پنوموکک #واکسن تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Chronic hepatitis E: هپاتیت مزمن E:  — Chronic HEV infection is defined empirically as detection of HEV RNA in serum or stool for longer than six months. Chronic HEV almost exclusively occurs in immunosuppressed patients (eg, those with HIV infection, following solid organ or bone marrow transplantation) . Chronic infection is typically with HEV genotype 3 infection, although chronic infection with genotype 4 has been documented in a transplant recipient . Chronic HEV infection with genotypes 1 and 2 have not been reported. As with most chronic viral hepatitis patients, symptoms are minimal and include fatigue and nonspecific findings until progression to decompensated cirrhosis occurs. Patients with chronic HEV have persistently elevated aminotransferase levels, detectable serum HEV RNA, and histologic findings compatible with chronic viral hepatitis. #hepatitis #HEV #هپاتیت تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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#UTI #عفونت_ادراری تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Roseola infantum: Laboratory features of roseola may include: ●Neutropenia and atypical lymphocytosis – Children with roseola may have relative neutropenia and mild atypical lymphocytosis . Early in the febrile period, the white blood cell count may be elevated but reaches its nadir (frequently in the range of 3000 cells/microL) by day 3 to 6 of illness, then gradually returns to normal over the following 7 to 10 days. ●Thrombocytopenia – Children with roseola also may have thrombocytopenia, which is thought to be caused by bone marrow suppression rather than immune-mediated peripheral consumption . ●Sterile pyuria – Children with roseola may have sterile pyuria. In a retrospective study from a single institution, 13 percent of 158 children with roseola had sterile pyuria . During the febrile phase, urinary tract infection (UTI) may be a diagnostic consideration in children with pyuria. UTI is a consideration among infants who present with fever before the onset of the characteristic roseola rash and are found to have pyuria during the evaluation of fever. Urine culture results will ultimately differentiate UTI from roseola in such children. A retrospective study of 158 young children (one month to three years) with roseola and 143 young children with UTI identified presenting clinical and laboratory findings more suggestive of UTI than roseola . Peripheral white blood cell (WBC) count >10,000 cells/microL was the most helpful single finding (occurring in 70 percent of children with UTI and only 4 percent of those with roseola). Additional findings that were more common among children with UTI than roseola included male sex, age <6 months, C-reactive protein >0.5 mg/dL (5 mg/L), and fever of <4 days duration at presentation. Although not examined in the study, a positive nitrite test by dipstick analysis is highly suggestive of UTI. Pending urine culture results, decisions regarding empiric antibiotics are best made on a case-by-case basis based upon the probability of UTI, which is determined by demographic and clinical factors (eg, age, circumcision status, urinary tract anomalies, etc) . To prevent unnecessary use of antibiotics in children in whom both UTI and roseola are being considered, it may be reasonable to withhold antibiotics pending urine culture results among those who are well-appearing, ≥6 months of age, have peripheral WBC count between 5000 and 10,000 cells/microL, and negative nitrites on dipstick analysis. اپتودیت #Roseola #رزئول تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Medication use and hyperprolactinemia: داروها وهیپر پرولاکتینمی: Medication use is a common cause of hyperprolactinemia, and it is important to differentiate this cause from pathologic causes, such as prolactinomas. To ascertain the frequency of this clinical problem and to develop treatment guidelines, the medical litera- ture was searched by using PubMed and the reference lists of other articles dealing with hyperprolactinemia due to specific types of medications. The medications that most commonly cause hyperprolactinemia are: antipsychotic agents; however, somenewer atypical antipsychotics do not cause this condition. Other classes of medications that cause hyperprolactinemia include antidepressants, antihypertensive agents, and drugs that in- crease bowel motility. Hyperprolactinemia caused by medicationsis commonly symptomatic, causing galactorrhea, menstrual dis-turbance, and impotence. It is important to ensure that hyperprolactinemia in an individual patient is due to medication and not to a structural lesion in the hypothalamic/pituitary area; this can be accomplished by : (1) stopping the medication temporarily to determine whether prolactin levels return to normal, (2) switch-ing to a medication that does not cause hyperprolactinemia (inconsultation with the patient’s psychiatrist for psychoactive medi- cations), or (3) performing magnetic resonance imaging or computed tomography of the hypothalamic/pituitary area. If the pa-tient’s hyperprolactinemia is symptomatic, treatment strategies include switching to an alternative medication that does not cause hyperprolactinemia, using estrogen or testosterone re- placement, or, rarely, cautiously adding a dopamine agonist. #hyperprolactinemia #هیپر پرولاکتینمی تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Biotin and thyroid function tests: تداخل مصرف بیوتین و تستهای تیروئید: There are numerous reports of biotin interference with laboratory testing, specifically with thyroid function tests. Most commonly, biotin use can result in falsely high levels of T4 and T3 and falsely low levels of TSH, leading to either a wrong diagnosis of hyperthyroidism or that the thyroid hormone dose is too high. The ATA has recommended that patients stop taking biotin for at least 2 days before thyroid testing to avoid the risk of having a misleading test. #بیوتین #تست های تیروئید #biotin #thyroid tests تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Jaundice: Evaluation: CONJUGATED HYPERBILIRUBINEMIA:   Defect of canalicular organic anion transport : Dubin-Johnson syndrome Defect of sinusoidal reuptake of conjugated bilirubin: Rotor syndrome Decreased intrahepatic excretion of bilirubin: Hepatocellular disease - Viral hepatitis A, B, D; alcoholic hepatitis; cirrhosis, nonalcoholic steatohepatitis, EBV, CMV, HSV, Wilson, autoimmune  Cholestatic liver disease -Primary biliary cholangitis, primary sclerosing cholangitis Infiltrative diseases (e.g., amyloidosis, lymphoma, sarcoidosis, tuberculosis) Sepsis and hypoperfusion states. Total parenteral nutrition Drugs & Toxins - oral contraceptives, rifampin, probenecid, steroids, chlorpromazine, herbal medications (e.g., Jamaican bush tea, kava kava), arsenic Hepatic crisis in sickle cell disease Pregnancy Extrahepatic cholestasis (biliary obstruction): Choledocholithiasis Tumors (e.g., cholangiocarcinoma, head of pancreas cancer) Extrahepatic biliary atresia Acute and chronic pancreatitis Strictures  Parasitic infections (e.g., Ascaris lumbricoides, liver flukes)  UNCONJUGATED HYPERBILIRUBINEMIA : 1- Excess production of bilirubin Hemolytic anemias, extravasation of blood in tissues, dyserythropoiesis 2-Reduced hepatic uptake of bilirubin: Gilbert syndrome  3-Impaired conjugation Crigler–Najjar syndrome type 1 and 2 Hyperthyroid Estrogen Evaluation: (After obtaining a thorough history and performing physicals, the most important laboratory test to be done is liver function tests. Liver function tests - to check serum levels of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma-glutamyltransferase, serum albumin, protein, and bilirubin AST, ALT and ALP levels: - if the liver transaminase levels increase but ALP levels are low, then the insult is hepatic in origin. AST/ALT ratio is more than 2 to 1 in alcoholic liver disease. AST and ALT values are in 1000s; then the hepatocellular disease is likely due to toxins like acetaminophen or ischemia or viral. If ALP levels are five times elevated than normal and liver transaminases are normal or less than two times normal, then the most likely cause is biliary obstruction. The high serum ALP levels due to a biliary injury can be differentiated from bone disorders by ordering a GGT serum profile, increased levels confirm hepatic origin. If AST, ALT and ALP levels are normal- then the jaundice is not due to liver or bile duct injury. The cause must probably be pre-hepatic inherited disorders of liver conjugation or blood disorders or defect in hepatic excretion (Rotor, Dubin-Johnson).  Serum Bilirubin - whether there is a rise in unconjugated or conjugated bilirubin  In addition to the liver panel, all jaundiced patients should have additional tests such as albumin and prothrombin time – which are indicative of chronic and acute liver function, respectively. The inability of prothrombin time to correct with parenteral administration of vitamin K suggests severe hepatocellular dysfunction.  The results of the bilirubin, enzymes, and liver function tests will direct the diagnosis towards a hepatocellular or cholestatic cause and offer some idea of the duration and severity of the disease.  Further evaluation can be conducted based on the initial assessment. Hepatocellular workup: viral serologies, autoimmune antibodies, serum ceruloplasmin, ferritin. Cholestatic workup: Additional tests include abdominal ultrasound, CT, magnetic resonance cholangiopancreatography (MRCP), endoscopic retrograde cholangiopancreatography (ERCP), percutaneous transhepatic cholangiography (PTC), endoscopic ultrasound (EUS). #jaundice تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Haemophilus influenzae: Haemophilus influenzae is a bacteria that has encapsulated (typeable) or unencapsulated (nontypeable) strains. Encapsulated strains express one of six antigenically capsular polysaccharides (types a, b, c, d, e, or f). Historically, type b (Hib) was the most common type to cause invasive disease, particularly in young children.  H.influenzae colonizes the upper respiratory tract of humans and is transmitted person-to-person by inhalation of respiratory droplets or by direct contact with respiratory tract secretions. Encapsulated H. influenzae nontype b strains, particularly type a, can cause invasive disease similar to Hib disease. Nontypeable strains also can cause invasive disease but more commonly cause mucosal infections such as otitis media, conjunctivitis, and sinusitis. Vaccines are only available for H. influenzae type b; Hib vaccines do not protect against disease caused by any other H. influenzae strains. #H_influenzae #هموفیلوس_آنفلوانزا تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Renal tubular ectasia: Renal tubular ectasia is an incidental finding that is seen more commonly on intravenous pyelography (IVP), but which can also occasionally be seen on CT urography (CTU). Terminology Renal tubular ectasia is also known as benign renal tubular ectasia. The term "benign" was used to differentiate it from medullary sponge kidney and the symptoms of medullary nephrocalcinosis; no tumor is associated with either condition. Pathology The appearance arises from congenital dilatation/ectasia of the distal tubules of the nephrons in a medullary pyramid. Some feel that the ectasia predisposes toward stone formation, but if this is the clinical case, the terms medullary sponge kidney and medullary nephrocalcinosis tend to be used instead. In the literature, there has been overlap in the use of the two terms, and some consider the two conditions to be different ends of spectrum of medullary tubular dilation. Radiographic features Both IVP and CTU show a similar "paintbrush" appearance to the medullary pyramid. The strands of the "brush" are mildly dilated tubules full of contrast (tubules dilated to ~0.2 mm). Unlike medullary nephrocalcinosis, renal tubular ectasia cannot be seen on a plain radiograph or a noncontrast CT. Treatment and prognosis No treatment or workup required. There is an association with congenital hepatic fibrosis 2, although this association may really be with medullary sponge kidney. Differential diagnosis medullary sponge kidney the difference is predominantly one of degree, renal tubular ectasia less pronounced than medullary sponge kidney medullary sponge kidney also predisposes to medullary nephrocalcinosis: the distal tubules accrete calcification which predisposes to renal stone formation normal faint blush of contrast in the medullary pyramid as contrast passes through the medullary pyramid, it will cause the pyramid to "blush"/enhance, but renal tubular ectasia is greater in degree. Radiopaedia 2022 تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Incident autoimmune conditions among males receiving quadrivalent human papillomavirus vaccine in the United States - ScienceDirect https://www.sciencedirect.com/science/article/pii/S0264410X2201307X
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Primary hypothyroidism : هیپوتیروئیدیسم اولیه: refers to inadequate thyroid hormone production in the gland itself. Following the inception of population-wide newborn screening programs in the 1970s, studies to determine the underlying etiology reported that approximately 85 percent were caused by thyroid dysgenesis, while 15 percent were caused by one of the inborn errors in thyroid hormone synthesis. On follow-up, the majority of these cases had permanent hypothyroidism. With lowering of the TSH screening cutoff and detection of milder cases of congenital hypothyroidism, more recent studies to examine the underlying etiology now report that a normal-sized or large thyroid gland in the normal location, so-called "gland in situ," is the most common finding . While the underlying cause of gland in situ is often unknown, it likely represents a mild form of thyroid dyshormonogenesis. On follow-up, approximately one-half of cases of thyroid gland in situ have transient hypothyroidism. #hypothyroidism #هیپوتیروئیدی تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Occult HBV infection:  — There exists a subset of patients with occult HBV infection, which is defined as the presence of detectable HBV DNA by polymerase chain reaction (PCR) in patients who are negative for HBsAg. Such patients have been further subclassified as having "seropositive" or "seronegative" occult HBV depending upon whether they are positive or negative for other HBV markers, most commonly anti-HBc . Seronegative occult HBV is rarely seen in humans, although it has been described in woodchucks . Most patients with occult HBV have very low or undetectable serum HBV DNA levels, accounting for the failure to detect HBsAg. Infections with HBV variants that decrease HBsAg production or have mutations in the S gene with altered S epitopes that evade detection in serology assays for HBsAg are uncommon. However, HBV DNA is often detected in the liver, and transplantation of livers from these persons can result in de novo HBV infection . In addition, patients with occult HBV infection, particularly those who are anti-HBc positive, are at risk of HBV reactivation if they receive potent immunosuppressive therapy such as anti-CD20 or myeloablative therapies for bone marrow or stem cell transplant. Occult HBV infection has been associated with chronic liver disease and should be considered in the differential diagnosis of patients with apparent cryptogenic chronic liver disease, especially those with risk factors for HBV infection . اپتودیت #HBV #HBsAg #Hepatitis_B #هپاتیت_بی تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Infection associated with eosinophilia: عفونت های همراه با ائوزینوفیلی: A variety of infections may be associated with eosinophilia; these include helminths (worms), fungi, protozoa, bacteria, the retroviruses human immunodeficiency virus (HIV) and human T cell lymphotropic virus type 1 (HTLV-1), in addition to arthropod infestations, such as scabies (a mite infestation). Most acute bacterial infections and viral infections are not associated with eosinophilia. A clinical approach focusing on infectious causes of eosinophilia based on epidemiologic exposure and clinical manifestations is outlined below. In general, helminths are the most commonly identified infectious causes of eosinophilia . Categories of helminths include flukes (trematodes), tapeworms (cestodes), and roundworms (nematodes). The major helminth infections associated with eosinophilia are discussed below; additional information regarding helminths associated with eosinophilia is summarized in the table . Fungal infections classically associated with eosinophilia include allergic bronchopulmonary aspergillosis and coccidioidomycosis. Less commonly, peripheral eosinophilia has been reported in patients with histoplasmosis, paracoccidioidomycosis, cryptococcosis, and basidiobolomycosis. Protozoal infections associated with eosinophilia include cystoisosporiasis, sarcocystosis, and Dientamoeba fragilis. Bacterial infections associated with eosinophilia include bartonellosis, syphilis, and resolving scarlet fever. Mycobacterial infections associated with eosinophilia include tuberculosis and leprosy. In the setting of HIV infection, eosinophilia may occur as a result of concomitant opportunistic infection or in the context of an associated condition such as eosinophilic folliculitis or adrenal insufficiency . HTLV-1 infection has been associated with adult T-cell leukemia/lymphoma (ATL); ATL may be associated with eosinophilia in some circumstances [10]. In addition, HTLV-1 infection is a risk factor for disseminated. اپتودیت #strongyloidiasis. #eosinophilia #ائوزینوفیلی تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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eosinophilia: ائوزینوفیلی: A variety of infections may be associated with eosinophilia; these include helminths (worms), fungi, protozoa, bacteria, the retroviruses human immunodeficiency virus (HIV) and human T cell lymphotropic virus type 1 (HTLV-1), in addition to arthropod infestations, such as scabies (a mite infestation). Most acute bacterial infections and viral infections are not associated with eosinophilia. A clinical approach focusing on infectious causes of eosinophilia based on epidemiologic exposure and clinical manifestations is outlined below. In general, helminths are the most commonly identified infectious causes of eosinophilia . Categories of helminths include flukes (trematodes), tapeworms (cestodes), and roundworms (nematodes). The major helminth infections associated with eosinophilia are discussed below; additional information regarding helminths associated with eosinophilia is summarized in the table . Fungal infections classically associated with eosinophilia include allergic bronchopulmonary aspergillosis and coccidioidomycosis. Less commonly, peripheral eosinophilia has been reported in patients with histoplasmosis, paracoccidioidomycosis, cryptococcosis, and basidiobolomycosis. Protozoal infections associated with eosinophilia include cystoisosporiasis, sarcocystosis, and Dientamoeba fragilis. Bacterial infections associated with eosinophilia include bartonellosis, syphilis, and resolving scarlet fever. Mycobacterial infections associated with eosinophilia include tuberculosis and leprosy. In the setting of HIV infection, eosinophilia may occur as a result of concomitant opportunistic infection or in the context of an associated condition such as eosinophilic folliculitis or adrenal insufficiency . HTLV-1 infection has been associated with adult T-cell leukemia/lymphoma (ATL); ATL may be associated with eosinophilia in some circumstances [10]. In addition, HTLV-1 infection is a risk factor for disseminated. اپتودیت #strongyloidiasis. #eosinophilia #ائوزینوفیلی تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Tetanus: کزاز: Because C. tetani will not grow in healthy tissues, a convergence of factors must be present in order for tetanus toxin to be elaborated in the human host. This combination of factors usually includes absence of antibodies (ie, from inadequate vaccination) plus two or more of the following: ●A penetrating injury resulting in the inoculation of C. tetani spores ●Coinfection with other bacteria ●Devitalized tissue ●A foreign body ●Localized ischemia The above factors explain why tetanus-prone injuries include splinters and other puncture wounds, gunshot wounds, compound fractures, burns, and unsterile intramuscular or subcutaneous injections (that often occur in injection drug users). These predisposing factors can also explain why tetanus can develop in unusual clinical settings such as in: ●Neonates (due to infection of the umbilical stump) ●Obstetric patients (after septic abortions) ●Postsurgical patients (with necrotic infections involving bowel flora) ●Adolescents and adults undergoing male circumcision in sub-Saharan Africa . ●Patients with dental infections ●Diabetic patients with infected extremity ulcers ●Patients who inject illicit and/or contaminated drugs Tetanus in patients without an identifiable cause:  — An identifiable antecedent cause for tetanus is obvious in most patients presenting with tetanus, but no cause can be identified in up to a quarter of patients with classic signs and symptoms of tetanus. Presumably, minor unnoticed abrasions or skin injuries are responsible for most or all of these "cryptogenic" cases. Tetanus has occurred rarely in patients who have received a timely and correct series of tetanus immunizations. اپتودیت #tetanus #کزاز تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Discrepancies between acute phase reactant levels:  — Although elevations in multiple components of APR commonly occur together, not all happen uniformly in all patients. Discordance between concentrations of different APR is common; some may be elevated while others are not. Differences in the production of specific cytokines or their modulators in different diseases may account in large part for these variations . Additionally, as a patient’s condition worsens or improves, the ESR changes relatively slowly, while CRP concentrations can change rapidly. Discrepancies between ESR and CRP are found with some frequency. An elevated ESR observed together with a normal CRP is often a misleading result that may, for example, reflect the effects of blood constituents, such as monoclonal immunoglobulins, that are not related to inflammation but that can influence the ESR. It should not be routine practice to order serum protein electrophoresis (SPEP) and urine protein electrophoresis (UPEP) in such instances, unless the clinical presentation suggests that a plasma cell dyscrasia may be present. Systemic lupus erythematosus (SLE) represents an exception to the generalization that CRP concentrations correlate with the extent and severity of inflammation in patients with rheumatic disorders . The ESR may be elevated, sometimes markedly, in patients with active SLE, while the CRP response is muted. The muted CRP response in SLE appears to result from the ability of type I interferons, which are highly expressed in most lupus patients, to inhibit CRP induction in hepatocytes . While many patients with active SLE do not have significantly elevated CRP concentrations , CRP concentrations may be quite elevated in patients with active lupus serositis or with chronic synovitis . In a febrile lupus patient, marked CRP elevation (greater than 6 mg/dL) favors the diagnosis of bacterial infection . In a landmark study, infection was present in all patients with CRP levels over 6 mg/dL (60 mg/L) except for those with serositis, supporting the clinical utility of regarding marked CRP elevation as strongly suggestive of infection . Another more common example reflects the acuity of the acute phase response. CRP levels measure a single molecule, and one will note acute and rapid rise and fall with an insult. By contrast, because ESR is the reflection of numerous factors and the interaction of these elements (ie, long half-life of some plasma proteins), ESR levels do not rapidly rise at the beginning of an inflammatory insult; similarly, normalization is slower. This difference between ESR and CRP can help clinicians distinguish between acute processes and a more chronic process (for example, high CRP and normal ESR may suggest an acute paronychia; by contrast, elevated CRP and ESR may suggest osteomyelitis). In patients with active rheumatoid arthritis, the ESR and CRP generally tend to be parallel (ie, both are elevated or not elevated in a single patient). However, one study found that results for the two tests were discordant (ESR >28 mm/hr with CRP ≤0.8 mg/dL or ESR ≤28 mm/hr with CRP >0.8 mg/dL) in about one-quarter of patients with active rheumatoid arthritis in a large practice-based registry . Several studies have suggested that elevations of the acute phase protein procalcitonin are highly specific for infection ; thus, procalcitonin may prove useful in differentiating infections from other inflammatory stimuli in autoimmune disease patients . A 2012 systematic review and meta-analysis of nine observational studies that evaluated procalcitonin as a marker of infection in patients with autoimmune disease found that procalcitonin and CRP exhibited similar sensitivity for infection (75 versus 77 percent), but that procalcitonin had significantly higher specificity (90 versus 56 percent) .Thus, procalcitonin determination was inadequate to exclude infection. #CRP #ESR تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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خلاصه اي راجع به زردي نوزادان: زردي كه در هنگام تولد موجود بوده يا در خلال 24 ساعت اول زندگي تظاهر مي كند ممكن است در اثر اريتروبلاستوز فتاليس، خونريزي پنهان، سپتي سمي ، CMV ، سرخجه يا توكسوپلاسموز مادرزادي باشد. زردي روز دوم يا سوم تولد معمولا فيزيولوژيك است. ولي ممكن است در اثرانواع شديد تر هيپر بيليروبينمي نوزاد  باشد. سندرم كليگلر نجار ابتدا روز دوم يا سوم تولد ديده مي شود. زردي كه بعد از روز سوم و در خلال هفته اول تولد تظاهر كند احتمال سپتي سمي ویا عفونت ادراری را مطرح مي كند و ممكن است در اثر عفونتهاي ديگري مانند سيفليس ، توكسوپلاسموز، CMV ،آنتروویروس باشد . زردي ثانويه به اكيموز وسیع يا هماتوم ممكن است روز اول يا ديرتر تظاهر كند. شروع زردي بعد از هفته اول : زردي ناشي از شير مادر (breast milk jaundice)                          ، سپتي سمي، آترزي مادرزادي مجاري صفراوي ، هپاتيت ، سرخجه ، هپاتيت هرپسي ، گالاكتوزمي ، هيپوتيروئيديسم ، اسفروسيتوز ارثي ، كمبود آنزيمي گلبول قرمز يا آنمي هموليتيك در اثر داروها . زردي مداوم در خلال ماه اول تولد در اثر:    هپاتيت ، CMV ، سيفليس ،توكسوپلاسموز ، آترزي مادر زادي  مجاري صفراوي ،inspissated bile syndrome ،گالاكتوزمي است . در صورتيكه نوزاد هيپوتيروئيديسم يا استنوز پيلور داشته باشد زردي فيزيولوژيك ممكن است چند هفته طول بكشد. در موارد زير بايد براي پيداكردن علت زردي اقدام كرد : اگر زردي در 24 ساعت اول تولد پيداشده باشد . اگر بيليروبين سرم بيش از mg 5 درصد در 24 ساعت بالا برود . اگر بيليروبين سرم بيش از 12 ميلي گرم درصد در نوزاد فول ترم و بيش از 14-10 ميلي گرم درصد درنوزاد  نارس باشد . اگرزردي كه بعد از هفته دوم زندگي طول بكشد . اگر بيليروبين مستقيم در هر زمانی بالا باشد. سابقه فاميلي بيماري هموليتيك ، رنگ پريدگي ، هپاتومگالي ، اسپلنومگالي ، اگر بافتوتراپي زردي كاهش نيابد ، استفراغ ، لتارژي ، اگر نوزاد خوب شير نخورد ، اگر وزن قابل توجهي كم كند ،اگر آپنه ،برادي كاردي، هيپوترمي ، مدفوع رنگ پريده ، ادرار تيره كه بيليروبين آن مثبت باشد و یاعلائم كرن ايكتروس موجودباشد. زردي ناشی از تغذيه با شير مادر :breast milk jaundice بين روزهاي 4-7 بعداز تولد شروع مي شود و حداكثر 10-30 ميلي گرم درصد در خلال 2-3 هفته ممكن است برسد . زردي بتدريج كاهش يافته و سپس مدت 10-3 هفته  در سطح پائين تري ادامه ميابد . اگر 1-2روز شير مادررا  به نوزاد نداده و بجاي آن شير خشك بدهيم بيليروبين سرم سريعا كاهش مي یابد ولی اینکاررا بطور روتین بجز درمواردی که مقدار بیلیروبین اندازه ای باشد که ارزش اینکار را داشته باشدتوصیه نمیکنم زیرا در این نوع زردی با گذشت زمان بیلیروبین بتدریج بطرف نرمال سیر میکند وقطع شیر مادرهم اثر روانی ناخوشایندی روی مادر دارد وگاهی مادران تشویق میشوند تغذیه با شیر خشک را قطع نکرده وادامه دهند .بنابراین شیر مادر را ادامه میدهیم ولی نوزاد را از نظر مقداربیلیروبین فالو میکنیم ودرصورت لزوم در صورت بالا بودن بیلیروبین از فتوتراپي استفاده و شیر مادر را موقتا با شیرخشک برای دو روز جایگزین میکنیم که باعث کاهش بیلیروبین شده و با شروع شیر مادر دوباره به مقدار قبلی باز نمیگردد. اين سندرم بايستي از هيپر بيليروبينمي غير كنژوگه تسريع شده با شروع زودرس در هفته اول زندگي افتراق داده شود كه در آن شير مادر خواران بيليروبين بالاتري نسبت به نوزاداني كه شير خشك ميخورند دارند. اين نوزادان دريافت شيرشان از طرف مادر كم است. و دهيدراتاسيون وكمبود كالري پيدا مي كنند . اين نوزادان را نبايد با آب قند سير كرد و بايد مكررا شير داد تا از پيدايش زردي در آنها جلوگيري شود. به اين مسئله breast feeding jaundice مي گويند. #هیپربیلیروبینمی_نوزادی #زردی_ناشی_از_شیر_مادر تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Ferritin is a marker of iron stores, but it may also be elevated as an acute phase reactant or due to massive cell and tissue death, especially in the liver and in the setting of hemophagocytosis. The absolute ferritin level cannot be interpreted in isolation and should not be the sole basis for treatment decisions. The pattern of ferritin increase (progressive, acute/marked increase, or chronic mild elevation) as well as the patient's underlying condition must be incorporated in the evaluation.
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The differential diagnosis for TBG deficiency: includes central hypothyroidism and euthyroid sick syndrome. Laboratory testing for patients with central hypothyroidism shows low FT4, low Total T4 along with low or inappropriately normal TSH levels. Central hypothyroidism may be congenital or acquired. Some critically ill euthyroid patients with non-thyroidal illness may also present with low FT4, low T4 along with low TSH. However, most of these patients present with high reverse T3 levels due to reduced clearance of Reverse T3. These abnormalities usually resolve with resolution of non-thyroid illness.
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Thyroxine-binding globulin (TBG): is one of three major transport proteins, which are primarily responsible for binding to and transporting thyroid hormones to the necessary tissues.  The other two serum transport proteins include transthyretin and human serum albumin.  While there are higher amounts of albumin in serum, TBG has a greater affinity to thyroxine (T4). Abnormalities in the functionality and amount of TBG can cause variations in the total amount of T4 in the serum, but not in the amount of bioactive free T4.  Since the amount of free T4 circulating in the serum remains the same, deficiency in thyroxine-binding globulin often does not lead to adverse metabolic effects seen in an individual with abnormal thyroid hormone levels. However, it can cause errors in the interpretation of thyroid hormone labs, which can ultimately lead to inappropriate treatment. Thyroxine-binding globulin (TBG) is a serine protease inhibitor produced in the liver. It belongs to the SERPINA7 family. The encoding gene for this protein is on the long arm of the X chromosome and as such, inherited forms of TBG tend to follow an X-linked pattern. Approximately 27 different mutations have been identified to play a role in the etiology of the inherited form of complete TBG deficiency thus far. These mutations seem to be caused by a nucleotide substation or by a frameshift.  Missense mutations have been the only type identified so far in an inherited form of partial TBG deficiency. Acquired forms of TBG deficiency are attributable to degradation and altered synthesis of the molecule. Patients with hyperthyroidism have been found to have an increase in the rate of turnover of TBG.  In terminal illness, interleukin-6 seems to play a role in altering the levels of TBG. Levels of TBG have been found to vary with fluctuations in sex hormones as well.  For example, estrogen has been known to cause an increase in TBG, while androgens have been found to decrease levels TBG. #thyroid #TBG #تیروئید 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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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
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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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Emphysematous urinary tract infections: عفونت ادراری آمفیزماتو: Emphysematous urinary tract infections (UTIs) are infections of the lower or upper urinary tract associated with gas formation. They may involve the bladder (cystitis), renal pelvis (pyelitis), or kidney (pyelonephritis). Diabetes mellitus is a major risk factor for these infections .  — Emphysematous UTIs are usually due to Escherichia coli or Klebsiella pneumoniae. These two organisms account for 65 to 100 percent of the isolates described in various retrospective reports . Other reported causative organisms include Proteus, Enterococcus, Pseudomonas, Clostridium, and, rarely, Candida spp and Aspergillus . Some infections are polymicrobial. The pathogenesis of emphysematous UTIs is poorly understood. Among patients with diabetes mellitus, elevated tissue glucose levels may provide a more favorable microenvironment for gas-forming microbes. However, bacterial gas production does not fully explain the pathologic and clinical manifestations of emphysematous UTIs . Diabetes mellitus and urinary tract obstruction are the major risk factors for emphysematous UTIs. They occur more commonly in females. Emphysematous pyelonephritis has also been rarely reported in renal transplant recipients . The clinical features of emphysematous pyelonephritis and pyelitis are indistinguishable from those seen in severe, acute pyelonephritis. Most patients complain of fevers, chills, flank or abdominal pain, nausea, and vomiting. The onset of symptoms may be abrupt or evolve slowly over two to three weeks. CT is the preferred imaging modality as it is more sensitive than other modalities and can delineate the extent of gas formation and any obstructing lesions in the urinary tract . CT findings have also been used for prognostic classification of emphysematous pyelonephritis. Air associated with emphysematous UTI can also be detected on plain films of the abdomen, with a reported sensitivity ranging from 50 to 85 percent . #UTI #عفونت_ادراری تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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The American Thyroid Association recommends that levothyroxine be consistently taken 60 minutes before breakfast or at bedtime, at least three hours after dinner. در زمان ثابتی استفاده شود.
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anion gap: آنیون گپ: Using the results of the comprehensive metabolic panel (CMP), the anion gap is the difference between measured cations (positively charged ions like Na+ and K+) and measured anions (negatively charged ions like Cl- and HCO3-). There are three types: serum, plasma, and urine anion gaps. The most common application of the anion gap is classifying cases of metabolic acidosis, states of lower than normal blood pH. Specifically, classifying into either those that do and those that do not have unmeasured anions in the plasma. The human body is electrically neutral; therefore, in reality, does not have a true anion gap. The calculation then finds utility in exposing variations in that balance. However, changes in albumin and bicarbonate concentrations warrant specific attention.  anion gap formula: ([Na+] +[K+]) – ([Cl-] + [HCO3-]) = [UA] – [UC] Anion Gap = UA – UC From this manipulation, a health care practitioner or researcher can see that the 4 to 12 mmol/L range of the anion gap is precisely equal to the difference between the unmeasured anions and cations. نکات قابل توجه: Every 1 g/L decrease in albumin will decrease the anion gap by 0.25 mmol/L. A patient with hypoalbuminemia may present with a normal anion gap when in actuality, they have a high anion gap acidosis. Consider in ICU patients. Another ratio worth adding to your anion gap toolkit is every decrease in 10 g/L albumin = 2.3 mmol/L decrease in the anion gap. Interestingly, paraproteins such as IgG also cause a reduction in anion gap due to their positive charge. Thus, patients with monoclonal proliferation such as those suffering from IgG myeloma have significant increases in cation or positive ion concentration resulting in decreased and rarely increased anion gaps. Likewise, a polyclonal proliferation of IgG would have the same effect, which can present in a patient with HIV. Finally, patients prescribed lithium carbonate for bipolar disorder can have reduced anion gap. At therapeutic doses of 1.0 mmol/L, no change in the anion gap materializes. However, in lithium intoxication, a noticeable reduction is appreciated. Other causes of reduced ion gap include hypoalbuminemia, hypertriglyceridemia, decreased unmeasured anions such as phosphorus, and increased unmeasured cations such as magnesium. increased anion gap metabolic acidosis: Carbon monoxide/cyanide Aminoglycosides Theophylline Methanol Uremia Diabetic ketoacidosis Paracetamol/acetaminophen Iron/isoniazid Lactic acidosis Ethanol/ethylene glycol Salicylate/ASA normal anion gap metabolic acidosis: Ureterostomy Small bowel fistula Extra chloride Diarrhea Carbonic anhydrase inhibitor Adrenal insufficiency Rental tubular acidosis Pancreatic fistula. #anion_gap #acidosis #آنیون_گپ #اسیدوز تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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#pneumococcal_vaccine #PCV #PPSV23 #واکسن_پنوموکک #واکسن تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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Chronic hepatitis E: هپاتیت مزمن E:  — Chronic HEV infection is defined empirically as detection of HEV RNA in serum or stool for longer than six months. Chronic HEV almost exclusively occurs in immunosuppressed patients (eg, those with HIV infection, following solid organ or bone marrow transplantation) . Chronic infection is typically with HEV genotype 3 infection, although chronic infection with genotype 4 has been documented in a transplant recipient . Chronic HEV infection with genotypes 1 and 2 have not been reported. As with most chronic viral hepatitis patients, symptoms are minimal and include fatigue and nonspecific findings until progression to decompensated cirrhosis occurs. Patients with chronic HEV have persistently elevated aminotransferase levels, detectable serum HEV RNA, and histologic findings compatible with chronic viral hepatitis. #hepatitis #HEV #هپاتیت تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles
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