Folate Deficiency in Children (folic acid)

Folate exists in a cardinal of altered actinic forms. Folic acerbic (pteroylglutamic acid) is the constructed anatomy acclimated in adherent foods and supplements. Naturally occurring folates in foods (pteroylpolyglutamate) are not acclimated as able-bodied as folic acid. Folate coenzymes are complex in a array of reactions, including amalgam of deoxyribonucleic acerbic and purine, amino acerbic interconversion, and about-face of homocysteine to methionine. Because of its role in protein synthesis, the accident of absence is added during periods of accelerated advance or added cellular metabolism.

Impaired folate cachet may be associated with abiding biologic analysis of assorted non-neoplastic diseases, including the use of high-dose nonsteroidal anti-inflammatory drugs; the anticonvulsants diphenylhydantoin and phenobarbital; and methotrexate acclimated in the analysis of rheumatoid arthritis, psoriasis, asthma, and anarchic bowel disease.

Folate absence may aftereffect from poor comestible assimilation or ailing able foods ; malabsorption (hereditary folate malabsorption, abdominals disease, anarchic bowel disease, alcoholism); diseases with a aerial corpuscle about-face amount (sickle corpuscle anemia, psoriasis); congenital errors of folate metabolism (methylene tetrahydrofolate reductase, methionine synthase reductase, glutamate formiminotransferase deficiencies) ; or autoantibodies adjoin the bookish folate receptor in the choroid plexus.

Anemia

Anemia due to decreased folate assimilation usually becomes apparent beneath analytic altitude that accept added vitamin requirements (e.g., pregnancy, advance in infancy, abiding hemolysis). The accustomed baby circadian claim is 25–35?g/day. The anemia is macrocytic (mean corpuscular aggregate >100 fL). Variations in RBC appearance and admeasurement are accepted . The reticulocyte calculation is low, and nucleated RBCs demonstrating megaloblastic analysis generally are apparent in the blood. Neutropenia and thrombocytopenia not often may be present, decidedly in patients with abiding and astringent deficiencies. The neutrophils are large, some with hypersegmented nuclei. The cartilage bottom is hypercellular because of erythroid hyperplasia, and megaloblastic changes are prominent. Large, aberrant neutrophilic forms (giant metamyelocytes) with cytoplasmic vacuolation additionally are seen.

Hereditary folate malabsorption presents aural 1–3 mo of age with alternate or abiding diarrhea, abortion to thrive, articulate ulcerations, neurologic deterioration, and megaloblastic anemia. Neurologic aftereffect is poor already axial afraid arrangement manifestations are present. It is not accessible to accomplish the accustomed cerebrospinal aqueous (CSF)-serum folate arrangement of 3:1 admitting normalization of serum levels. Children with this anarchy additionally accept depressed idmmunity and are affected to adept infections.

Treatment of ancestral folate malabsorption may be accessible with intramuscular folinic acid; some patients may acknowledge to high-dose articulate folinic acerbic therapy.

Cerebral folate absence presents aural 4–6 mo of age with irritability, microcephaly, adorning delay, cerebellar ataxia, cone-shaped amplitude signs, choreoathetosis, ballismus, and seizures. Subsequently, amaurosis due to optic decline develops. Serum and red claret corpuscle 5-methyltetrahydrofolate levels are normal, but clearly low in the CSF. A high-affinity blocking autoantibody adjoin the membrane-bound folate receptor in the choroid abdomen may be the account of the baby bookish folate deficiency.

Treatment with articulate folinic acerbic corrects the low CSF folate levels and improves the analytic manifestations

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Overweight and Obesity in Children

 
Obesity and overweight are terms that are commonly used interchangeably in children, with overweight being the preferred term. As the prevalence of overweight has increased in children and adolescents, complications of overweight are now well recognized in children.
Pathogenesis:
Overweight results from a dysregulation of caloric intake and energy expenditure. A complex interplay between each individual’s genetic predispositions and the environment affects an intricate system that controls appetite and energy expenditure. Prehistoric ancestors of humans experienced long periods of food scarcity, so energy conservation and storage during times of food availability had a survival advantage.
Diagnositic Criteria for Overweight:
The diagnosis of obesity in adults is based on calculation of the BMI by dividing the weight in kilograms by the height in meters squared (kg/m²). The calculated BMI can overestimate adiposity in trained athletes or muscular children, but it is generally recognized as the most reliable method to determine healthy and unhealthy adiposity. Other methods of determining adiposity are useful, but are either too expensive to be of practical use in a clinical setting (ultrasound, CT, MRI, DEXA, total body conductivity, air displacement plethysmography), require specialized training (skinfold thickness), have poor reproducibility (waist-hip ratios), or lack extensive normative data in children (bioelectric impedance analysis). Therefore, BMI in combination with clinical assessment is sufficient to make the diagnosis.
Children’s adiposity rises in the 1st year of life, reaches a nadir around 5–6 yr of age, and then increases again throughout childhood. This is called the adiposity rebound. The 95th percentile BMI for a 4 yr old is approximately 19, but it is 25 in a 13 yr old. Consistent use of the BMI growth chart aids in early identification of children at risk for later obesity; an earlier adiposity rebound (increase in BMI younger than 5 yr of age) coincides with later obesity.
Evaluation Of Overweight Child:

  

Evaluation of overweight children and their families requires sensitivity and compassion, because the general public often perceives overweight individuals as unhealthy, unintelligent, unhygienic, and lazy. Overweight children often have decreased self-esteem, and their overweight parents may have similar psychosocial issues due to the stigma of being overweight. Obesity is a chronic medical problem that requires management in a manner similar to that of other chronic disorders. Explaining this construct to the family in an objective and nonjudgmental manner helps in building a trusting relationship that is important for successful treatment. The initial evaluation is focused on exploring dietary practices, family structure, and habits because alteration of these factors is usually the basis of successful treatment. It is also important to determine if there may be an underlying secondary cause of obesity or if there are current comorbidities from being overweight.
History:
A family history of Type 2 diabetes, a high-risk ethnicity (African-American, Hispanic, Native American), and central adiposity increase the risk of hyperinsulinism or Type 2 diabetes. Symptoms of polyuria, nocturia, polydipsia, and unexplained rapid weight loss are all associated with the onset of Type 2 diabetes. A history of maternal diabetes or obesity and being large or small for gestational age increase the risk of metabolic syndrome. Snoring, episodes of nighttime coughing fits, or excessive daytime sleepiness can be due to obstructive sleep apnea, which warrants further investigation with referral to a sleep laboratory for polysomnography. A history of wheezing, shortness of breath, or coughing can be due to asthma. Hip, knee, or leg pain is often present due to orthopedic complications. Asthma and orthopedic problems may require treatment and/or alterations in prescribed exercise programs, so identification of these problems during the initial evaluation is important. Irregular menses occur in overweight females with polycystic ovary syndrome.
Physical Findings and Laboratry Screening:
Careful screening for hypertension using an appropriately sized blood pressure cuff is important. Acanthosis nigricans suggests insulin resistance. Tanner staging is useful to identify premature adrenarche. Hirsutism, male pattern baldness, and severe acne are noted with polycystic ovary syndrome.

Treatment:

  

Successful treatment of obesity is challenging, and treatment goals vary, depending on the age of the child and the severity of complications from being overweight. Children are still growing, so severe caloric restriction and weight loss may be detrimental. Weight maintenance rather than weight loss is frequently a reasonable initial goal. As children grow in stature, BMI decreases. Weight loss should be attempted only in skeletally mature children or in those with serious complications from obesity. Weight loss should be slow (1 lb or 0.5 kg or less/wk), because more rapid weight loss requires overly restrictive dieting. An initial goal of a 10% reduction in weight is reasonable because this amount of weight loss has been shown to significantly improve overall health. Once achieved, the new weight should be maintained for 6 mo before further weight loss is attempted.

Successful long-term weight loss in adults is uncommon, despite the wide variety of diet plans and commercial products. There is a propensity to regain weight and adapt unhealthy behaviors with recurrent fad dieting. The most successful approach to weight maintenance or weight loss requires substantial lifestyle changes that include increased physical activity and altered eating habits. Similar approaches are used to prevent weight gain in children who are at risk for overweight and to promote weight maintenance or weight loss in overweight children. Therapies often combine diet, exercise, behavior modification, medications, and rarely, surgery. There is no clear and universally accepted treatment approach, but there are some generally accepted principles.
source:http://easypediatrics.com

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Hypokalemia in Children (low potassium)

Hypokalemia is generally defined as a serum potassium level of less than 3.5 mEq/L in children, although exact values for reference ranges of serum potassium are age-dependent, and vary among laboratories. It is frequently present in pediatric patients who are critically ill and reflects a total body deficiency of potassium or, more commonly, reflects conditions that promote the shift of extracellular potassium into the intracellular space.
Potassium is the most abundant intracellular cation and is necessary for maintaining a normal charge difference between intracellular and extracellular environments. Potassium homeostasis is integral to normal cellular function and is tightly regulated by specific ion-exchange pumps, primarily by cellular, membrane-bound, sodium-potassium adenosine triphosphatase (ATPase) pumps. Derangements of potassium regulation may lead to neuromuscular, GI, and cardiac conduction abnormalities.

Definition and Etiology

• Hypokalemia is defined as a serum potassium <3.5 mEq/L.
• It is a result of potassium losses in excess of replacement. Potassium can be lost through the GI tract as well as the kidneys.
  
  

  • Hypokalemia may be due to a total body deficit of potassium, which may occur chronically with the following:
    

    • Prolonged diuretic use
    • Inadequate potassium intake
    • Laxative use
    • Diarrhea
    • Hyperhidrosis
    • Hypomagnesemia
  • Acute causes of potassium depletion include the following:
    

    • Diabetic ketoacidosis
    • Severe GI losses from vomiting and diarrhea
    • Dialysis and diuretic therapy
  • Hypokalemia may also be due to excessive potassium shifts from the extracellular to the intracellular space, as seen with the following:
    

    • Alkalosis
    • Insulin use
    • Catecholamine use
    • Sympathomimetic use
    • Hypothermia
  • Other recognizable causes of hypokalemia include the following:
    

    • Renal tubular disorders, such as Bartter syndrome and Gitelman syndrome
    • Type I or classic distal tubular acidosis
    • Periodic hypokalemic paralysis
    • Hyperaldosteronism
  • Other states of mineralocorticoid excess that may cause hypokalemia include the following:
    

    • Cystic fibrosis with hyperaldosteronism from severe chloride and volume depletion
    • Cushing syndrome
    • Exogenous steroid administration, including fludrocortisone and other mineralocorticoids
    • Excessive licorice consumption
  • Other conditions that may cause hypokalemia include acute myelogenous, monomyeloblastic, or lymphoblastic leukemia.
  • Drugs that may commonly cause hypokalemia include the following:
    

    • Furosemide, bumetanide, and other loop diuretics
    • Methylxanthines (theophylline, aminophylline, caffeine)
    • Verapamil (with overdose)
    • Amphotericin B
    • Quetiapine (particularly in overdose)
    • Ampicillin, carbenicillin, high-dose penicillin
    • Drugs associated with magnesium depletion, such as aminoglycosides, amphotericin B, and cisplatin

Clinical Presentation and Physical Examination

• Symptoms: constipation, fatigue, muscle weakness, and paralysis
• Physical examination
  • Check for possible irregular heartbeat.
  • Evaluate for signs of muscle weakness/paralysis.

Differential Diagnosis

• Decreased intake as a result of low dietary intake or IV fluids without potassium
• Increased GI losses from vomiting, nasogastric suction, or diarrhea
• Increased urinary losses because of loop and thiazide diuretics
• Mineralocorticoid excess
• Liddle syndrome (autosomal dominant with increased sodium resorption)
• Bartter or Gitelman syndromes
• Amphotericin
• Hypomagnesemia

Treatment

• Administer oral or IV potassium supplements.
• Correct hypomagnesemia.
• Stop diuretics and amphotericin if possible.
   source:http://emedicine.medscape.com/article/907757-overview#a0199

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