Protein-calorie malnutrition in Children

Nutrition No Responses »
Aug 252010
One of the most prevalent and serious depletion disorders, protein-calorie malnutrition occurs as marasmus (protein-calorie deficiency), characterized by growth failure and wasting; and as kwashiorkor (protein deficiency), characterized by tissue edema and damage. Both forms vary from mild to severe and may be fatal, depending on accompanying stress (particularly sepsis or injury) and duration of deprivation. Protein-calorie malnutrition increases the risk of death from pneumonia, chickenpox, or measles.
Causes
Both marasmus (nonedematous protein-calorie malnutrition) and kwashiorkor (edematous protein-calorie malnutrition) are common in underdeveloped countries and in areas where dietary amino acid content is insufficient to satisfy growth requirements. Kwashiorkor typically occurs at about age 1, after infants are weaned from breast milk to a protein-deficient diet of starchy gruels or sugar water, but it can develop at any time during the formative years. Marasmus affects infants ages 6 to 18 months as a result of breast-feeding failure or a debilitating condition such as chronic diarrhea.
In industrialized countries, protein-calorie malnutrition may occur secondary to chronic metabolic disease that decreases protein and calorie intake or absorption or trauma that increases protein and calorie requirements. In the United States, protein-calorie malnutrition is estimated to occur to some extent in 50% of surgical and 48% of medical patients. Those who aren’t allowed anything by mouth for an extended period are at high risk for developing protein-calorie malnutrition. Conditions that increase protein-calorie requirements include severe burns and injuries, systemic infections, and cancer (accounts for the largest group of hospitalized patients with protein-calorie malnutrition.) Conditions that cause defective utilization of nutrients include malabsorption syndrome, short-bowel syndrome, and Crohn’s disease.
Signs and symptoms
Children with chronic protein-calorie malnutritioin are small for their chronological age and tend Continue reading »
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Severe combined immunodeficiency disease

Immunology No Responses »
Aug 212010
Both cell-mediated (T-cell) and humoral (B-cell) immunity are deficient or absent in severe combined immunodeficiency disease (SCID). This results in susceptibility to infection from all classes of microorganisms during infancy.
At least three types of SCID exist: reticular dysgenesis, the most severe type, in which the hematopoietic stem cell fails to differentiate into lymphocytes and granulocytes; Swiss-type agammaglobulinemia, in which the hematopoietic stem cell fails to differentiate into lymphocytes alone; and enzyme deficiency, such as adenosine deaminase (ADA) deficiency, in which

the buildup of toxic products in the lymphoid tissue causes damage and subsequent dysfunction.
Incidence
SCID affects more males than females; its estimated incidence is 1 in every 100,000 to 500,000 births. Most untreated patients die from infection within 1 year of birth.

Causes
SCID is usually transmitted as an autosomal recessive trait, although it may be X-linked. In most cases, the genetic defect seems associated with failure of the stem cell to differentiate into T and B lymphocytes.
Many molecular defects, such as mutation of the kinase ZAP-70, can cause SCID. X-linked SCID results from a mutation of a subunit of the interleukin-2 (IL-2), IL-4, and IL-7 receptors. Less commonly, it results from an enzyme deficiency.
Signs and symptoms
An extreme susceptibility to infection becomes obvious in the infant with SCID in the first months of life. The infant fails to thrive and develops chronic otitis, sepsis, watery diarrhea (associated with Salmonella or Escherichia coli), recurrent pulmonary infections (usually caused by Pseudomonas, cytomegalo-virus, or Pneumocystis carinii), persistent oral candidiasis (sometimes with esophageal erosions), and possibly fatal viral infections (such as chickenpox).
P. carinii pneumonia usually strikes a severely immunodeficient infant in the first 3 to 5 weeks of Continue reading »
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Staphylococcal scalded skin syndrome in Children

Infectious Diseases No Responses »
Aug 212010
A severe skin disorder, staphylococcal scalded skin syndrome (SSSS) is marked by epidermal erythema, peeling, and superficial necrosis that give the skin a scalded appearance. SSSS is most prevalent in infants ages 1 to 3 months but may develop in children; it’s rare in adults.
This disease follows a consistent pattern of progression, and most patients recover fully. Mortality is 2% to 3%, with death usually resulting from complications of fluid and electrolyte loss, sepsis, and involvement of other body systems.

Causes
The causative organism in SSSS is Group 2 Staphylococcus aureus, primarily phage type 71. Predisposing factors may include impaired immunity and renal insufficiency—present to some extent in the normal neonate because of immature development of these systems.
Signs and symptoms
SSSS commonly can be traced to a prodromal upper respiratory tract infection, possibly with concomitant purulent conjunctivitis. Cutaneous changes progress through three stages.

Erythema
In the first stage, erythema becomes visible, usually around the mouth and other orifices, as well as body fold areas, and may spread in widening circles over the entire body surface. The skin becomes tender; Nikolsky’s sign (sloughing of the skin when friction is applied) may appear.
Exfoliation
About 24 to 48 hours later, exfoliation occurs. In the more common, localized form of this disease, superficial erosions and minimal crusting develop, generally around body orifices, and Continue reading »
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