An excessive accumulation of cerebrospinal fluid (CSF) within the ventricular spaces of the brain, hydrocephalus occurs most commonly in neonates. It can also occur in adults as a result of injury or disease. In infants, hydrocephalus enlarges the head, and in both infants and adults, the resulting compression can damage brain tissue.
With early detection and surgical intervention, the prognosis improves but remains guarded. Even after surgery, such complications as developmental delay, impaired motor function, and vision loss can persist. Without surgery, the prognosis is poor: Mortality may result from increased intracranial pressure (ICP) in people of all ages; infants may also die prematurely of infection and malnutrition.
Hydrocephalus may result from an obstruction in CSF flow (noncommunicating hydrocephalus) or from faulty absorption of CSF (communicating hydrocephalus).
In noncommunicating hydrocephalus, the obstruction occurs most commonly between the third and fourth ventricles, at the aqueduct of Sylvius, but it can also occur at the outlets of the fourth ventricle (foramina of Luschka and Magendie) or, rarely, at the foramen of Monro.
This obstruction may result from faulty fetal development, infection (syphilis, granulomatous diseases, meningitis), a tumor, a cerebral aneurysm, or a blood clot (after intracranial hemorrhage).
A medical emergency, septic (infectious) arthritis is caused by bacterial invasion of a joint, resulting in inflammation of the synovial lining. If the organisms enter the joint cavity, effusion and pyogenesis follow, with eventual destruction of bone and cartilage.
Septic arthritis can lead to ankylosis and even fatal septicemia. However, prompt antibiotic therapy and joint aspiration or drainage cures most patients.
In most cases of septic arthritis, bacteria spread from a primary site of infection, usually in adjacent bone or soft tissue, through the bloodstream to the joint.
Common infecting organisms include four strains of gram-positive cocci—Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and Streptococcus viridans—and two strains of gram-negative cocci—Neisseria gonorrhoeae and Haemophilus influenzae. Various gram-negative bacilli—Escherichia coli, Salmonella, and Pseudomonas, for example—also cause infection.
Anaerobic organisms such as gram-positive cocci usually infect adults and children older than age 2. H. influenzae most often infects children younger than age 2.
The essential features of bulimia nervosa include eating binges followed by feelings of guilt, humiliation, and self-deprecation. These feelings cause the patient to engage in self-induced vomiting, the use of laxatives or diuretics, following a strict diet, or fasting to overcome the effects of the binges. Electrolyte imbalances (including metabolic alkalosis, hypochloremia, and hypokalemia) and dehydration can occur, increasing the risk of physical complications.
Bulimia nervosa usually begins in adolescence or early adulthood and can occur simultaneously with anorexia nervosa. It affects nine women for every man affected. Nearly 2% of adult women meet the diagnostic criteria for bulimia nervosa; 5% to 15% have some symptoms of the disorder.
Bulimia nervosa has no known cause, but psychosocial factors may contribute to its development, including family disturbance or conflict, sexual abuse, maladaptive learned behavior, struggle for control or self-identity, cultural overemphasis on physical appearance, and parental obesity.
Signs and symptoms
Hypothyroidism, a state of low serum thyroid hormone, results from hypothalamic, pituitary, or thyroid insufficiency. The disorder can progress to life-threatening myxedema coma. Hypothyroidism is more prevalent in women than in men.
Hypothyroidism results from inadequate production of thyroid hormone, usually because of dysfunction of the thyroid gland due to surgery (thyroidectomy), radiation therapy (particularly with 131I), inflammation, chronic autoimmune thyroiditis (Hashimoto’s disease) or, rarely, conditions such as amyloidosis and sarcoidosis. It may also result from pituitary failure to produce thyroid-stimulating hormone (TSH), hypothalamic failure to produce thyrotropin-releasing hormone, inborn errors of thyroid hormone synthesis, inability to synthesize thyroid hormone because of iodine deficiency (usually dietary), or the use of antithyroid medications such as propylthiouracil.
In patients with hypothyroidism, infection, exposure to cold, and sedatives may precipitate myxedema coma.
Signs and symptoms:
Typically, the early clinical features of hypothyroidism are vague and may include fatigue, forgetfulness, sensitivity to cold, unexplained weight gain, and constipation. As the disorder progresses, characteristic myxedematous signs and symptoms appear, such as decreasing mental stability; dry, flaky, inelastic skin; puffy face, hands, and feet; hoarseness; periorbital edema; Continue reading “Hypothyroidism in adults”
Before chronic transfusions are initiated, the diagnosis of B0-thalassemia should be confirmed and the parents counseled about this lifelong therapy. Initiating transfusion and chelation therapy can be difficult for parents to face early in their child’s life.
If there is the possibility of a bone marrow transplant, the blood should be negative for cytomegalovirus and irradiated.
Blood Transfusion therapy:
Transfusion therapy promotes general health and well-being and avoids the consequences of ineffective erythropoiesis. A transfusion program generally requires monthly transfusions, with the pretransfusion hemoglobin level >9.5 and <10.5 g/dL. In patients with cardiac disease, higher pretransfusion hemoglobin levels may be beneficial. Some blood centers have donor programs that pair donors and recipients, decreasing the exposure to multiple red cell antigens.
Transfusional hemosiderosis causes many of the complications of thalassemia major. Accurate assessment of excessive iron stores is essential to optimal therapy. The serum ferritin level is useful in assessing iron balance trends, but does not accurately predict quantitative iron stores. Undertreatment or overtreatment of presumed excessive iron stores can Continue reading “Treatment Options for Thalassemia Major”
A common, slowly progressive megaloblastic anemia, folic acid deficiency anemia is most prevalent in infants, adolescents, pregnant and lactating females, alcoholics, elderly people, and people with malignant or intestinal diseases.
Folic acid deficiency anemia results from a decreased level or lack of folate, a vitamin that’s essential for red blood cell production and maturation. Causes include:
alcohol abuse (may suppress metabolic effects of folate)
inadequate diet (common in alcoholics, elderly people who live alone, and infants, especially those with infections or diarrhea)
impaired absorption (due to intestinal dysfunction from such disorders as celiac disease, tropical sprue, and regional jejunitis and from bowel resection)
bacteria competing for available folic acid
overcooking, which can destroy a high percentage of folic acids in foods
limited storage capacity in infants
prolonged drug therapy (with anticonvulsants and estrogens)
- increased folic acid requirement during pregnancy, during rapid growth in infancy (common because of increased survival rate of preterm infants), during childhood and adolescence (because of general use of folate-poor cow’s milk), and in patients with neoplastic diseases and some skin diseases (chronic exfoliative dermatitis).
Signs and symptoms