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Identifying Data: Patient's name; age, sex. List the patient’s significant medical problems. Name and relationship to child of informant (eg, patient, parent, legal guardian). Chief Complaint: Reason given for seeking medical care and the duration of the symptom(s). History of Present Illness (HPI) : Describe the course of the patient's illness, including when it began and the character of the symptom(s); aggravating or alleviating factors; pertinent positives and negatives. Past diagnostic testing. Past Medical History (PMH): Past diseases, surgeries, hospitalizations; medical problems; history of asthma. Birth History: Gestational age at birth, whether preterm, obstetrical problems. Developmental History: Motor skills, language development, self-care skills. Medications: Include prescription and over-the-counter drugs, vitamins, herbal products, homeopathic drugs, natural remedies, nutritional supplements. Feedings: Diet, volume of formula per day. Immunizations: Up-to-...

DEF: Elevated serum bilirubin. ETIOL: In the first 3 to 4 postnatal days, healthy term infants can experience a physiologic increase in unconjugated serum bilirubin from cord levels of 1.5 mg/dL or less at birth to a mean value of 6.5 ± 2.5 mg/dL, with means of 7.3 ± 3.9 mg/dL and 5.7 ± 3.3 mg/dL for breast-fed infants and formula-fed infants, respectively. Although most new-borns have hyperbilirubinemia by adult standards, physiologic jaundice is linked to normal development and is usually benign and self-limited. It arises from a developmental delay in the conjugation and excretion of bilirubin; thus, preterm infants can have maximum serum bilirubin levels 30% to 50% higher than term babies, with elevated levels persisting for 6 to 7 days postnatally. Unconjugated or indirect hyperbilirubinemia is also caused by isoimmune hemolytic disease (e.g., ABO, Rh, or minor blood group incompatibilities); structural or metabolic abnormalities of RBCs (e.g., G6PD deficiency, hereditary sphero...

DEF: Infectious or idiopathic inflammation of the liver. ETIOL: Neonatal hepatitis can be caused by a variety of infectious agents, including cytomegalovirus (CMV), rubella, reovirus type 3, herpes simplex, herpes zoster, herpesvirus type 6, adenovirus, enteroviruses, parvovirus B19, hepatitis viruses, human immunodeficiency virus, bacterial sepsis (gram-negative rods, staphylococci, streptococci), syphilis, listeriosis, tuberculosis, and toxoplasmosis. Idiopathic neonatal hepatitis describes neonatal cholestatic liver disease for which all other known causes, including metabolic, infectious, and extrahepatic obstruction, have been ruled out. The incidence of idiopathic neonatal hepatitis is 1 in 5,000 births and accounts for 50% of cases of prolonged neonatal jaundice. CLIN/STUDIES/TX: The history should focus on maternal infection during pregnancy and delivery and family history of pediatric liver disease. The major types of neonatal hepatitis are as follows: Idiopathic: More comm...

DEF: Chronic lung disease characterized by persistent tachypnea, dyspnea, hypoxemia, and hypercarbia in neonates surviving hyaline membrane disease. ETIOL: BPD occurs in neonates with a history of pulmonary immaturity and acute lung injury who have been treated with ventilatory support. The premature lung is believed to be particularly susceptible oxygen (O2) toxicity and iatrogenic barotrauma, resulting in persistent respiratory insufficiency. Whether infection (e.g., Ureaplasma), oxidant injury, or barotrauma is the primary insult, the inflammatory process likely exacerbates the prolonged lung damage characteristic of BPD. CLIN: Most neonates with acute lung disease recover completely within the first week of life. The diagnosis of BPD is suspected when an affected neonate (typically premature) fails to recover as anticipated and instead may have a gradual increase in O2 and ventilatory requirements during the first month of life. STUDIES: No specific tests exist to confirm the di...

DEF: Neurotoxicity caused by Clostridium botulinum exotoxin, which irreversibly blocks acetylcholine release from presynaptic terminals of cholinergic neurons at the neuromuscular junction. ETIOL : Infant botulism is distinct from food-borne and wound botulism in that it is caused by ingestion of C. botulinum spores rather than the exotoxin itself. Spores germinate in the intestine and generate exotoxin, which is distributed hematogenously. Infant botulism accounts for two-thirds of reported botulism cases in the United States. Although the toxin does not cross the blood–brain barrier, it accesses the cyto-plasmic membrane of peripheral cholinergic nerve endings, preventing exocytosis of acetylcholine at the neuromuscular junction. The resulting flaccid paralysis is potentially fatal. Infant botulism occurs almost exclusively within the first year of life and typically between 5 and 12 weeks of life. Honey has been implicated as the source of spores in 20% of cases; the contaminants ha...

DEF: Progressive atresia or hypoplasia of any portion of the biliary system. ETIOL: The incidence of biliary atresia ranges from 1 in 8,000 to 1 in 20,000 live births. The disorder appears to be acquired rather than a result of abnormal development, based on the rarity of biliary atresia in autopsied fetuses and premature newborns. One causative factor is believed to be infection with reovirus type 3. CLIN: Infants with biliary atresia are typically born at term and have a normal birth weight. Jaundice develops at age 3 to 6 weeks in otherwise well-appearing, thriving infants. Fifteen percent of infants may have associated defects, including polysplenia (i.e., splenic tissue divided into several equally sized masses), cardiovascular anomalies, and malrotation of the intestine. Family history is usually negative. STUDIES: Stool is acholic, collected duodenal fluid lacks bilirubin pigment or bile acids, and abdominal ultrasound may show absence of the gallbladder. Radionuclide hepato...

ANEMIA DEF : Hematocrit and hemoglobin concentration below normal levels. CONDITION : Physiologic anemia of infancy/anemia of prematurity. ETIOL/CLIN : Soon after birth, erythropoiesis almost ceases because of the oxygen-rich milieu and relative excess of red blood cells (RBCs); this results in a decrease in hemoglobin values during the first several months of life, the severity of which is related to birth weight, perinatal complications, blood transfusion history, and vitamin E deficiency. Nadir hemoglobin values can reach 9.5 g/dL at 3 months in term infants and 6 g/dL in 6- to 8-week-old premature infants. Recovery is heralded by a slight elevation in the reticulocyte count and a rise in hemoglobin levels to those seen throughout the remainder of infancy. Tx : Healthy term infants and asymptomatic growing premature infants require no therapy. Iron supplementation may be indicated during the recovery phase to support erythropoiesis. CONDITION : Blood loss. ETIOL/CLIN : Anemia owing ...