ABSTRACT
The authors describe an educational software program to use to administer medicines. They describe how a computer can help become an educational resource in nursing and the phases used to develop and evaluate this program. This program has five modules: 1. General instruction, 2. Avoiding errors, 3. Procedures, materials and supervision, 4. Possible complications, 5. Professional orientation; in addition, there is a summary module. This system has a total of 27 study units, 7 knowledge tests, 17 videos, and 34 photos. 24 students in undergraduate nursing were the study group on which this program was evaluated. Results were positive and some suggestions to improve this program were obtained. The authors concluded that this study is an improvement in teaching since this proposes a technological innovation which has possibilities for future development and due to its application of the latest technology for the nursing profession.
Subject(s)
Computer-Assisted Instruction , Drug Therapy , Humans , SoftwareSubject(s)
Alleles , Gene Deletion , Gene Frequency , Mutation , Brazil , Chromosomes , DNA Mutational Analysis , Fetal Blood , Hearing Loss, Sensorineural/genetics , Heterozygote , Humans , Infant, Newborn , Polymerase Chain ReactionABSTRACT
We describe the behavior of hemostatic variables in children with portal vein thrombosis (PVT) and in a control pediatric population. Hereditary protein C (PC) or protein S (PS) deficiency was not a etiologic factor for PVT in children. Minor signs of consumption of coagulation factors II, V, fibrinogen and hyperfibrinolysis were detected. One child had lupus anticoagulant (LA).
Subject(s)
Hemostasis , Portal Vein/pathology , Venous Thrombosis/blood , Child , Child, Preschool , Female , Humans , Infant , MaleABSTRACT
Portal vein thrombosis (PVT) is a rare condition affecting both children and adults, and occurs in association with a wide variety of clinical situations. On the other hand, the development of PVT in patients under these situations indicates that other contributing factors could be involved. Recently a missense mutation in the factor V gene (1691G-->A), known as factor V Leiden, has been identified and results in abnormal factor V product, resistant to proteolytic inactivation by activated protein C and thus predisposes to thrombosis. This study was carried out to verify if children with PVT have an increase in frequency of factor V Leiden. Allele-specific restriction analysis and single strand conformational polymorphism (SSCP) were used to test for factor V Leiden in 20 children with PVT and 64 normal children. None of the PVT children were heterozygous or homozygous for the factor V Leiden, and one control child was heterozygous. This study demonstrates that factor V Leiden is not common in children with PVT, and is not a prerequisite for this thrombotic event.
