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drug therapy in pregnancy and pediatrics

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Question
Answer
Kernicterus   competition between drugs and bilirubin with plasma protein binding sites  
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Tetracycline effects   teeth  
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amphetamine and methylphenidate   growth retardation  
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aspirin in children   reyes syndrome  
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Routes   oral and rectal. Avoid parenteral  
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why do you avoid parenteral admin   phase II metabolism is slower to develop  
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Drug Dosage   dose= adult dose X (kg/150)  
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preferred method of drug dosage   surface area  
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when is adult renal fucntion attained   1 year  
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pediatric absorption   variations in peripheral blood flow makes unpredictable absorption of parenteral drugs. Gastric pH and emptying time vary during development  
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Distribution   differences in amount of body water, fat and plasma protein results in Vd differences from adult  
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Metabolism   phase I metabolism more developed than Phase II in neotates. Phase I activates, phase II conjugates  
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teratogenesis   defined as induction of alterations of somatic cells of a developing organism causing defects in organ systems  
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Factors determining placental drug transfer   placental blood flow, molecular size of drug, lipid solubility of drug, pKa of drug, fetal pH  
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basic drugs and fetus   increased ion trapping on fetal side  
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acidic drugs and fetus   increased ion trapping on fetal side  
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fetal pH   slightly less than maternal pH resulting in increased ion trapping of basic drugs on fetal side  
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protein binding in fetus   fetus has lower total plasma protein  
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fetal distribution   significant amount of umbilical venous blood flow enters fetal liver before reaching general circulation  
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metabolism   drug metabolizing systems present and functional early n gestation. Phae I reactions generally more developed than Phase II  
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fetal excretion   via placenta (early) and kidneys (late)  
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factors which control susceptiblity of teratogenesis   cell proliferation, organogenesis, growth and functional maturation, most organs have a period of particular susceptiblitiy, dose dependant  
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drug classifications (risk factors)   A, B, C, D, X  
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Class A   vitamins  
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Category B   no demonstrated fetal risk but are no controlled studies in pregnant women or animal-reproduction studies have shown an adverse effect  
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Category C   have revealed adverse effects on the fetus but potential benefit justifies the potential risk to fetus  
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Category D   beneftis from use in pregnant women may be acceptable despite the risk. Used in a life threatening situation. There is positive evidence of human fetal risk  
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Category X   studies in animals or human beings have demonstrated fetal abnormaliteiis or there is evidence of fetal risk based on human experience or both. Use of drug in pregnant woemen clarly outweighs any possible benefit  
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Analgesia during pregnancy   APAP best choice. NSAIDs increase risk of miscarriage  
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Anemia during pregnancy   prevention – oral ferrous suphate – tx, oral ferrous sulphate x3 dayliy and folic acid 5 mg daily  
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nausea and vomiting   PremesisRx  
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Preeclampsia (early)   treat with bed rest and sedate with phoneobarbital. ASA effects on platelets decrease clotting and increase placental perfusion  
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Eclampsia   bed rest magnesium sulfate and hydralizine  
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folic acid   prevention of neural tube defects  
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depression   SSRIs  
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Diethylstilbestrol   vaginal adenosis, clear cell vaginal adenocarcinoma  
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Ethanol   risk of fetal alcohol syndrome and alcohol-related neurodevelopmental defects  
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methotrexate   multiple congenital malformations  
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phenytoin   fetal hydantoin syndrome  
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thalidomide   phocomelia (absent long bones)  
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warfarin first triemester   hypoplastic nsal bridge, chondrodysplasia  
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warfarin second trimester   CNS malformations  
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Warfarin third trimester   risk of bleeding. Discontinue use 1 month before delivery  
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