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