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[의학] 간이식, liver trnasplantation

Liver transplantationIntroduction간이식은 다른 치료로 호전이 불가능한 급성, 만성 간질환에서 가장 확실한 치료방법 중 하나이다. 1963년 미국 Starzl에 의해 최초로 시행되었고 초기 성적은 만족스럽지 못했다. 현재는 새로운 면역억제제의 등장, 장기 보전 능력의 발전, 수술 수기의 향상, 술 후 처치의 향상으로 1980년경부터 간이식의 성적이 향상되고 있다. 현재 간이식의 1년 생존율은 약 85%이고 5년 생존율도 70%에 이르고 있다.우리나라에서는 1988년도 윌슨병 때문에 말기 간질환인 14세 여아에게 최초로 이식에 성공하였고 그 이후로 산발적으로 시도되었다. 현재는 뇌사자 장기 이식뿐만 아니라 생체간이식, 분할간이식이 활발히 시행되는 상황이다.Indication금기가 없고 더 이상 내외과적인 치료가 불가능한 심각하고 비가역적인 간질환을 가진 모든 환자가 대상이 될 수 있다. 일반적으로 간 기능부전에 의한 혈액응고장애와 황달의 생화학적 이상 정도에 따라 생활의 정도에 따라서, 또는 문맥압항진증의 합병증인 복수나 정맥류 출혈의 정도에 따라서, 또는 간성 뇌증의 정도에 따라서 적응증이 결정되기도 한다. 그러나 질환에 따라 적응증이 변경될 수 있는데 담즙울체성 간질환의 경우 병의 자연경과에 바탕을 둔 예후모델이 있어서 이것을 참조할 수 있고 심한 가려움증, 뼈 질환, 반복적인 담관염, 신경질환 등이 있을 경우에 간이식의 대상이 될 수 있다.소아의 경우 이식 대상은 Table 1에 정리되어있다. Biliary atresia가 가장 흔한 원인이다. 물론 Kasai 수술이 담관폐쇄의 첫 번째 치료방법이지만 간의 부전이 나타나 성장하지 않는 경우 간이식이 대상이 된다. 유전성 대사질환이 다음 흔한 원인이다.성인에서의 모든 원인의 end-stage liver disease에서 간이식이 가능하다. (table 1 참조)전격성간부전 (과거 간질환이 없는 상태에서 증상 발현 후 8주 이내에 간성 뇌증 발생)의 경우 2기 간성뇌증 발생하는 경우 간stoma, epitheloid hemangioma, multiple hepatic adenoma)은 간이식의 대상이 될 수 있다. HCC의 경우 1996년도 발표된 연구에서 5cm미만의 단일결정 혹은 3cm미만의 3개 이하 결절의 HCC 환자에서 간이식을 시행할 경우 75% 5년 생존율을 보고하여 non-HCC 환자와 비슷한 생존율을 보고 하였다. 이를 Milan criteria 하여, 여러 나라에서 이식 기준으로 시행하고 있다. 최근에는 이보다 확대된 기준으로 한국을 비롯한 여러 나라에서 적용하고 있다.Contraindication절대적인 금기증은 조절되지 않는 패혈증, 선행하고 있는 심폐질환, 전이된 악성 종양, 알코올이나 약물 중독등이 있다. 현재 60대, 70대에서도 간이식을 성공적으로 시행하고 있는 상태로 고령 단독으로는 절대적인 금기증은 아니다. 다른 동반질환을 제외하기 위해서 철저한 술 전 검사가 필요하다고 하겠다. 다른 상대적인 금기증은 Table 3.에 기술하였다.Technical considerationCadaver donor selectionABO blood group와 organ size의 compatibility가 수혜자 선택하는데 가장 중요한 고려사항이다. 하지만 응급상황이거나 donor 부족한 상황에서는 시행하기도 한다. Tissue HLA matching은 시행하지 않으며 cytotoxic HLA 항체가 있어도 시행 제외하지 않는다. 장기 획득 시 UW (University of Wisconsin) solution 사용하여 cold ischemic time을 20까지 확장하였고 보통 12h 이내에 시행한다.과거 CTP score와 대기시간을 기준으로 배분하였으나 현재는 MELD score 대체하고 있다. MELD score는 bilirubin, creatinine, PT(INR)을 사용하며 CTP score가 가진 주관적 관점이 배제하고 정확한 이식 후 예후를 반영한다.Living donor transplantation응급환경이 tation)은 1988년 Pichlmayr등에 의해서 시작되었다. 뇌사자의 간을 체외에서 일반적인 술식으로 절제한 후 체외에서 분할 하였다. 이런 체외에서 분할하는 간이식 (ex-vivo liver transplantation)은 일반 간이식보다 예후가 좋지 못하다. 냉한 보존 중에 간을 박리하여 절단하는 술식으로 시간이 많이 걸리고 조작 중에 간조직의 온도가 상승하는 것을 피할 수 없다. 또한 허혈 상태에서 간 단면을 처리하기 때문에 혈관과 담관을 완벽하게 처리하기 힘들다. 이러한 단점을 극복하기 위해서 생체 내 분할하는 간이식 (in-situ split liver transplantation)이 시행되고 있다. 이 술식의 경우 체외 분할간이식의 단점을 크게 향상시켜 1년 생존율을 92%까지 보고하고 있어 일반적인 간이식과 큰 차이를 보이지 않는다. 혈연간의 생체간이식은 1988년 브라질의 Raia에 의해 처음 시도된 이래 2008년도 우리나라에서 4288건이 시행되었다. 소아의 경우 어른 간의 왼쪽 외측이나 왼쪽 내측을 포함하면 소아 환자의 표준 간 용적에 접근하게 되고, 따라서 이 부위의 이식으로 충분한 간 용적을 줄 수 있다. 어른의 경우에는 간 용적에 한계가 있기 때문에 문제가 된다. 문헌상에서는 환자의 표준 간 용적의 약 32% 이상이거나 환자 체중의 1% 이상이 되어야 한다. 최근 환자 상태에 따라서 0.8%까지 가능한 것으로 보고되고 있다. 과거에는 왼쪽간을 많이 이용하였으나 오른쪽 간을 생체간이식에 많이 이용되고 있다.보조 간이식(auxiliary liver transplantation)은 환자의 병든 간 일부 또는 전부를 그냥 둔 채 공여자의 일부 또는 전부를 이식하는 방법이다. 전격성 간부전에 시행함으로써 괴사된 환자의 간이 회복될 때까지만 간기능을 대신하고 그 후 본인의 간이 회복하면 이식 간을 면역억제제의 투여 중지로 없애거나 수술로 제거하는 방법이다.Postoperative managementImmunosuppressive theraaft의 survival에는 차이가 없었지만 tacrolimus는 rejection 횟수의 최소화, 추가적인 glucocorticoid 필요성 감소, 세균이나 CMV 감염 가능성의 감소등을 보여 이식 후 환자 관리를 단순화가 가능하게 되었다. Cyclosporine 경우, 수술 직후에 T-tube drainage로 enterohepatic circulation의 장애로 흡수율 예측이 힘들다. 그에 비해 경구 투약 시 cyclosporine보다 흡수율이 예측하기 더 수월한 장점을 가진다. Nephrotoxicity와 neurotoxicity가 가장 흔한 부작용이다. 당뇨의 경우에는 두 가지 약물에서 다 발생 가능하지만 hirsutism과 gingival hypertrophy는 tacrolimus에서 발생하지 않는다. Cyclosporine과 tacrolimus는 toxicity를 overlap한다. Tacrolimus는 cyclosporine의 clearance 감소시키므로 동시에 사용하지 않는다. 수술 직후에 생긴 신기능 저하 시에는 tacrolimus나 cyclosporine 사용은 부적절하다. 이 경우 T cell의 monoclonal antibody인 OKT3 사용 가능하다. OKT3는 이식 후 급성 거부반응 시에 효과적이며 methylprednisolone에 반응하지 않는 급성 거부반응에 표준치료이다.Transplant rejection면역억제제 사용에도 불구하고 이식 후 1~2주부터 시작되는 거부반응이 아직도 큰 부분이다. 거부반응의 임상적 증상은 발열, 우상복부 통증, bile 분비 감소이다. 가장 의미 있는 검사 소견은 bilirubine, aminotransferase 수치의 상승이다. 이식 거부가 의심되는 경우 methylprednisolone 투여하고 반응이 없는 경우에는 OKT3나 polyclonal antilymphocyte globulin을 사용한다. 만성 거부반응은 상대적으로 드물고, 반복적인 급성 반응 후에 발생하거나 이전에 거부반응lson's diseaseFulminant hepatitisTyrosinemia, ProtoporphyriaAlcoholic cirrhosisGlycogen storage diseasesChronic viral hepatitisLysosomal storage diseasesPrimary hepatocellular malignanciesCrigler-Najjar disease type IHepatic adenomasFamilial hypercholesterolemiaNonalcoholic steatohepatitisPrimary hyperoxaluria type IFamilial amyloid polyneuropathyHemophiliaTable 2. Indication to liver transplantation of fulminant hepatitis (O’Grady criteria)Acetaminophen tocixitiypH6.5(INR), serum creatinine>3.4mg/dlNon-Acetaminophen tocixitiyPT>6.5(INR) or3 or more of 5 criteria are requiredAge : 40원인 : NANB 간염, 할로테인간염, 특이체질 약물반응PT>3.5(INR)Serum bilirubin>17.6mg/dl뇌병증 전 황달의 기간 >7일Table 3. Contraindications to liver transplantationAbsoluteRelativeUncontrolled extrahepatobiliary infectionActive, untreated sepsisUncorrectable, life-limiting congenital anomaliesActive substance or alcohol abuseAdvanced cardiopulmonary diseaseExtrahepatobiliary malignancy (not including nonmelanoma skin cancer)Metastatic m

의/약학| 2011.06.07| 7페이지| 2,500원| 조회(267)

간이식, Liver transplantatio, 생체 간이식, 사체 간이식

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Achalasia & Esophageal motility disorders

Esophageal motility disorders AchalasiaNormal physiology of esophagusNormal eosphageal manometer and fluroscopy of barium swallowExamples of esophageal peristalsis and LES relaxation during three swallows each of 5 mL of water.Classification of esophageal motility abnormalitiesInadequate LES relaxation Classic achalasia Atypical disorders of LES relaxationUncoordinated contraction Diffuse esophageal spasmHypocontraction Ineffective esophageal motilityHypercontraction Nutcracker esophagus Isolated hypertensive LESGut 2001;49:145–151Motility patterns in esophageal smooth muscle disorders. Harrison's Principles of Internal Medicine. 16th ed 1739–1745.Esophageal manometric findings in classic achalasia and vigorous achalasiaEsophageal manometric findings in diffuse esophageal spasm.Esophageal manometric findings in Nutcracker esophagusEsophageal manometric findings in systemic sclerosis.AchalasiaIntroductionSir Thomas Willis, first described in 1674 who described a man in good health who vsulting from loss of inhibitory neurons results in elevation in basal LESP and absence of relaxation of LES Achalasia with complete loss of myenteric neurons. basal LESP is below normal owing to absent excitatory neurons,Pathophysiologyneurodegenerative insult inflammatory origin with possibly (slow) viral involvement. genetic, autoimmune or infectious origin of the neural damage, secondary achalasia associated with Chagas disease caused by trypanozoma cruzi endemic to Southern AmericaImportant causes of achalasiaClinical featureAchalasia is a rare disease affecting both genders annual incidence between 0.5~1/100.000 per yr incidence peaks in the 3rd and 7th life decade chest pain is reported by 1/3~1/2 of pt with achalsia wt. loss is common, confused with eating disorder combination of dysphagia for both “solid and liquids” suggesting achalasia over mechanical obstruction “symptoms rather than physical finding are hallmark”Diagnosistypically delayed 2-3 yrs from onset of symptoms suspiographic findings smooth tapering in the distal esophagus with “bird´s beak” or “champagne glass” appearance lack of primary peristalsis noticed during fluoroscopy formation of a contrast column above LES none be present in early phase of disease normal barium esophagogram not rule out achalasiaConventional barium esophagogram in achalasiaBird's beak“Timed barium” swallow in achalasia. Images were 1, 3 and 5 min after ingestion of 50-100ml barium. monitor patients after therapy in order to detect recurring disease before becoming clinically overt. Before (A), after (B) treatment.Esophageal manometry“gold standard” in diagnosing calssic achalasia three characteristic manometric features elevated resting LES pr (above 45 mmHg) incomplete LES relaxation after swallow aperistalsis in smooth muscle portion of esophageal body Vigorous achalasia simultaneous esophageal contractions amplitudes 60 mmHg prognostic therapeutic value of this separation controversialEsophageal manometric findings otulinum toxin injections Pneumatic balloon dilatation Surgical lower esophageal myotomyOral pharmacologic treatmentsmooth muscle relaxants CCB, nitrates and phosophodiestarase inhibitors aimed at reducing LES pr. clinically available pharmacologic therapies limited value in treatment of achalasia. Indication pts not willing or unable to undergo any other procedure pts waiting for more definitive therapy supportive treatment for refractory chest pain in achalasia.Botulinum toxin injectionsPasricha et al reported on use of botulinum toxin A (Botox) injections in LES to treat achalasia. NEJM 1995;332:774-778. original protocol, 80~100IU of BoTox are injected in 4 quadrants just above Z-line, an area LES Initial beneficial effect occurs in 60~75% duration of BoTox treatment varies according to various studies , generally on average 6-12 mo.Mechanism of Action of Botulinum ToxinJAMA 2001;285;1059~1070Dilatationoldest treatment modality and first described 300 yrs ago with a tool of time – phamacologic treatment and BoToxEfficacy reduced by half for subsequent dilatation poor initial result or rapid recurrence lesser response Morbidity in 3% of patients, Mortality rarely reported most related to esophageal perforation, Perforation more likely in severe malnurished pt. Disadvantages - lesser short- and long-term efficacy in comparison with myotomy, particlularly in young patientsEsophagomyotomyGoal of surgical theraphy to reduce LES resting pr without completely compromising refluxErnst Heller first described in 1914 two-cardiomyotomy technique (one ant. and one post.) along GEJ Modification of this procedure (Heller myotomy and Toupet posterior fundoplication)EsophagomyotomyGood results from open myotomy occur in 80~90% reduces LED pr. more than pneumatic dilatation accounting for greater efficacy Minimally invasive approaches to myotomy as effective as open counterpart surgical procedure of choice as limited long-term dataComparison of Primary Treatments for Idiopathic ow}

의/약학| 2009.07.29| 33페이지| 2,000원| 조회(285)

Botulinum, 이완불능증, achalasia, Esophagomyotom..

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[의학] malignant hyperthermia (악성 고열 증후군)

Review : Malignant hyperthermiaIntroductionMalignant hyperthermia (MH) uncommon, potentially fatal pharmacogenetic disorder uncontrolled release of cytoplasmic free Ca from sarcoplasmic reticulum of skeletal m. leading to increased metabolism incidence of MH in North America and Europe 1:15 000 anaesthetics for children and adolescents 1:50 000~1:150 000 anaesthetics for adults prevalence in general population :unknown may be as common as one in 2000IntroductionMH may occur whenever 'triggering' agents are used in susceptible pts susceptible to MH , develop heat stroke, exercise induced rhabdomyolysis and hyperthermia with use of certain drugs – methamphetamine 1st recognized as complication of anaesthesia, case-fatality rate was 70%. Today, with prompt use dantrolene, widespread education, diagnostic testing, mortality rate is 5%Trigger agents and safe agents for malignant hyperthermia.PathophysiologyMuscle PhysiologyCross-bridge CycleThis animation by Mike Geeves, Laboratory of Molece responsible for RYR1, located on chr. 19. Administration of triggering agents, all halogenated anaesthetic agents , succinylcholine increase RYR1 activity and disturb Ca++ regulation, leading to sustained m. contraction and hypermetabolism.Muscle membrane breakdownUncontrolled release of Ca2+ from sarcoplasmic reticulumIntracellular Ca2+ in skeletal muscleIntense muscle contractionSustained and enhanced ATP activityUncontrolled in aerobic and anerobic metabolism (hypermetabolism)O2 consumptionCO2 productionSympathetic toneacidosishyperkalemiaVentricular fibrillationDEATHClinical feature and diagnosisMasseter muscle spasm or trismus occur in up to 1% of children induced with inhalation agents and then given succinylcholine. Succinylcholine - induced masseter rigidity : predictive sign of MH elective surgery postponed. Urgent surgery continued using non-trigger agents unit for observation for 24 hours and myoglobin and CKMimics of MHThyroid storm Neuroleptic malignant syndrome IatrogenmyopathyTreatmentDantrolene sodiumInitially synthesized as antibiotic, found to cause muscle weakness in animals dantrolene inhibits excitation-contraction coupling RYR1 is direct molecular target slows Ca release by sarcoplasmic reticulum and decreases total amount released no direct effect on actin/myosin binding and no effect on neuromuscular junctionDantrolene sodiumelimination half-life : approximately 9 hrs not significantly influenced by pregnancy or preoperative medication with diazepam or Phenobarbital pharmacokinetics are similar in paediatric pts 5-OH dantrolene, metabolized in liver from dantrolene excreted in urine half activity of parent compound and has a half-life of approximately 15 hrs cannot be removed to appreciable extent by dialysisClinical Indicators for use in Determing the Malignant Hyperthermia (MH) Raw Score Anesthesiology. V 80, No 4, Apr 1994 Process Indicator points Process I: Rigidity Generalized muscular rigidity (in absence of shivering 15 due to hypothted creatine kinase 10,000 IU after anesthetic 15 without succinylcholine Cola colored urine in preoperative period 10 Myoglobin in urine 60 μg/L 5 Myoglobin in serum 170μg/L 5 Process III: Respiratory Acidosis PETCO2 55 mmHg with appropriately controlled ventilation 15 Arterial Paco2 60 mmHg with appropriately controlled ventilation 15 PETCO2 60 mmHg with spontaneous ventilation 15 Arterial Paco2 65 mmHg with spontaneous ventilation 15 Inappropriate hypercarbia ( in anesthesiologist's judgment) 15 Inappropriate tachypnea 10Process IV: Temperature increase Inappropriately rapid increase in temperature 15 (in anesthesiologist's judgment) Inappropriately increased temperature 38.8℃ 10 (101.8℉) in the perioperative period (in anesthesiologist's judgment) Process V: Cardiac Involvement Inappropriate sinus tachycardia 3 Process VI: Family History Positive MH family history in relative of first degree 15 (used to determine MH susceptibility) Positive MH family history in relative not of firsr 10 indicator from the patient's own anesthetic experience other than elevated resting serum CK Resting elevated serum creatine kinase (in patient with 10 a family history of MH). Anesthesiology. V 80, No 4, Apr 1994 -----------------------------------------------------------------------------Raw Score Range MH Rank Description of Likelihood 0 1 Almost never 3-9 2 Unlikely 10-19 3 Somewhat less than likely 20-34 4 Somewhat greater than likely 35-49 5 Very likely 50+ 6 Almost certain Anesthesiology, V80, No 4, Apr 1994Evaluation of susceptibility to MHcaffeine-halothane contracture test (CHCT) standard test for diagnosing susceptibility to MH obtained by muscle biopsy (vastus lateralis) bathed on a solution containing 1-3% halothane and caffeine they decrease the threshold for muscle contraction and therefore facilitate diagnosis. standardized test protocols : sensitivity 97–99% specificity 85–90%Mutation in gene, calcium release channel (the ryanodine receptor, RYR-1)---Porcine RYR-1

의/약학| 2007.09.17| 20페이지| 2,000원| 조회(810)

의학, malignant hypertherm, 악성 고열 증후군

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Pheochromocytoma(갈색세포종) 진단

Review of Pheochromocytoma -diagnosis 중심으로-Pheochromocytomascatecholamine-producing neuroendocrine tumors arising from chromaffin cells of adrenal medulla or extra-adrenal paraganglia. tumors from extra-adrenal chromaffin tissue : extra-adrenal phaeochromocytomas or paragangliomas.Frequency of signs and symptoms of pheochromocytomaLancet 2005; 366: 665–675Classic triadHypertension is often paroxysmal in nature background of sustained HTN or normal BP can severe and result in HTN emergencies be consistently normal, esp in adrenal incidentalomas dopamine-producing paragangliomas normal BP or even hypotension is common predominantly epinephrine-secreting tumors present with hypotension or even shock contributing factors intravascular vol. depletion, abrupt cessation of catecholamine secretion d/t tumour necrosis, desensitisation of adrenergic receptors, hypoCaDifferential diagnosis of pheochromocytomaEndocrine Hyperthyroidism Carcinoid Hypoglycaemia Medullary thyroid carcinoma Mastocytosirdia syndromeCardiovascular Heart failure, Arrhythmias Ischaemic heart disease Baroreflex failure Miscellaneous Porphyria Panic disorder or anxiety Factitious disorders (sympathomimetic drugs such as ephedrine) Drug treatment (MAO inhibitors, sympathomimetic drugs, withdrawal of clonidine) Illegal drugs (eg, cocaine)Pheochromocytoma in genetic disorderMost catecholamine-secreting tumors are sporadic. Some pts (15~20%) have disease as part of familial disorder. ; in these patients catecholamine-secreting tumors are more likely to be bilateral adrenal pheochromocytomas or paragangliomas. Familial pheochromocytoma There are two primary familial disorders associated with pheochromocytoma, both of which have autosomal dominant inheritance: von Hippel-Lindau (vHL) syndrome MEN2Indications for screeningHyperadrenergic spells (eg, self-limited episodes of nonexertional palpitations, diaphoresis, headache, tremor, or pallor) Hypertension – sustained or paroxysmal Familial syndrome (eg, MEN 2, Vor angiography Onset of hypertension at young ageDiagnotic approach to pheocromocytoma1.2.3.TyrosineL-DopaDopamineNorepinephrineEpinephrineCatecholaminesNormetanephrineMetaneprinePNMTDBHCOMTCOMTMetabolitesHomovanillic acid (HVA)MAO, COMTVanillymandelic Acid (VMA)MAOMAOTHCatecholamines synthesis and metabolismTH : tyrosine hydroxylase DBH : Dopamine β-hydroxylase PNMT : phenylethanolamine N-methyl-transferase MAO : monoamine oxidase COMT : catechol-O-methyltransferase24h Urine Collection24h urine collection: Creatinine, catecholamines, metanephrines, vanillymandelic acid (VMA) HPLC with electrochemical detection or mass spect Positive results ( 2-3 fold elevation): 24h Ucatechols 2-fold elevation ULN for total catechols 591-890 nmol/d 24h Utotal metanephrines 1.2 ug/d (6.5 umol/d) 24h UVMA 3-fold elevation ULN 35 umol/d for most assays24h Urine: False PositiveDrugs: TCAs, MAO-i, levodopa, methyldopa, labetalol, propanolol, clonidine (withdrawal), ilicit drugs (opiods, amphetamines, cocaycemia, stroke, raised ICP, etc.)Plasma CatecholaminesDrawn with patient fasting, supine, with an indwelling catheter in place 30 min Plasma total catechols 11.8 nM (2000 pg/mL) SEN 85% SPEC 80% False positives: same as for 24h urine testing, also with diuretics, smoking CRF ESRD: Oliguric to Anuric  24h Urines inaccurate Plasma epinephrine best test for pheo in ESRD Plasma norepi and metanephrines falsely elevated in ESRDPlasma MetanephrinesNot postural dependent: can draw normally Secreted continuously by pheo SEN 99% SPEC 89% False Positive: acetaminophenSensitivity and specificity of biochemical tests for diagnosis of pheochromocytomaLancet 2005; 366: 665–675Sources of variable interference with measurements of catecholamines and catecholamine metabolitesLancet 2005; 366: 665–675Suppression/Stimulation TestingClonidine suppression clonidine po 0.3mg plasma catecholamine and metaneprines measured before and after 3hrs normal subjects – norepi. + epi. 500pg/mL, normetanephrine into ate – 92% May precipitate hypotensive shock!Radiologic testAbout 10% of tumors are extraadrenal, but 95% are within abdomen and pelvis Any site containing paraganglionic tissue can be involved Superior and inferior abdominal paraaortic arears (75%) urinary bladder (10%), thorax (10%), head neck (5%)ADRENAL GLANDS – NORMAL APPEARANCEImaging characteristicsEnhancement with IV contrast on CT scan High signal intensity on T-2 weighted MRI scan May have cystic and hemorrhagic changes Variable size and may be bilateralUNILATERAL PHEOCHROMOCYTOMABILATERAL PHEOCHROMOCYTOMASPHEOCHROMOCYTOMA – HYPERINTENSITY ON MRIMIBG Scan123I or 131I labelled metaiodobenzylguanidine MIBG catecholamine precurosr taken up by the tumor Inject MIBG, scan @ 24h, 48h, 72h Lugol's 1 gtt tid x 9d (from 2d prior until 7d after MIBG injection to protect thyroid) False negative scan: Drugs: Labetalol, reserpine, TCAs, phenothiazines Must hold these medications for 4-6 wk prior to scanEvaluation and treatment of catechola}

의/약학| 2007.09.14| 26페이지| 2,000원| 조회(1,821)

갈색세포종, Pheochromocytoma, paragangliomas

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[내과, 산부인과]임신시 항고혈압제와 면역억제제 사용

immunosuppressive antihypertensive drugs in pregnancyimmunosuppressive drugs in pregnancyGLUCOCORTICOIDScleft palate, mental retardation, and fatal adrenal hypoplasia reported in humans after in utero steroid exposure during preg. PROM and intrauterine growth restriction. pregnancy-induced HTN, gestational DM, osteoporosis suppression of the hypothalamic pituitary adrenal axis in newborn : infrequent and transientRecommendations : lowest effective glucocorticoid dose possible, avoidance of therapy during 1st trimester 20 mg PDL, interval of breast feeding – 4hrs FDA use in pregnancy rating - BCYCLOPHOSPHAMIDE1st trimester : cyclophosphamide embryopathy – growth restriction, ear facial abnormalities, absence of digits, hypoplastic limbs 2nd,3rd trimester : 2 women treated for SLE fetal demise. (Clowse et al. 2005) 36 women treated for breast cancer without reported adverse pregnancy or neonatal events (Berry et al. 1999)Recommendations : avoid during preg. except life-threatening, no alternative. breast feeding is prohibited preg. test before theraphy if, child bearing age FDA use in pregnancy rating - DAZATHIOPRINE64 ~ 93% administered to mothers appears in fetal blood as inactive metabolites. - fetal liver lack of inosinate pyrophosphorylase lower birth wt., prematurity, jaundice, RDS, aspiration, dose-related myelossupresionRecommendations : can be used ,necessary during pregnancy. feeding no recommended d/t excreted in to breast FDA use in pregnancy rating - DCYCLOSPORINEconflicting reports on transfer of cyclosporine across the human placenta during preg. PROM and intrauterine growth restriction. pregnancy-induced HTN, gestational DM complication rate in newborns was slightly lower in cyclosporine group and no malformations were seen. (Armeti et al. Transplantation 1994, 27 : 502)CYCLOSPORINEcyclosporine metabolism increased during preg. - higher dose requirement to therapeutic level pre-eclampsia complicated by cyclosporin - limited to 2~4mg/kg/dayRecommendations : alternative to other immunosuppressant during preg. long-term effects, exposed in utero is unknown. breast feeding not recommended FDA use in pregnancy rating - CTACROLIMUSpaucity of data about effect of tacrolimus 60% premature among 100 pregnancies in 84 women (Kaniz et al. Transplantation 2000) 4 babies with malformations - no consistent pattern of anatomic abnormalityFDA use in pregnancy rating - CMYCOPHENOLATE MOFETILanimals, cause problems with development of ova humans, case report of in utero exposure causing hypoplastic nails ,short 5th fingers ; no other abnormalities were notedRecommendations : avoid using medication during preg.,nursing d/t paucity of available information, FDA use in pregnancy rating - COKT3Immunoglobulin G - cross placenta 4 surviving infants among 5 woman with OKT3 - NTPR reported, 1997FDA use in pregnancy rating - CCONCLUSIONimmunosuppressive regimen of transplant recipients - glucocorticoids, azathioprine, cyclosporine.for pregnant ,autoimmune disease mild – immunosuppressant avoided. low dose glucocorticoids (PDL 5~15mg/day) moderate to severe - glucocorticoids, azathioprine, cyclosporine, IVIG tolerated by fetus. life-threatening - high-dose steroid, cyclosporine azathioprine cyclophosphamide reserved for cases of no alternative available.CONCLUSIONNephrol Dial Transplant 2002 17: 703Treatment of hypertension in pregnancyBlood pressure goalpreg. without end-organ damage systolic pr. -140~150 mmHg diastolic pr. - 90~100 mmHg preg. with end-organ damage below 140/90 mmHg , go as low as 120/80 mmHg.methyldopa : most widely used in preg. and long-term safety hydralazine : safe and used frequently Beta-blocker : generally safe labetalol is the preferred agent. atenolol - impair fetal growth early in preg non selective BB – not used d/t risk of uterine contractionACEi and angiotensin receptor antagonists : serious adversed effects – oligohydroamnios, neonatal anuria, renal failure, death Calcium channel blocker : no incresed congenital anomaliesFirst choice : methyldopa or labetalol. 2nd or 3rd line : long acting calcium channel blocker (nifedipine or amlodipine) normal fall in BP during 2nd trimester reduction in dose or cessationBreastfeeding mothersBeta blockers and calcium channel blockers : enter breast milk; safe during lactation labetalol propranolol preferred for initial choice SR nifedipine or verapamil alternatives ACE inhibitors and angiotensin receptor : avoided in the neonatal period, but considered after time. Diuretics reduce milk volume and should be avoided.{nameOfApplication=Show}

의/약학| 2006.10.28| 19페이지| 2,000원| 조회(512)

임신, 면역억제제, pregnanacy, 항고혈압, immunosuppressi..

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