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pheochromocytoma (갈색세포종)

Pheochromocytoma차례Catecholamine producing tumor Physiology/Pathophysiology Clinical Presentation Epidemiology Signs Symptoms Diagnosis Biochemical Localization Management Preoperative Operative Postoperative PregnancyCatecholamine Producing TumorsNeural CrestSympathoadrenal Progenitor Cell (Neuroblasts)Chromaffin CellSympathetic Ganglion CellIntra-adrenal Extra-adrenal PheochromocytomaGanglioneuromaNeuroblastomaCatecholamine Producing TumorsPheochromocytoma Paraganglioma (extra-adrenal pheo) Originate in extra-adrenal sympathetic chain/chromaffin tissue Ganglioneuroma Behave like paraganglioma biochemically Neuroblastoma Common malignancy in children, adrenal or sympathetic chain Catecholamine humoral effects usually minor Rapid growth widespread metastasis Some differentiate and spontaneously regress Rx complex (surgery, RTx, chemotherapy)Catecholamine Producing TumorsCheodectoma Carotid body, behave like paraganglioma biochemically Glomus jugulare tumor Intracranial branch of CN IX a Precipitated: Diagnostic procedures, I.A. Contrast (I.V. is OK) Drugs (opiods, unopposed -blockade, anesthesia induction, histamine, ACTH, glucagon, metoclopramide) Strenuous exercise, movement that increases intra-abdo pressure (lifting, straining) Micturition (bladder paraganlgioma)Pheo: Hypotension!Hypotension (orthostatic/paroxysmal) occurs in many patients Mechanisms: ECF volume contraction Loss of postural reflexes due to prolonged catecholamine stimulation Tumor release of adrenomedullin (vasodilatory neuropeptide)Pheo: Signs SymptomsN/V, abdo pain, severe constipation (megacolon) Chest-pains Anxiety Angina/MI with normal coronaries: Catecholamine induced:  myocardial oxygen consumption or coronary vasospasm CHF HTN  hypertrophic cardiomyopathy  diastolic dysfn. Catechols induce dilated cardiomyopathy  systolic dysfn. Cardiac dysrhythmia conduction defectsPheo: Signs (metabolic)Hypercalcemia Associated MEN2 HPT PTHrP secretion by pheo Mild glucose intolerance Lipolysis Wei UVMA Sen 63% Spec 94% Sensitivity increased if 24h urine collection begun at onset of a paroxysm24h Urine: False PositiveDrugs: TCAs, MAO-I, levodopa, methyldopa, labetalol, propanolol, clonidine (withdrawal), ilicit drugs (opiods, amphetamines, cocaine), ethanol, sympathomimetics (cold remedies) Hold these medications for 2 weeks! Major physical stress (hypoglycemia, 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: acetaminophenBiochemical Tests: Summary80%85%Plasma catecholamines89%99%Plasma metanality: 0 - 2.7 % Preoperative preperation, -blockade? New anesthetic techniques? Anesthetic agents Intraoperative monitoring: arterial line, EKG monitor, CVP line, Swan-Ganz Experienced Coordinated team: Endocrinologist, Anesthesiologist and SurgeonPreop workupCBC, electrolytes, creatinine, INR/PTT CXR EKG Echo (r/o dilated cardiomyopathy 2º catechols)Preop Preperation RegimensCombined  +  blockade Phenoxybenzamine Selective 1-blocker (ex. Prazosin) Propanolol Metyrosine Calcium Channel Blocker (CCB) Nicardipine No Randomized Clinical Trials to compare various regimens!Preop:  +  blockadeStart at least 10-14d preop Allow sufficient time for ECF volume re-expansion Phenoxybenzamine Drug of choice Covalently binds -receptors (1 2) Start 10 mg po bid  increase q2d by 10-20 mg/d Increase until BP control and no more paroxysms Maintenance 40-80 mg/d (some need 200 mg/d) Salt load: NaCl 600 mg od-tid as toleratedPreop:  +  blockadePhenoxybenzamine (cont'd) Side-effect: orthostati adjunct to  +  blockade or other preop prepTyrosineL-DopaDopamineNorepinephrineEpinephrinePNMTDBHTHPreop: CCBCleveland Clinic Experience Only 6 cardiovascular complications All occurred in patients with preop -blockade 30% received no medications preop if no HTN Patients not receiving phenoxybenzamine required less fluids (956 cc intraop, 479 cc POD#1) CCB Block norepi mediated Ca transport into vascular smooth muscle Nicardipine: most commonly used agentPreop: CCBNicardipine (France Study) Started po 24h to few weeks preop to control BP and allow ECF volume restoration After intubation  IV Nicardipine gtt (start 2.5 ug/kg/min) IV Nicardipine adjusted to SBP Stopped prior to ligation of tumor venous drainage Tachycardia Rx with concurrent IV esmolol Advantage: periop hypotension may still respond to pressor agents as opposed to those patients who are completely -blockedPreop: CCBCleveland Clinic: Only 10% received phenoxybenzamine CCB 1st line agents as preop po med Selective 1w}

의/약학| 2008.07.25| 49페이지| 10,000원| 조회(118)

고혈압, 갈색세포종, Hypertension, Pheochromocytoma, epidemiology

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일반인과 의대생을 위한 간경화 총정리

간 경화간 경화간 경화 간경화증 또는 간경변증 (liver cirrhosis(LC))은 '간이 딱딱해지는 병'을 말함 즉, 간조직에 만성적으로 염증이 있어서 간세포가 광범위하게 파괴되고, 그 자리에 섬유조직의 증식과 재생성 결절 (regenerative nodule, 간경변증 등에 특징적인 작은 덩어리)이 형성되어, 2차적으로 간 내 혈관의 변형과 간 기능의 저하를 초래하는 질환을 말합니다 ☞ 간 경화 : 간염이 오래 지속되어, 간 조직이 섬유화, 경화 되는 것간 경화가 중요한 이유 → 간경변증은 간암(liver cancer)으로 발전할 수 있을 뿐 만 아니라 그 자체만으로도 간기능의 부전 등을 초래하여 사망에 이를 수 있는 질환이기 때문 간 경화의 원인 바이러스 B 형 간염, C 형 간염, D 형 간염 알코올 독성 간염 비알콜성 지방간 자가 면역성 질환바이러스가 원인이 되는 간염 A형, B형, C형, D형, E형, G형 그외 기타 : 단순포진 바이러스(Herpes simplex virus), 거대세포바이러스(Cytomegalovirus, CMV), 엡스타인-바 바이러스 (Epstein-Barr virus), 황열 바이러스(yellow fever virus), 아데노바이러스(adenovirus) A 형 간염 A형간염바이러스(hepatitis A virus, HAV)에 의해 감염되어 발생하는 간의 염증성 질환 바이러스에 오염된 음식물 등을 섭취함으로 감염 대부분 공중위생 상태가 나쁜 경우에 잘 생기며 감염자와의 직접적인 신체 접촉을 통하여 감염될 수도 있다증상 4주간의 잠복기를 거친 후 급성간염 증상이 나타남 위장관 증세 : 식욕부진(anorexia)·오심(nausea)·구토(vomiting)·설사(diarrhea) 전신증상 : 피로·무력감·권태감·발열·두통(headache) 황달(jaundice) 치료 특별한 치료법이 없어서 증상이 심한 경우에는 증상에 대한 치료 대증요법만 시행 대부분 대증요법만으로 서서히 임상증상이 호전되면서 황달이 없어지고 후유증 없이 완. 모유에서도 B형간염바이러스가 아주 소량이나마 검출 모유 수유는 지양증상 급성B형간염(acute hepatitis B) : 전황달기(preicteric phase), 황달기(icteric phase), 회복기(recovery phase) 전황달기 : 황달(jaundice)이 나타나기 1∼2 주 전 피로감, 식욕부진, 오심 및 구토, 미열, 근육통 담배를 즐기던 사람이 담배맛을 잃어버리거나 우측 상복부에 불쾌감을 호소 95%에서 소변 색깔이 진해짐 관절통, 발진, 혈관부종 등이 발생하기도 함. 전격성간염 만성간염 - 간경변증/ 간암치료 항바이러스제 투여 + 증상에 따른 보존 치료 항바이러스제 라미부딘(Lamivudine, 상품명 제픽스(Jeffix)) 아데포비어(Adefovir depivoxil, 상품명 헵세라(Hepsera)) 클레부딘(Clevudine, 상품명 레보비르(Levovir)) 텔비부딘 인터페론 알파(interferon-α) 페그인터페론 알파(pegylated interferon-α) 예방 B형간염 예방 백신 : 0, 1, 6개월, 또는 0, 1, 2개월 접종 표면항체(anti-HBs)의 역가가 10mIU/ml 이상이면 B형간염바이러스에 면연력이 있음 저(底)반응자/ 무(無)반응자 - 저반응자는 다시 3회의 재접종을 시행하면 대부분 항체가 형성됨 - 무반응자도 3회의 재접종을 시행하면 30~50%에서 항체가 형성됨C 형 간염 C형간염바이러스(hepatitis C virus, HCV)에 의해 주로 혈액을 통해 감염되는 간의 염증성 질환 혈액을 통해서 감염, 바이러스에 오염된 주사바늘이나 혈액제제 등이 원인 C형간염은 60~85%가 만성간염으로 진행될 정도로 만성화율이 높음 급성C형간염(acute hepatitis C) C형간염바이러스에 감염되고 난 후 6개월까지 감염된 환자의 60~70%에서는 전혀 증상이 나타나지 않음 식욕감퇴, 피로감(fatigue), 복통 등의 일반적이고 비특이적인 증상이나 독감과 같은 증상 만성C형간염(chronic hepat없으며(poor appetite) 헛배가 부르고(abdomina discomfort and distension) 구역감이 생기고(nausea and retching) 설사 또는 변비(diarrhea or constipation) 등을 호소 ☞ 만성간염의 전신증상과 매우 유사황달(Jaundice) 황색의 빌리루빈(bilirubin, 담즙색소)이 몸에 필요 이상으로 과다하게 쌓여 눈의 흰자위(공막, sclera)나 피부, 점막(mucosa) 등에 노랗게 착색되는 것 간의 섬유화 때문에 미세담도가 막혀서 배설되지 못한 직접빌리루빈이 피부로 역류하여 발생 간경변증이 간염과 혼재되어 있을 때에는 간세포의 손상이 동반복수(ascites) 및 부종(edema) 알부민(albumine) 간에서 합성 복수(腹水, ascites) 부종(edema) 간기능부전이 발생한 간경변증 환자에서는 간에서의 알부민의 합성이 저하되기 때문에 혈관 내외의 삼투압 차이로 부종(edema)이나 복수가 발생 자발성(특발성) 복막염(spontaneous peritonitis) 복수가 차있는 간경변증 환자에서는 저절로 세균에 감염되어 복막염 발생 복강내의 복수 때문에 장벽이 약해져서 장 속의 세균들이 복강내로 빠져 나와 발생 사망률이 높은 합병증 ☞ 복수가 찬 간경변증 환자에서 복통과 발열 등의 증상이 나타난다면 자발성 복막염을 생각하고 신속히 치료 자발성 복막염이 발생한 간경변증 환자의 평균 생존 기간은 1~2년여성화(feminization) 현상 유방이 커지는 여성형 유방(gynecomastia) 고환 위축(testicular atrophy) 치모(pubic hair) 소실거미양 혈관종(spider angioma) 및 수장홍반(palmar erythema) 거미양 혈관종(spider angioma) 일종의 모세혈관 확장증(telangiectasis) 피부밑의 세동맥(arteriole)을 중심으로 확장된 모세혈관(capillary)이 방사선으로 뻗어나간 형태 얼굴과 목, 가슴에 잘 발생하며 팔, 다리내의 모세혈관에서 나온 혈액과 비장(spleen)을 거쳐서 나온 혈액이 간문맥(portal vein)을 통해 간으로 들어간 후 간정맥(hepatic vein), 상대정맥(superior vena cava)을 거쳐서 심장으로 들어가는 과정간의 혈관 구조문맥고혈압증(portal hypertension, 문맥압 항진증) 문맥순환의 일부가 막혀 문맥압이 상승하는 상태 간의 섬유화 때문에 간 내부의 혈관이 막혀서 간문맥으로 들어온 혈액이 간정맥으로 빠져나갈 수가 없게되므로 결국은 문맥압이 상승하여 문맥고혈압증 발생함 문맥고혈압증을 일으키는 원인중 90% 정도가 간경변증 우회로 문맥내의 혈액이 간을 통하지 않고 심장으로 들어가기 위한 통로 정상적으로는 아주 작은 정맥혈관들이 수 배, 혹은 수 십배 팽창 → 정맥류(varix)간 문맥 항진증 시 우회로합병증 '메두사 머리(Caput Medusae)' 우회 정맥의 하나로 배꼽 주면의 복벽정맥(abdominal wall vein)이 확장 배꼽을 중심으로 구불구불한 정맥이 뻗어나가는 것을 관찰할 수 있음 상부위장관출혈(upper gastrointestinal hemorrhage) 늘어난 식도정맥류(esophageal varix)와 위정맥류(gastric varix)의 파열로 인해 다량의 출혈 발생간 경화와 출혈혈액응고 장애(coagulopathy) 간기능부전이 진행된 간경변증 환자에게서 지혈이 잘 되지 않음 특별한 이유 없이 코피가 나거나 잇몸에 피가 나는 등의 출혈성 경향(hemorrhagic tendency) ☞ 혈액응고 장애(cagulopathy) 원인 혈소판감소증(thrombocytopenia) 비종대(splenomegaly)로 인한 비기능항진증(hypersplenism) 문맥고혈압증으로 인하여 비장내에 혈액이 저류되어 비장이 커지는 울혈성 비종대(congestive splenomegaly)가 발생 기능이 비정상적으로 항진된 비기능항진증(hypersplenism)까지 동반되면 비장에서 많은 양의 혈소판이 파괴되어 결국 혈경계가 억압되어 의식의 변화를 초래 증상 기분 및 성격 변화 지남력 장애 혼수 및 사망위험 인자 변비, 탈수, 염증, 위장관 출혈, 안정제 및 과량의 이뇨제 복용 치료 단백질 섭취를 제한 위험인자를 해소 관장(enema) 등을 통해서 변비를 해소 수분 및 전해질을 보충하여 탈수를 개선 항생제 등을 사용하여 염증을 치료 위장관 출혈에 대한 처치 투여되는 약물을 조절 글루탐산(glutamic acid)이나 아르기닌(arginine) 등을 투여 간신증후군(hepatorenal syndrome) 저혈당(hypoglycemia) 간암(liver cancer)간경변증의 발생 원인이 되는 인자를 가지고 있는 사람에게서 문맥고혈압증의 징후(sign)를 발견함으로 일차적으로 간경변증을 진단 만성 B형간염이나 만성 C형간염 등에 대한 검사 및 만성 알코올성간염에 대한 과거력을 파악 혈액검사 간기능검사(liver function test, LFT) B형간염바이러스에 대한 항원, 항체(HBsAg/Ab) 검사 C형간염바이러스에 대한 항체검사(HCV Ab) 복부 초음파검사(abdominal sonography)/ 복부 전산화단층촬영(abdominal CT) 상부위장관 내시경검사 식도정맥류나 위정맥류를 확인함 간의 조직검사 간경변증을 진단하기 위하여 조직검사를 하는 경우는 거의 없음알파 태아단백(alpha-fetoprotein, AFP) 검사 간경변증이 발생한 경우 간암이 발생할 위험성이 높음 간암의 혈액 표지자간경변증의 치료 목표 완치가 아니라, 증상의 진행 및 그로인한 간기능의 저하를 최대한 늦추는 데 있음 원인 질환에 대한 치료 간경변증으로 진행하게 된 원인에 대한 치료를 먼저 시행 바이러스성 간염 항바이러스제를 투여 인터페론 알파(interferon-α)나 페그인터페론 알파(pegylated interferon-α)를 주사 알코올성 간염 금주 및 영양상태 개선 합병증 증상에 따라 치료 복수 이뇨제(diuretics) 복수 천자자발성 세균성 복막염(spontaneous bacter}

의/약학| 2010.12.11| 39페이지| 8,000원| 조회(571)

간경화, 간경변, 간경화치료, 바이러스간염, liver cirrhoisis

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gout (통풍)

GOUTThe Clinical ProblemAt least 1 percent of men in Western countries A male:female ratio ranging from 7:1 to 9:1 Humans do not express the enzyme uricase Hyperuricemia is central to gout but does not inevitably cause disease Predictors of the development of clinical gout, other than the serum urate level: Hypertension the use of thiazides and loop diuretics Obesity a high alcohol intakeThe Clinical ProblemThe classic symptoms of gouty arthritis recurrent attacks of acute markedly painful monoarticular or oligoarticular inflammation polyarthritis and chronic arthritis A definitive diagnosis the direct identification of urate crystals in the joint the exclusion of infection Serum urate levels are frequently normal during attacks of acute goutThe Clinical Problemamong postmenopausal women in association with diuretic-treated hypertension and renal insufficiency organ-transplant recipients who are treated with cyclosporine have an increased risk of goutClinical FeaturesHave hyperuricemia hyperuricemia Acute gouty arthritis Gout attack Most significant presentation Intercritical asymptomatic gout Between attacks Chronic tophaceous gout Long term problemRenal manifestationsNephrolithiasis Acidic urine saturated with uric acid crystals As a nidus for calcium oxalate or phosphate stone Acute gouty nephropathy Massive malignant cell turnover With treatment of myeloproliferative or lyphoproliferative disorders Blockage of urine flow secondary to the precipitation of uric acid in the CD and ureter Chronic urate nephropathy Long-term deposition of crystals in the parenchyma Giant cell inflammatory reaction Proteinuria Inability of the kidney to concentrate urineBiochemical Basis of GoutElevated uric acid levels in blood (hyperuricemia) and urine Overproduction of purine nucleotides via the de novo pathway End product of purine degradation is uric acid Deposition of uric acid crystals Inflammatory response  PAIN! Long-term cartilage destructionClassification of goutAcute (cry Thiazide Salicylates Niacin Cyclosporine LevodopaADDITIONAL RISK FACTORSRenal impairment Alcohol consumption Obesity Hypertension Gender Lead exposureClinical DiagnosisH P for hyperuricemia Obesity? Alcoholism? Drugs like diuretics? Lead exposure? Renal disease? Acute arthritis? Hypertension or CVD? Family history?Clinical DiagnosisLab tests - CBC - Urinalysis - Creatinine clearance - Liver function - Uric acid levels (serum and urine)Clinical DiagnosisSynovial fluid aspiration - Usually of 1st MTP joint (big toe) - Increased white cell count (neutrophils) - Monosodium urate crystals Needle shaped Strong, negative birefringence with compensated polarized light IntraleukocyticClinical DiagnosisMonosodium Urate CrystalsClinical DiagnosisRadiology Plain film X-ray S.T. swelling and edema in joints Punched out lesions and fractures Interosseous tophi and joint space narrowing CT scan Nuclear medicine (triphasic bone scan) MRIClinical DiagnosisPlain film X-rays of foot and hand of gout affan be used as follows for prophylaxis against acute gout particularly before the initiation of antihyperuricemic therapy Side Effects: Diarrhea Nausea, Vomiting BM suppression for IV.Colchicine0.6 mg orally twice daily in patients with creatinine clearance ≥50 ml/min 0.6 mg orally per day in patients with creatinine clearance of 35–49 ml/min 0.6 mg every 2–3 days in patients with creatinine clearance of 10–34 ml/min Avoid in patients with creatinine clearance 10 ml/min, patients receiving hemodialysis patients with clinically significant hepatic or hepatobiliary dysfunction, Reduce the maintenance doses recommended above by half in patients ≥70 yr of ageNSAID'SAcute Gout Daily doses (2-5 days.) Indomethacin Reduce inflammation Inhibits phagocytosis of crystals Naxopren, sulidac, naproxen, ibuprofen, oxaprozin *Aspirin is contraindicated w/ uricosuric useNSAID'SSelective COX-2 inhibitors Rofecoxib Celecoxib Major considerations Avoid in patients with renal or hepatic failure patients at excretion 24-hour urinary urate excretion to identify patients who overproduce urate a daily urinary urate excretion in excess of 800 to 1000 mg the xanthine oxidase inhibitor allopurinol which inhibits uric acid synthesis, whether or not the patient overproduces urateUricosuric Therapy: Creatinine Clearence: 80 mLProbenecid (500mg) Decreases renal reabsorption of Urate. Sulfinpyrazone (100mg) Greater effect than probenecid *Aspirin antagonizes the effect of both drugsAllopurinol…..AllopurinolXanthine Oxidase inhibitor Normal Renal Function: 300 mg/day Impaired Renal Function: 100 mg/day Creatinine clearence should be monitored (24 hr urine collection)AllopurinolMinor hypersensitivity reactions pruritus and dermatitis: 2% Severe allopurinol-induced toxic effects: mortality rate - 20% Fever Eosinophilia Dermatitis Hepatic dysfunction Renal failure Vasculitis Cuation: Renal failure Azathiopurine, mercaptopurine, wafarineAllopurinolTo reduce the risk of full-blown allopurinol hypersensitow}

의/약학| 2008.02.26| 47페이지| 10,000원| 조회(891)

gout, 통풍, arthritis, cholchin, tophi

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dyslipidemia treatment (고지혈증 치료)

Dyslipidemia treatment : current considerations and unmet needsThere were approximately 500,000 deaths from cardiovascular disease in the USA in 2001. Elevated LDL-C level is a known risk factor for coronary artery disease. Reducing LDL-C can decrease the overall risk for CVD morbidity and mortality by up to 40%. The principal goal of risk reduction therapy is to lower LDL-C levels.Risk factor : LDL-C, HDL-C and subfractions, non-HDL-C, lipoprotein (Lp)(a) and nonlipid biomarkers, such as CRP, fibrinogen and homocysteine. Refining ASCVD risk assessment and substantially reducing this risk level further, with the ultimate aim of almost eliminating it.Risk assessment emerging risk facotorsRisk assessment emerging risk facotorsNon-coronary atherosclerotic clinicical disease : carotid disease, peripheral arterial disease, abdominal aortic aneurysm. Risk factor : age, T-cho, LDL-C, HDL-C, blood pressure, smoking, diabetes, sex. No specific therapy goals were established for HDL-C, or TG levnts in HDL are increasingly thought to reduce ASCVD risk reverse cholesterol transport(RCT) from extrahepatic, peripheral tissues, atheroscelerotic plaques antioxidant and anti-inflammatory effectsRisk assessment emerging risk facotorsStabilize prostacyclin production, decrease endothelial expression of cell adhesion molecules and restore endothelial dysfunction by improvements in nitric oxide Drug therapy that targets HDL-C reduces ASCVD events independent of LDL-C loweringLCATCETPClinical dyslipidemia assessmentComplete lipid profile Secondary cause of hyperlipidemia need to excluded : hypothyroidism, nephrotic syndrome, renal failure, diabetes, obstructive liver disase, hyperparathyroidism and alcoholism medication (β-blocker, diuretics, estrogens/progestins, glucocorticoids, antiretrovirals, isotretinoin, tamoxifen, cyclosporin, etretinate and antipsychotics)Clinical dyslipidemia assessmentClinical dyslipidemia assessmentTherapeutic goalsTabel 1 HDL : The ADA has indicated a goal osterol esters from HDL-C to VLDL-CAvailable pharmacologic agentsStatins increase hepatocyte apoA-I secretion. Gastrointestinal upset, muscle aches and hepatic dysfunction. Drug interactions can be significant with fibrates and to a much lesser extent with niacin, azole, cyclosporin, verapamil, grapefruit juice, marcrolide antibiotics and nefazodone. RhabdomyolysisAvailable pharmacologic agentsAvailable pharmacologic agentsNiacin Most potent drug for increasing HDL-C Reduction in coronary artery disease events and overall morbidity and mortality. TC, LDL-C, VLDL-C, small dense LDL-C, apoB, Lp(a), HDL-C and TGs Increase HDL-C by 15-30% and lower Lp(a) by 20-40%Availablel pharmacologic agentsIncrease the HDL2-C and LP-AI subfractions, which are considered to be cardioprotective. Increasing HDL-C, decreasing Lp(a) It raises HDL-C and apoA-I by decreasing the hepatic catabolism of apoA-I. Niacin decrease adipose tissue TG lipolysis. Niacin reduces plamsa TGs and VLDL-C by reducing the rate e HDL-C by 5-15%. LDL-C levels may increase slightly(in severe hyperTG pt), remain unchanged or decrease. Gastrointestinal disturbances, rash and rarely myotoxicity. Renal insufficiency, liver disease, or gall bladder disease pt By inhibiting DGAD, a key enzyme for TG synthesisAvailable pharmacologic agentsBile acid sequestrants(cholecystramine, colestipol) Combination tx with statins for pt that require further reduction in LDL-C. Effective in lowering plasma levels of LDL-C. Increase TG levels, especially in the insulin resistant pt Abdominal fullness, gas and constipation in 30% of patients Colesevelam(Welchol) - fewer adverse effects and better compliance, lower efficacyAvailable pharmacologic agentsCholesterol absorption inhibitors (ezetimibe, ZetiaTM) Inhibits dierary and biliary cholesterol absorption at the brush border of the intestine without affecting the absorption of TGs or fat loluble vitamines. Rapidly absorbed, extensively conjugated, excreted primarily in the stool. (h/dl Familial hypercholesterolemic heterozygotes with LDL-C 200mg/dl and documented CHDMechanical approaches for removing atherogenic lipoproteinsMechanical approaches for removing atherogenic lipoproteinsPlasma exchange LDL apheresis life long therapy (1- to 2weeks intervals in order to lower LDL-C levels) diet and cholesterol-lowering medications while receiving LDL-apheresisClinical approach to dyslipidemia threatment : monotherapy versus combination therapyIf the pt is medication naïve, monotherpy may be used as first line tx. Lowering LDL-C in high risk pt results in further event reduction regardless of baseline LDL-C. First line therapy for most high risk pt should consist of statins.Clinical approach to dyslipidemia threatment : monotherapy versus combination therapyThe rationale for using combination therapy includes achieving target goals where monotherapy has failed. Combination therapy allows the use of low does of two agents, thus minimizing side effects increased. But somew}

의/약학| 2008.03.13| 44페이지| 5,000원| 조회(674)

dyslipidemia, hypercholesterolemia, Lipito..

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gout (통풍, tophi, gouty arthritis)의 모든 것

GoutN Engl J Med 2003;349:1647-55The disease of kings (and the king of diseases) Pride or punishment?Cosmo de MediciElizabeth INostradamusBen FranklinMarcus AgrippaA 59-year-old man with bilateral olecranon-bursa tophi has frequent bouts of acute gouty arthritis, including three in the past year. His serum uric acid level is consistently above 9 mg per deciliter (535 μmol per liter). He is moderately obese and has mild, untreated hypertension. Allopurinol was discontinued after a maculopapular rash developed. How should this patient's condition be treated?The Clinical ProblemAt least 1 percent of men in Western countries A male:female ratio ranging from 7:1 to 9:1 Humans do not express the enzyme uricase Hyperuricemia is central to gout but does not inevitably cause disease Predictors of the development of clinical gout, other than the serum urate level: Hypertension the use of thiazides and loop diuretics Obesity a high alcohol intakeThe Clinical ProblemThe classic symptoms of gouty a the great toe experiences agonizing pain followed by inflammation, swelling, warmth and tenderness A low grade fever may occur Attacks last from a few days to a couple weeksExtremities Decreased temperature Lower extremities Routine activities of weight bearing joints accumulate slight edema During rest at night, water is reabsorbed from the joint spaces leaving a supersaturated concentration of uric acidClinical phases of goutAsymptomatic hyperuricemia Acute gouty arthritis Gout attack Most significant presentation Intercritical asymptomatic gout Between attacks Chronic tophaceous gout Long term problemRenal manifestationsNephrolithiasis Acidic urine saturated with uric acid crystals As a nidus for calcium oxalate or phosphate stone Acute gouty nephropathy Massive malignant cell turnover With treatment of myeloproliferative or lyphoproliferative disorders Blockage of urine flow secondary to the precipitation of uric acid in the CD and ureter Chronic urate nephropathy Long-term deposistructionMonosodium urate crystals from a tophus, observed with polarized light microscopyIntracellular monosodium urate crystal from synovial fluid, observed with polarized light microscopyCotran: Robbins Pathologic Basis of Disease, 6th ed.,1999NUTRITIONAL FACTORSTea Coffee Cocoa Chocolate High purine foodsMEDICATIONSDiuretics Thiazide Salicylates Niacin Cyclosporine LevodopaADDITIONAL RISK FACTORSRenal impairment Alcohol consumption Obesity Hypertension Gender Lead exposureClinical DiagnosisH P for hyperuricemia Obesity? Alcoholism? Drugs like diuretics? Lead exposure? Renal disease? Acute arthritis? Hypertension or CVD? Family history?Clinical DiagnosisLab tests - CBC - Urinalysis - Creatinine clearance - Liver function - Uric acid levels (serum and urine)Clinical DiagnosisSynovial fluid aspiration - Usually of 1st MTP joint (big toe) - Increased white cell count (neutrophils) - Monosodium urate crystals Needle shaped Strong, negative birefringence with compensated polarized light InterventionColchicine NSAID'S Corticosteroids Uricosuric Therapy AllopurinolColchicineAcute Gout Within the first few hours hours: 0.6 mg once every hour for up to 3 hr (maximum, 3 pills) low-dose oral colchicine can be used as follows for prophylaxis against acute gout particularly before the initiation of antihyperuricemic therapy Side Effects: Diarrhea Nausea, Vomiting BM suppression for IV.Colchicine0.6 mg orally twice daily in patients with creatinine clearance ≥50 ml/min 0.6 mg orally per day in patients with creatinine clearance of 35–49 ml/min 0.6 mg every 2–3 days in patients with creatinine clearance of 10–34 ml/min Avoid in patients with creatinine clearance 10 ml/min, patients receiving hemodialysis patients with clinically significant hepatic or hepatobiliary dysfunction, Reduce the maintenance doses recommended above by half in patients ≥70 yr of ageNSAID'SAcute Gout Daily doses (2-5 days.) Indomethacin Reduce inflammation Inhibits phagocytosis of crystals Naxopren, sulerproductionThe Choice?between a medication that reduces urate production and one that increases urate excretion 24-hour urinary urate excretion to identify patients who overproduce urate a daily urinary urate excretion in excess of 800 to 1000 mg the xanthine oxidase inhibitor allopurinol which inhibits uric acid synthesis, whether or not the patient overproduces urateUricosuric Therapy: Creatinine Clearence: 80 mLProbenecid (500mg) Decreases renal reabsorption of Urate. Sulfinpyrazone (100mg) Greater effect than probenecid *Aspirin antagonizes the effect of both drugsProbenecidAllopurinol…..AllopurinolXanthine Oxidase inhibitor Normal Renal Function: 300 mg/day Impaired Renal Function: 100 mg/day Creatinine clearence should be monitored (24 hr urine collection)AllopurinolMinor hypersensitivity reactions pruritus and dermatitis: 2% Severe allopurinol-induced toxic effects: mortality rate - 20% Fever Eosinophilia Dermatitis Hepatic dysfunction Renal failure Vasculitis Cuation: Renal fa}

의/약학| 2008.03.13| 50페이지| 10,000원| 조회(1,040)

gout, 통풍, tophi, colchin, Hyperuricemia

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