آنزيم شناسي باليني. Transaminases GOT or AST GPT or ALT.

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Presentation transcript:

آنزيم شناسي باليني

Transaminases GOT or AST GPT or ALT

AST ALT Heart Liver Sk-muscle Kidneys Pancrease Spleen70080 Lungs50045 RBC157 serum11

روش هاي اندازه گيري كالريمتريك فتومتريك

مقادير نرمال adultsinfantsNewborn AST ALT

CPK Mg coenzyme Inhibitors: Ca, Zn, Cu, Mn, iodoacetate Activators: N-acetylcysteine CK-MB- α2 glubolin

CK Ck activity Ck3-MM % Ck2-MB % Ck1- BB % SK- muscle brain heart liver~

Aldolase ALD A : FDP ALD B : F1P ALD C : ? Disease of Skeletal muscle times Duchenne disease Myasthenia gravis & MS In MI 5-8 times Pattern parallel AST Injection of cortisone & ACTH times

LDH pH optimum in L P = pH optimum in P L = 7.8 Inhibitors: reagents against thiol (Hg), Borate & Oxalate, EDTA HBDH = LD1

ALP boneIsoenzyme: liver, bone, intestinal, placental, renal Activators: Mg, Co, Mn Inhibotors: phosphate, borate, oxalate, cyanide 56º & 65º Urea inhibition Phe inhibited intestinal & placental

5‘-Nucleotidase (NTP) Localized in cytoplasmic cell membrane pH optimum = 6.6 – 7 In hepatobiliary disease increased 2-6 times increase: stone, tumor, biliary cirrhosis In early hepatitis NTP normal or slightly elevated In hepatobiliary disease ALP & NTP elevated similarly

Comparison of ALP & NTP In hepatobiliary disease ALP & NTP elevated similarly In Skeletal disease, late pregnancy, childhood ALP increased & NTP normal

Gamma-glutamyl transferase (GGT) GGT present in all cells except muscle Small in cytosol & large fraction in cell membrane GGT elevated in all liver disease GGT more sensitive than ALP, NTP, LAP, GOT, GPT in obstructive jaundice Normal: skeletal disease, children older than 1 y, pregnancy

Comparison of GGT, ALP & NTP ALPNTPGGT Biliary tract disease Acute & chronic hepatitis

Amylase Amylase hydrolased α-1,4 linkage Types of amylase: –Beta: plant & bacterial. Terminal reducing, splits a maltose at a time –Alpha: animal & human. Random hydrolased α-1,4 linkage

Human amylase pH optimum = 6.9 – 7 Q 10 =1.6, up to 50° active Calcium metalloenzyme Activator ions: chloride, bromide, nitrate, phosphate MW= – Electrophoresis: β & γ globulins

Types of human amylase P – type & S – Type (ptyalin) Macroamylase : usually S-type with IgA, IgG or other normal proteins

Causes of hyperamylasemia Pancreatic disease (P) Renal insufficiently (mixed) Mumps (s) Diabetic ketoacidosis (M) Acute alcoholism (M) Medicinal opiates (p) Heroin lung (s)

Amylase/creatinine clearance ratio (ACCR) ACCR (%) = (urine clearance of amylase/ urine clearance of creatinine) X 100 ( urine amylase (U/L) X serum creatinine (mg/L) / serum amylase (U/L) X urine creatinine (mg/L) X 100 Normal ACCR = 2 – 5 % Acute pancreatitis > 8% Macroamylasemia < 2%

Lipase Glycoprotein MW = Concentration lipase in pancreas ~ serum alpha position carbons Lipase activated by NaCl

Cholinesterase Choline esterase I = true cholinesterase –RBC, lung, spleen, nerve endings, gray matter of the brain Choline esterase II = pseudocholinesterase –Serum, Liver, pancreas, heart, white matter of the brain

Cholinesterase Liver function Insecticide poisoning Normal range – U/L –Level at birth = ¼ adults –In 2 month = adults

Cholinesterase 30-50% decrease –Acute & chronic hepatitis 50-70% decrease –Advanced cirrhosis & carcinoma Decrease slightly in pregnancy

Acid phosphatase ایزوآنزیم های زیادی دارد که مهمترین آنها ایزوآنزیم پروستاتیک است. در تشخیص اختلالات خوش خیم و بدخیم پروستات نقش دارد. ایزوآنزیم پروستاتیک حساس به تارتارات است. نگهداری سرم حتی در یخچال سبب کاهش فعالیت اسید فسفاتاز می گردد. بهترین راه نگهداری نمونه جهت انجام آزمایش اسیدفسفاتاز اسیدی کردن سرم می باشد

Angiotensine converting enzyme (ACE)