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

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Presentation on theme: "آنزيم شناسي باليني. Transaminases GOT or AST GPT or ALT."— Presentation transcript:

1 آنزيم شناسي باليني

2 Transaminases GOT or AST GPT or ALT

3 AST ALT Heart7800450 Liver71002850 Sk-muscle5000300 Kidneys45001200 Pancrease1400130 Spleen70080 Lungs50045 RBC157 serum11

4 روش هاي اندازه گيري كالريمتريك فتومتريك

5 مقادير نرمال adultsinfantsNewborn AST8-209-8047-150 ALT10-407-40

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

7 CK Ck activity Ck3-MM % Ck2-MB % Ck1- BB % SK- muscle 250098.91.10.06 brain55502.797.3 heart47378.7201.3 liver~ 100100

8

9 Aldolase ALD A : FDP ALD B : F1P ALD C : ? Disease of Skeletal muscle 10-50 times Duchenne disease Myasthenia gravis & MS In MI 5-8 times Pattern parallel AST Injection of cortisone & ACTH 10-18 times

10 LDH pH optimum in L P = 8.8-9.8 pH optimum in P L = 7.8 Inhibitors: reagents against thiol (Hg), Borate & Oxalate, EDTA HBDH = LD1

11

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

13 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

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

15 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

16 Comparison of GGT, ALP & NTP ALPNTPGGT Biliary tract disease 4.06.211.9 Acute & chronic hepatitis 1.51.12.3

17 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

18 Human amylase pH optimum = 6.9 – 7 Q 10 =1.6, up to 50° active Calcium metalloenzyme Activator ions: chloride, bromide, nitrate, phosphate MW= 55000 – 60000 Electrophoresis: β & γ globulins

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

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

21 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%

22 Lipase Glycoprotein MW = 54000 Concentration lipase in pancreas ~ 20000 serum alpha position carbons Lipase activated by NaCl

23 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

24 Cholinesterase Liver function Insecticide poisoning Normal range –4000-12000 U/L –Level at birth = ¼ adults –In 2 month = adults

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

26 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

27 Angiotensine converting enzyme (ACE)


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