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http://www.bio-rad.com/B2B/BioRad/product/br_category.jsp?BV_SessionID=@@@@1855363217.1233317879@@@@&BV_EngineID=ccciadegggdfjlgcfngcfkmdhkkdfll.0&divName=Life+Science+Research&categoryPath=Catalogs/Life%20Science%20Research&lang=English&country=HQ&catLevel=2&loggedIn=false&serviceLevel=Lit+Request&catOID=-9263&isPA=false&cat_index=yes
bir çok ingilizce slayt
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http://www.sigmaaldrich.com/life-science/cell-biology/learning-center/pathway-slides-and.html
Şeker Yüklemesi yaptıracak kişilerin test öncesi uygulaması tavsiye edilen 3 günlük diyet
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ÖRNEK MENÜ
SABAH: 1 su bardağı süt
1 adet yumurta veya;
1 kibrit kutusu kadar beyaz peynir
1 tatlı kaşığı reçel, bal, pekmez
1 tatlı kaşığı yağ veya 5 zeytin
50 gr. Ekmek
Saat : 10.00 1 porsiyon meyve
ÖĞLE: 2 köfte büyüklüğünde et
1 porsiyon sebze yemeği
1 porsiyon tahıl yemeği (pilav, makarna, çorba, börek, vb.)
…Salata
1 porsiyon meyve
50 gr. Ekmek
Saat : 16.00 1 porsiyon meyve
AKŞAM: Öğle yemeği gibi
SABAH: 1 su bardağı süt
1 adet yumurta veya;
1 kibrit kutusu kadar beyaz peynir
1 tatlı kaşığı reçel, bal, pekmez
1 tatlı kaşığı yağ veya 5 zeytin
50 gr. Ekmek
Saat : 10.00 1 porsiyon meyve
ÖĞLE: 2 köfte büyüklüğünde et
1 porsiyon sebze yemeği
1 porsiyon tahıl yemeği (pilav, makarna, çorba, börek, vb.)
…Salata
1 porsiyon meyve
50 gr. Ekmek
Saat : 16.00 1 porsiyon meyve
AKŞAM: Öğle yemeği gibi
Kan alımında tavsiye edilen tüp sırası: (CLSI H3-A5 Standartlarına göre)
|
Kan alımında tavsiye edilen tüp sırası: (CLSI H3-A5 Standartlarına göre)
1● Kan kültürü
2● Koagulasyon
3● Jelli/Jelsiz Serum
4● Jelli/Jelsiz Heparin
5●EDTA
6● Diğerleri
1● Kan kültürü
2● Koagulasyon
3● Jelli/Jelsiz Serum
4● Jelli/Jelsiz Heparin
5●EDTA
6● Diğerleri
faydalı
|
http://www.chemistryonline.com/news/16/clinicalbiochemistry.html
http://www.chemistryonline.com/news/13/medicalbiochemistry.html
http://www.chemistryonline.com/news/13/medicalbiochemistry.html
Newborn Screening Tests
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Organic acid metabolism disorders:
* IVA (isovaleric acidemia)
* GA I (glutaric acidemia)
* HMG (3-OH 3-CH3 glutaric aciduria)
* MCD (multiple carboxylase deficiency)
* MUT (methylmalonic acidemia due to mutase deficiency)
* Cbl A,B (methylmalonic acidemia)
* 3MCC (3-methylcrotonyl-CoA carboxylase deficiency)
* PROP (propionic acidemia)
* BKT (beta-ketothiolase deficiency)
Fatty acid oxidation disorders
* MCAD (medium-chain acyl-CoA dehydrogenase deficiency)
* VLCAD (very long-chain acyl-CoA dehydrogenase deficiency)
* LCHAD (long-chain L-3-OH acyl-CoA dehydrogenase deficiency)
* TFP (trifunctional protein deficiency)
* CUD (carnitine uptake defect)
Amino acid metabolism disorders:
* PKU (phenylketonuria)
* MSUD (maple syrup urine disease)
* HCY (homocystinuria due to CBS deficiency)
* CIT (citrullinemia)
* ASA (argininosuccinic acidemia)
* TYR I (tyrosinemia type I)
Hemoglobinopathies:
* Hb SS (sickle cell anemia)
* Hb S/Th (hemoglobin S/beta-thalassemia)
* Hb S/C (hemoglobin S/C disease)
Others:
* CH (congenital hypothyroidism)
* BIOT (biotinidase deficiency)
* CAH (congenital adrenal hyperplasia due to 21-hydroxylase deficiency)
* GALT (classical galactosemia)
* HEAR (hearing loss)
* CF (cystic fibrosis)
* IVA (isovaleric acidemia)
* GA I (glutaric acidemia)
* HMG (3-OH 3-CH3 glutaric aciduria)
* MCD (multiple carboxylase deficiency)
* MUT (methylmalonic acidemia due to mutase deficiency)
* Cbl A,B (methylmalonic acidemia)
* 3MCC (3-methylcrotonyl-CoA carboxylase deficiency)
* PROP (propionic acidemia)
* BKT (beta-ketothiolase deficiency)
Fatty acid oxidation disorders
* MCAD (medium-chain acyl-CoA dehydrogenase deficiency)
* VLCAD (very long-chain acyl-CoA dehydrogenase deficiency)
* LCHAD (long-chain L-3-OH acyl-CoA dehydrogenase deficiency)
* TFP (trifunctional protein deficiency)
* CUD (carnitine uptake defect)
Amino acid metabolism disorders:
* PKU (phenylketonuria)
* MSUD (maple syrup urine disease)
* HCY (homocystinuria due to CBS deficiency)
* CIT (citrullinemia)
* ASA (argininosuccinic acidemia)
* TYR I (tyrosinemia type I)
Hemoglobinopathies:
* Hb SS (sickle cell anemia)
* Hb S/Th (hemoglobin S/beta-thalassemia)
* Hb S/C (hemoglobin S/C disease)
Others:
* CH (congenital hypothyroidism)
* BIOT (biotinidase deficiency)
* CAH (congenital adrenal hyperplasia due to 21-hydroxylase deficiency)
* GALT (classical galactosemia)
* HEAR (hearing loss)
* CF (cystic fibrosis)
faydalı siteler
|
Online biyokimya(güzel site)
http://employees.csbsju.edu/hjakubowski/classes/ch331/bcintro/default.html
Medikal ingilizce eğitim
http://www.englishmed.com/
TÜM LABORATUVAR CİHAZLARI ile ilgili aradığınız bilgiler, teknik şartnameleri vs
http://www.labworld-online.com/index.html
"Nomenclature Committee of the International Union of Biochemistry and Molecular Biology (NC-IUBMB)"nin ENZİMLERE ilişkin kapsamlı bir sitesi
http://www.chem.qmw.ac.uk/iubmb/enzyme
International Federation Of Clinical Chemistry and Laboratory Medicine (IFCC)'nın Web Sitesi
http://www.ifcc.org/
OLDUKÇA YARARLI bir site
http://www.lib.washington.edu/Subject/Biochemistry/
"Online" olarak ulaşabileceğiniz BİYOKİMYA KİTABI ve DERGİLERİ
http://www.sc.edu/library/science/elbch.html
http://employees.csbsju.edu/hjakubowski/classes/ch331/bcintro/default.html
Medikal ingilizce eğitim
http://www.englishmed.com/
TÜM LABORATUVAR CİHAZLARI ile ilgili aradığınız bilgiler, teknik şartnameleri vs
http://www.labworld-online.com/index.html
"Nomenclature Committee of the International Union of Biochemistry and Molecular Biology (NC-IUBMB)"nin ENZİMLERE ilişkin kapsamlı bir sitesi
http://www.chem.qmw.ac.uk/iubmb/enzyme
International Federation Of Clinical Chemistry and Laboratory Medicine (IFCC)'nın Web Sitesi
http://www.ifcc.org/
OLDUKÇA YARARLI bir site
http://www.lib.washington.edu/Subject/Biochemistry/
"Online" olarak ulaşabileceğiniz BİYOKİMYA KİTABI ve DERGİLERİ
http://www.sc.edu/library/science/elbch.html
Summary of rejection characteristics
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Error Condition High Pfr High Ped
No errors 12s
Random error 12.5s, 13s, 13.5s
R4s, R0.05, R0.01
Systematic error 22s, 41s, 2of32s, 31s
6x, 8x, 9x, 10x, 12x
x0.05, x0.01
cusum
No errors 12s
Random error 12.5s, 13s, 13.5s
R4s, R0.05, R0.01
Systematic error 22s, 41s, 2of32s, 31s
6x, 8x, 9x, 10x, 12x
x0.05, x0.01
cusum
Diabet
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Secondary, or other specific types of diabetes mellitus are the result of many causes including:
1. Maturity onset type diabetes of the young (MODY) was previously considered to be a third form of type 2 diabetes. However, with the discovery of specific mutations leading to MODY, it is now classified under secondary or other specific types of diabetes. MODY is characterized by onset prior to age 25. All cases to date have shown impaired β-cell function. Patients may also exhibit insulin resistance and late β-cell failure. Evidence indicates that mutations in 10-12 different genes have been correlated with the development of MODY. Mutations in the 6 genes described here are all clearly correlated to MODY:
MODY1: the transcription factor identified as hepatic nuclear factor-4α (HNF-4α). This gene is also called transcription factor-14 (TCF14). Expression of HNF-4α is associated with the growth and normal functioning of the pancreas. Genes known to be regulated by HNF-4α include the insulin gene, glucose-6-phosphatase, GLUT2, the liver pyruvate kinase isoform (L-PK) which is also expressed in the pancreas, glyceraldehyde-3-phosphate dehydrogenase (G3PDH), aldolase B and thermogenin (uncoupling protein, UCP).
MODY2: pancreatic glucokinase
MODY3: the transcription factor HNF-1α. This gene is also called hepatocyte transcription factor-1 (TCF1). HNF-1α is known to regulate expression of the HNF-4α gene and also the GLUT2 and L-PK genes.
MODY4: the homeodomain transcription factor insulin promoter factor-1 (IPF-1). This gene is more commonly called PDX1 derived from pancreas duodenum homeobox-1.
MODY5: the transcription factor HNF-1β. This gene is also called hepatocyte transcription factor-2 (TCF2). HNF-1β is a critical regulator of a transcriptional network that controls the specification, growth, and differentiation of the embryonic pancreas. In humans, mutations in the HNF-1β gene are associated with pancreatic hypoplasia, defective kidney development and genital malformations.
MODY6: the bHLH transcription factor NeuroD1. NeuroD1 was first identified as a neural fate-inducing gene. The hamster β2 gene, shown to regulate insulin transcription is identical to NeuroD1 so the gene is often called NeuroD/β2.
2. Pancreatic disease: Pancreatectomy leads to the clearest example of secondary diabetes. Cystic fibrosis and pancreatitis can also lead to destruction of the pancreas.
3. Endocrine disease: Some tumors can produce counter-regulatory hormones that oppose the action of insulin or inhibit insulin secretion. These counter-regulatory hormones are glucagon, epinephrine, growth hormone and cortisol.
a. Glucagonomas are pancreatic cancers that secrete glucagon.
b. Pheochromocytomas secrete epinephrine.
c. Cushing syndrome results in excess cortisol secretion.
d. Acromegaly results in excess growth hormone production.
4. Drug-induced diabetes; treatment with glucocorticoids and diuretics can interfere with insulin function.
5. Anti-insulin receptor autoantibodies (Type B insulin resistance).
6. Mutations in the insulin gene.
7. Mutations in insulin receptor gene which lead to the syndromes listed below. Two clinical features are common in all syndromes that result from mutations in the insulin receptor gene: acanthosis nigricans and hyperandrogenism (the latter being observed only in females).
a. Donohue syndrome (also referred to as Leprachaunism)
b. Rabson-Mendenhall syndrome
c. Type A insulin resistance
8. Gestational diabetes; this syndrome sets in during pregnancy and usually resolves itself following childbirth.
9. Many other genetic syndromes have either diabetes or impaired glucose tolerance associated with them; lipoatrophic diabetes, Wolfram syndrome, Down syndrome, Klinefelter syndrome (XXY males), Turner syndrome, myotonic dystrophy, muscular dystrophy, Huntington disease, Friedreich ataxia, Prader-Willi syndrome, Werner syndrome, Cockayne syndrome, and others such as those indicated above
1. Maturity onset type diabetes of the young (MODY) was previously considered to be a third form of type 2 diabetes. However, with the discovery of specific mutations leading to MODY, it is now classified under secondary or other specific types of diabetes. MODY is characterized by onset prior to age 25. All cases to date have shown impaired β-cell function. Patients may also exhibit insulin resistance and late β-cell failure. Evidence indicates that mutations in 10-12 different genes have been correlated with the development of MODY. Mutations in the 6 genes described here are all clearly correlated to MODY:
MODY1: the transcription factor identified as hepatic nuclear factor-4α (HNF-4α). This gene is also called transcription factor-14 (TCF14). Expression of HNF-4α is associated with the growth and normal functioning of the pancreas. Genes known to be regulated by HNF-4α include the insulin gene, glucose-6-phosphatase, GLUT2, the liver pyruvate kinase isoform (L-PK) which is also expressed in the pancreas, glyceraldehyde-3-phosphate dehydrogenase (G3PDH), aldolase B and thermogenin (uncoupling protein, UCP).
MODY2: pancreatic glucokinase
MODY3: the transcription factor HNF-1α. This gene is also called hepatocyte transcription factor-1 (TCF1). HNF-1α is known to regulate expression of the HNF-4α gene and also the GLUT2 and L-PK genes.
MODY4: the homeodomain transcription factor insulin promoter factor-1 (IPF-1). This gene is more commonly called PDX1 derived from pancreas duodenum homeobox-1.
MODY5: the transcription factor HNF-1β. This gene is also called hepatocyte transcription factor-2 (TCF2). HNF-1β is a critical regulator of a transcriptional network that controls the specification, growth, and differentiation of the embryonic pancreas. In humans, mutations in the HNF-1β gene are associated with pancreatic hypoplasia, defective kidney development and genital malformations.
MODY6: the bHLH transcription factor NeuroD1. NeuroD1 was first identified as a neural fate-inducing gene. The hamster β2 gene, shown to regulate insulin transcription is identical to NeuroD1 so the gene is often called NeuroD/β2.
2. Pancreatic disease: Pancreatectomy leads to the clearest example of secondary diabetes. Cystic fibrosis and pancreatitis can also lead to destruction of the pancreas.
3. Endocrine disease: Some tumors can produce counter-regulatory hormones that oppose the action of insulin or inhibit insulin secretion. These counter-regulatory hormones are glucagon, epinephrine, growth hormone and cortisol.
a. Glucagonomas are pancreatic cancers that secrete glucagon.
b. Pheochromocytomas secrete epinephrine.
c. Cushing syndrome results in excess cortisol secretion.
d. Acromegaly results in excess growth hormone production.
4. Drug-induced diabetes; treatment with glucocorticoids and diuretics can interfere with insulin function.
5. Anti-insulin receptor autoantibodies (Type B insulin resistance).
6. Mutations in the insulin gene.
7. Mutations in insulin receptor gene which lead to the syndromes listed below. Two clinical features are common in all syndromes that result from mutations in the insulin receptor gene: acanthosis nigricans and hyperandrogenism (the latter being observed only in females).
a. Donohue syndrome (also referred to as Leprachaunism)
b. Rabson-Mendenhall syndrome
c. Type A insulin resistance
8. Gestational diabetes; this syndrome sets in during pregnancy and usually resolves itself following childbirth.
9. Many other genetic syndromes have either diabetes or impaired glucose tolerance associated with them; lipoatrophic diabetes, Wolfram syndrome, Down syndrome, Klinefelter syndrome (XXY males), Turner syndrome, myotonic dystrophy, muscular dystrophy, Huntington disease, Friedreich ataxia, Prader-Willi syndrome, Werner syndrome, Cockayne syndrome, and others such as those indicated above
Diabetik ketoasidoz ve tedavi
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Treatment of Diabetic Ketoacidosis
The following is not intended to be considered as routine orders for the diagnosis and treatment of all cases of DKA but is presented only as one possible treatment regimen. Each case of DKA must be treated on an individual basis.
Initial Assessment of DKA
blood glucose > 250mg/dL
arterial pH <7.3
serum bicarbonate <15mEq/L
urinary ketones ≥ 3+ and/or serum ketones are positive
Monitoring
vital signs every hour
serum glucose every hour and as needed
blood gas pH every 2 hrs (use arterial for 1st measurement then can use venous)
electrolytes every 1-2 hrs
urine ketones on each void
fluid input and output continuously
magnesium and phopshorous immediately and then every 1-2 hrs
Fluid Management
start normal saline at 1L/hr or 15-20ml/kg/hr initially
determine hydration status, goal being to replace 50% of estimated volume loss in the 1st 4hrs then remainder over next 8-12 hrs
infuse normal saline 125-500 ml/hr, rate dependent on hydration status
once serum Na+ is corrected infuse 1/2 normal saline at 4-14ml/kg/hr
when serum glucose reaches 250mg/dL change fluid to D5W 1/2 normal saline at same rate
Insulin Managementdiscontinue all oral diabetic medications and
previous insulin orders
give regular insulin iv bolus of 10 units
start insulin infusion usually at a rate of 0.15units/kg
insulin administration goal is to reduce serum glucose 50-70mg/dL/hr
when serum glucose is ≤ 150mg/dL then can switch to adult sq insulin with basal insulin
Potassium Management
if serum K+ is <3.3 give 40mEq/hr until it is >3.3
if serum K+ is >3.3 but <5.0 give 20-30mEq/L of iv fluids to keep serum K+ between 4-5mEq/L
if serum K+ is ≥5.0 do not give K+ but check serum levels every 2hrs
when replacing K+ both potassium chloride and potassium phosphate can be used
hold K+ replacement if patient urine output is <30ml/hr
Bicarbonate Management
assess need for bicarbonate by arterial pH measurement
if pH <6.9 give 100mEq sodium bicarbonate in 1L D5W and infuse at 200ml/hr
if pH is 6.9 - 7.0 give 50mEq sodium bicarbonate in 1L D5W and infuse at 200ml/hr
if pH >7.0 do not give bicarbonate
continue sodium bicarbonate administration until pH is >7.0
monitor serum K+
The following is not intended to be considered as routine orders for the diagnosis and treatment of all cases of DKA but is presented only as one possible treatment regimen. Each case of DKA must be treated on an individual basis.
Initial Assessment of DKA
blood glucose > 250mg/dL
arterial pH <7.3
serum bicarbonate <15mEq/L
urinary ketones ≥ 3+ and/or serum ketones are positive
Monitoring
vital signs every hour
serum glucose every hour and as needed
blood gas pH every 2 hrs (use arterial for 1st measurement then can use venous)
electrolytes every 1-2 hrs
urine ketones on each void
fluid input and output continuously
magnesium and phopshorous immediately and then every 1-2 hrs
Fluid Management
start normal saline at 1L/hr or 15-20ml/kg/hr initially
determine hydration status, goal being to replace 50% of estimated volume loss in the 1st 4hrs then remainder over next 8-12 hrs
infuse normal saline 125-500 ml/hr, rate dependent on hydration status
once serum Na+ is corrected infuse 1/2 normal saline at 4-14ml/kg/hr
when serum glucose reaches 250mg/dL change fluid to D5W 1/2 normal saline at same rate
Insulin Managementdiscontinue all oral diabetic medications and
previous insulin orders
give regular insulin iv bolus of 10 units
start insulin infusion usually at a rate of 0.15units/kg
insulin administration goal is to reduce serum glucose 50-70mg/dL/hr
when serum glucose is ≤ 150mg/dL then can switch to adult sq insulin with basal insulin
Potassium Management
if serum K+ is <3.3 give 40mEq/hr until it is >3.3
if serum K+ is >3.3 but <5.0 give 20-30mEq/L of iv fluids to keep serum K+ between 4-5mEq/L
if serum K+ is ≥5.0 do not give K+ but check serum levels every 2hrs
when replacing K+ both potassium chloride and potassium phosphate can be used
hold K+ replacement if patient urine output is <30ml/hr
Bicarbonate Management
assess need for bicarbonate by arterial pH measurement
if pH <6.9 give 100mEq sodium bicarbonate in 1L D5W and infuse at 200ml/hr
if pH is 6.9 - 7.0 give 50mEq sodium bicarbonate in 1L D5W and infuse at 200ml/hr
if pH >7.0 do not give bicarbonate
continue sodium bicarbonate administration until pH is >7.0
monitor serum K+
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