Biochemical examination refers to the physical examination of a person by analyzing the blood components of the human body by biological or chemical means. Different hospitals, biochemical group inspection items will be different, but the approximate project will not be too different.

Biochemical full inspection use

1, for routine physical examination screening 2, disease screening and confirmation test

 The biochemical full-scale examination is a comprehensive examination of the body and an understanding of the physical condition. Sometimes, the hidden diseases can be detected. For example, hepatitis B virus carriers need to regularly check the liver function to prevent sudden onset of the disease and promptly treat.

Biochemical full inspection project

liver function

α-L fucosidase

Alanine aminotransferase

Aspartate aminotransferase

4. Total protein

5. Albumin

6.A/G

7. Alkaline phosphatase

8. Glutamyltranspeptidase

9. Total bilirubin

10. Direct bilirubin

11. Cholinesterase

12. Total bile acid

13. Adenosine deaminase

14. Prealbumin

15. Homocysteine

16. Glucose

Blood lipid

17. Triglycerides

18. Total cholesterol

19. High density lipoprotein

20. Low density lipoprotein

21. Apolipoprotein A1

22. Apolipoprotein B

23. Apolipoprotein a

Renal function

24. Creatinine

25. Urea

26. Uric acid

27. Cystatin-C

28. β2-microglobulin

29. Potassium

30. Sodium

31. Chlorine

32. Total carbon dioxide

33. Anion gap

34. Phosphorus

35. Calcium

36. Magnesium

Four anemia

37. Iron

38. Unsaturated iron

39. Total iron binding force

40. Transferrin

41. Transferrin saturation

Myocardial enzyme

42. Lactate dehydrogenase

43. Hydroxybutyrate dehydrogenase

44. Creatine kinase

45. Creatine kinase isoenzyme

46. Myoglobin

Rheumatism

47. Anti-chain O

48. Rheumatoid factor

49. Hypersensitive C-reactive protein

Pancreas

50. Amylase

51. Lipase

Glycated hemoglobin (this is a single item)

Clinical significance

01α-L fucosidase (AFU)

Increased: suggesting that liver cells develop lesions for the diagnosis of primary liver cancer.

Reduction: seen in the fucosal storage disease caused by hereditary AFU deficiency, the children died at 5 and 6 years old.

02 alanine aminotransferase (ALT or GPT)

Increased: common in acute and chronic hepatitis, drug-induced liver damage, fatty liver, cirrhosis, myocardial infarction, myocarditis and biliary diseases.

03 aspartate aminotransferase (AST or GOT)

Increased: common in the onset of myocardial infarction, acute and chronic hepatitis, toxic hepatitis, cardiac insufficiency, dermatomyositis and so on.

04 total protein (TP)

Increased: Common in high dehydration (such as diarrhea, vomiting, shock, high fever) and multiple myeloma.

Reduction: common in malignant tumors, severe tuberculosis, nutritional and malabsorption disorders, cirrhosis, nephrotic syndrome, ulcerative colitis, burns, blood loss, etc.

05 albumin (ALB)

Increased: It is common for severe water loss to cause plasma concentration and increase albumin concentration.

Reduced: Basically the same as total protein, especially liver disease, kidney disease is more obvious.

06 alkaline phosphatase (ALP)

Increased: common in liver cancer, cirrhosis, obstructive jaundice, acute and chronic jaundice hepatitis, osteoblastoma, bone metastases, fracture recovery period. In addition, children and adolescents are active in the skeletal system during growth and development, which can increase ALP.

Note: With different buffers, the results can vary significantly.

07 glutamyl transpeptidase (γ-GGT)

Increased: common in primary or metastatic liver cancer, acute hepatitis, chronic hepatitis active cirrhosis, acute pancreatitis and heart failure.

08 total bilirubin (TBIL)

Increased: liver disease, extrahepatic disease, primary biliary cirrhosis hemolytic jaundice acute jaundice hepatitis neonatal jaundice chronic active hepatitis occlusive jaundice viral hepatitis cholelithiasis obstructive jaundice pancreatic head cancer liver cirrhosis transfusion error.

09 direct bilirubin (DBIL)

Increased: common in obstructive jaundice, liver cancer, pancreatic head cancer, cholelithiasis and so on.

10 cholinesterase (CHE)

Increased: mainly seen in hyperthyroidism, diabetes, nephrotic syndrome, fatty liver, obesity, nervous system diseases, hypertension, bronchial asthma and so on.

Reduced: liver disease, hereditary serum CHE abnormalities, hunger, infection and anemia.

11 total bile acid (TBA)

Increased: mainly seen in acute and chronic hepatitis, cirrhosis, obstructive jaundice, primary liver cancer, acute intrahepatic cholestasis, primary biliary cirrhosis and extrahepatic obstructive jaundice.

12 adenosine deaminase (ADA)

Increased: seen in tuberculous chest, ascites, intracranial tumors and central nervous system leukemia slightly increased.

Reduction: visible in severe immunodeficiency disease (red blood cells lack this enzyme).

13 prealbumin (PALB)

Acute phase response protein

Increased: can be seen in Hodgkin's disease, oral contraceptives and the use of steroids.

Nephrotic syndrome >500mg / L (at this time ALB <30g / L), the incidence of PA increased ALB decreased.

Reduce: malnutrition, severe liver disease patients, malignant tumors, inflammation and kidney disease.

14 homocysteine (HCY)

Increased: It can stimulate the blood vessel wall to cause damage to arterial blood vessels, leading to inflammation and the formation of plaques.

15 glucose (GLU)

Hyperglycemia: Some physiological factors (such as emotional stress, 1-2 hours after a meal) and intravenous injection of adrenaline can cause blood sugar to increase. Pathological increases are common in a variety of diabetes, chronic pancreatitis, myocardial infarction, acromegaly, some endocrine diseases, such as hyperthyroidism, anterior pituitary eosinophilic adenoma, anterior pituitary basophilic hyperfunction Adrenal hyperfunction. Intracranial hemorrhage, cranial trauma, etc. also cause blood sugar to increase.

Hypoglycemia: abnormal glucose metabolism, islet cell tumor, pancreatic tumor, severe liver disease, neonatal hypoglycemia, pregnancy, breastfeeding, etc. can cause hypoglycemia.

16 triglyceride (TG)

Increase: can be caused by genetic, dietary factors or secondary to certain diseases, such as diabetes, kidney disease. The TG value was increased by 2.26 mmol/L or more; and 5.65 mmol/L or more was severe hypertriglyceridemia.

Reduction: common in hyperthyroidism, adrenal insufficiency, liver parenchymal disease, primary B lipoprotein deficiency, and malabsorption.

17 total cholesterol (TCHO)

(1) diagnosis and classification of hyperlipoproteinemia and dyslipoproteinemia; (2) judgment of risk factors for cardiac and cerebrovascular diseases; (3) increase or decrease in CHO may be primary (including hereditary ), nutritional factors or secondary to certain diseases, such as thyroid disease, kidney disease. When the CHO value is 5.17-6.47mmol/L, it is the risk of atherosclerosis; 6.47-7.76mmol/L is the risk of atherosclerosis; >7.76mmol/L is the high risk level of atherosclerosis; <3.1 Methylene/L or <2.59 mmol/L is hypocholesterolemia.

18 high density lipoprotein (HDL)

Conducive to the clearance of arterial intima cholesterol, and negatively correlated with the incidence of cardiovascular and cerebrovascular diseases.

Increased: can be seen in primary high HDL, insulin, estrogen, exercise, drinking and so on.

Reduction: common in hyperlipoproteinemia, cerebral infarction, coronary atherosclerosis, chronic renal insufficiency, cirrhosis, diabetes, obesity and long-term smoking.

19 low density lipoprotein (LDL)

Increased: can be seen in 1. hypothyroxinemia, nephrotic syndrome, diabetes, liver disease and chronic renal failure, etc. 2. blood porphyria, neurotic phobia and pregnancy 3. obesity and long-term high cholesterol and saturated fatty acid diet.

Reduce: 1. High thyroxemia, acute myocardial infarction, myeloma, trauma, severe liver disease and Reye syndrome. 2. Malnutrition and chronic anemia.

20 apolipoprotein A1 (ApoA1)

Apolipoprotein AI is the major structural protein of high-density lipoprotein, which is the best indicator of HDL levels. Reduction: coronary heart disease, liver parenchymal disease, nephrotic syndrome, malnutrition, diabetes, etc.

ApoA1 deficiency, familial hypoalphalipoproteinemia, fisheye disease and other serum levels are extremely low.

21 apolipoprotein B (ApoB)

Apolipoprotein B is a structural protein of low-density lipoprotein, which mainly represents the level of LDL. The change of APOB in pathological state is often more obvious than that of LDL.

Increased: common in hepatitis, hyperlipidemia, coronary heart disease, diabetes, nephrotic syndrome and psoriasis.

Reduction: common in liver parenchymal lesions.

22 lipoprotein a (Lp(a))

Lp(a) is a recognized independent risk factor for atherosclerosis.

Increase: atherosclerosis, cerebral infarction, cerebral arteriosclerosis, acute phase reaction.

Reduced: seen in severe liver disease.

23 creatinine (CREA)

Elevation: common in severe renal insufficiency, various renal disorders, acromegaly and so on. Reduction: Common in muscle loss (such as malnutrition, elderly), polyuria.

24 uric acid (UA)

Elevation: common in gout, eclampsia, leukemia, polycythemia, multiple myeloma, acute and chronic glomerulonephritis, severe liver disease, lead and chloroform poisoning. Reduction: common after medications such as pernicious anemia, celiac disease and adrenocortical hormone.

25 urea nitrogen (BUN or UREA)

Elevation: It can be roughly divided into three stages. When the concentration is 8.2-17.9mmol/L, it is common in UREA excess (such as high protein diet, diabetes, severe liver disease, high fever, etc.), or UREA diarrhea (such as mild renal dysfunction, high blood pressure, gout, multiple Myeloma, urinary tract occlusion, postoperative oliguria, etc.). When the concentration is 17.9-35.7mmol/L, it is common in pre-uremic disease, cirrhosis, bladder tumor and so on. The concentration is above 35.7mmol / L, which is common in severe renal failure and uremia.

26 Cystatin C (Cys-C)

Can be used as a marker of early kidney damage.

27β2-microglobulin (β2-MG)

It is a sensitive indicator for diagnosing damage to proximal convoluted tubules.

28 potassium (K)

Increase: (1), oral and intravenous intake increased. (2) Potassium influx into the extracellular fluid is severely hemolyzed and infected with burns, tissue destruction, and insulin deficiency. (3), tissue hypoxia, cardiac insufficiency, respiratory disorders, shock. (4), urinary excretion disorders renal failure and adrenal insufficiency. (5), taking digoxigenin in large quantities. Reduce: (1), oral intake decreased. (2), potassium is transferred into the cells, liquid alkali poisoning and IRI secretion increases after insulin is used. (3), potassium loss in the digestive tract Frequent vomiting and diarrhea. (4), urinary potassium loss, renal tubular acidosis.

Clinical significance of urinary potassium: urinary potassium excretion increases when diuretics are used. The ratio of sodium to potassium in the urine of patients with primary aldosteronism was reduced to 0.6:1. When aldosterone secretion increases, urinary potassium excretion increases.

29 sodium (NA)

Elevation: (1), severe dehydration, excessive sweating, high fever, burns, diabetic polyuria. (2) Adrenal hyperfunction, primary and secondary aldosteronism. Reduce: (1), kidney loss of sodium such as renal cortical insufficiency, severe pyelonephritis, diabetes. (2), gastrointestinal sodium loss, such as gastrointestinal drainage, vomiting and diarrhea. (3), excessive antidiuretic hormone.

Clinical significance of urine sodium determination: The important clinical significance of urine sodium determination is to know whether there is a large amount of salt loss, to determine whether the intake is sufficient, and to assist in monitoring the low-salt diet and postoperative electrolyte supervision, to help determine vomiting, serious Electrolyte balance in patients with diarrhea and heat failure. It is also used for the definitive diagnosis of patients with salt-deficient water shortage and water-deficient water shortage; the sodium chloride in the urine is quite low, and the sodium chloride in the urine is normal or elevated. Central nervous system diseases, cerebral hemorrhage, inflammation, tumors, Edison's disease, adrenal insufficiency, severe tubular damage, bronchogenic lung cancer, etc., increased sodium in the urine.

30 chlorine (CL)

Elevation: common in hypernatremia, respiratory alkalosis, hyperosmotic dehydration, nephritis oliguria and urethral infarction.

Reduction: common in hyponatremia, severe vomiting, diarrhea, loss of pancreatic juice in the pancreatic juice, renal dysfunction and Addison's disease. Clinical significance of chlorine determination in urine: In general, sodium and chlorine in urine remain relatively balanced. But the two are not always balanced.

For example, after continuous administration of sodium chloride or potassium chloride, urine chlorine is higher than urine sodium, and when a large amount of alkaline sodium salt is continuously taken, sodium in urine is higher than chlorine. In addition, the urine is alkaline and it is likely that the urine sodium content is higher than chlorine.

31 total carbon dioxide (TCO2)

Increase: excess alkali storage (1) metabolic alkalosis: pyloric infarction (a large loss of gastric acid), upper intestinal obstruction, lack of potassium, taking alkaline drug overdose (or poisoning). (2) Respiratory acidosis: obstruction of the respiratory tract, severe emphysema, bronchiectasis, pneumothorax, emphysema, lung consolidation, pulmonary fibrosis, respiratory muscle paralysis, compensatory respiratory acidosis. (3) High fever, exhaled carbon dioxide. (4) Adrenal hyperfunction, excessive use of adrenocortical hormone.

Decrease: insufficient alkali reserve (1) Metabolic acidosis: diabetic ketoacidosis, renal failure, uremia, septic shock, severe dehydration, epidemic hemorrhagic fever (hypotension and oliguria), chronic adrenal gland Decreased cortical function and taking too much acidic drug. (2) Respiratory alkalosis: Respiratory center excitement (breathing increases, hyperventilation, excessive carbon dioxide inhalation). (3) Kidney disease: glomerulonephritis, renal tubular acidosis, pyelonephritis, kidney tuberculosis. Mild acidosis: CO2CP 23-18mmol/L moderate acidosis: CO2CP 18-14mmol/L severe acidosis: CO2CP<14mmol/L extreme acidosis: CO2CP <7mmol/L

32 anion gap (AG)

One of the important indicators reflecting metabolic acid-base poisoning.

33 phosphorus (P)

Elevation: common in hypoparathyroidism, acute and chronic renal insufficiency, uremia, myeloma and fracture healing.

Reduced: common in hyperthyroidism, metabolic acidosis, rickets, renal failure, long-term diarrhea and malabsorption.

34 mg (Mg)

Elevation: common in acute and chronic renal insufficiency, hypothyroidism, Addison's disease, multiple myeloma, severe dehydration and diabetic coma.

Reduction: common in congenital familial hypomagnesemia, hyperthyroidism, long-term diarrhea, vomiting, malabsorption, diabetic acidosis, primary aldosteronism, and long-term use of corticosteroids.

35 calcium (CA)

Elevation: common in bone tumors, hyperparathyroidism, acute bone atrophy, adrenal sebum dysfunction and excessive intake of vitamin D.

Reduced: common in vitamin D deficiency, rickets, rickets, pediatric hand and foot convulsions, senile osteoporosis, hypoparathyroidism, chronic nephritis, uremia, low calcium diet and malabsorption.

36 iron (FE)

Increased: seen in hemolytic anemia, aplastic anemia, megaloblastic anemia, acute hepatitis and lead poisoning.

Reduced: seen in iron deficiency anemia, chronic blood loss, menorrhagia, pregnancy, infectious diseases, evil

37 total iron binding capacity (TIBC)

The maximum amount of iron bound by transferrin in serum is called total iron binding capacity (TIBC), which is equal to the sum of the binding force of serum iron and unsaturated iron. The determination of total iron knot and force is conducive to the diagnosis of a variety of diseases.

Increased: seen in iron deficiency anemia and hepatocyte necrosis.

Reduced: seen in hereditary ferritin deficiency, kidney disease, uremia, cirrhosis, hemolytic anemia, chronic infection and leukemia.

38 unsaturated iron binding force (UIBC)

Usually only one-third of the transferrin in the serum binds to iron, and the other potential of transferrin to bind iron is called unsaturated iron binding (UIBC).

Increased: seen in hemolytic anemia, pernicious anemia, thalassemia, iron poisoning, nephritis.

Reduced: seen in iron deficiency anemia, chronic infectious anemia, malignant tumor anemia.

39 transferrin (TRF)

Increased: common in iron deficiency, pregnancy, control of estrogen and fat-like kidney disease.

Reduction: Common in hereditary defects, control of testosterone, infection, acute inflammation, certain types of nephritis, tumors, hemoglobin deficiency, acute malaria, and malnutrition.

40 transferrin saturation (TS)

Increase: can be seen in aplastic anemia, hemolytic anemia, megaloblastic anemia.

Reduction: can be seen in iron deficiency anemia, polycythemia and inflammation.

41 lactate dehydrogenase (LDH)

LDH is present in various tissues of the human body, and the content of LDH is highest in heart, kidney and red blood cells. Under normal circumstances, the activity of this enzyme in serum is 1000 times lower than that in cell tissue. When a small amount of tissue necrosis occurs, the enzyme is released into the blood to increase its activity in the blood. The serum LDH of patients with myocardial infarction, hepatitis, cirrhosis, and kidney disease is significantly increased.

42 hydroxybutyrate dehydrogenase (HBDH)

Elevation: It is roughly the same as LDH. In acute myocardial infarction, the enzyme maintains a high value in the blood by about 2 times.

43 creatine kinase (CK)

Elevation: Myocardial infarction begins to rise 4-6 hours, 18-36 hours to normal value is indeed 20-30 times, the highest peak, 2-4 days return to normal. In addition, viral myocarditis, dermatomyositis, muscle damage, muscular dystrophy, pericarditis, cerebrovascular accidents, and cardiac surgery can all increase CK.

44 creatine kinase isoenzyme (CKMB)

CK-MB is mainly present in the myocardium, which is about 14% of the total myocardial CK. The serum CK-MB rises before the total activity, peaks at 24 hours, and its fluctuation curve is parallel with the total activity within 36 hours. The hour disappears.

45 myoglobin (Mb or MYO)

Myoglobin is the earliest measurable marker of myocardial damage after acute myocardial infarction (AMI). The AMI increased 2 hours after the onset of AMI, reached the peak at 6~9h, and returned to normal level at 24~36h. Its negative predictive value is 100%.

46 anti-chain O (ASO)

The ASO test provides evidence for early streptococcal infections, primarily for acute rheumatic fever, glomerulonephritis following streptococcal infection, individuals with pharyngitis, and other acute infections. Typically, antibodies corresponding to antigens peak at about three weeks after acute streptococcal infection and remain at peak levels for 3-4 months, then gradually decrease to normal levels.

47 rheumatoid factor (RF)

It has certain clinical significance for the diagnosis and prognosis of patients with rheumatoid arthritis (RA).

Can be used for the auxiliary diagnosis of autoimmune diseases.

48 hypersensitive C-reactive protein (HCRP)

HCRP is a non-specific acute phase response protein that appears in the blood during inflammation. The change in CRP concentration in patients with acute inflammation is faster than the change in red blood cell deposition. Studies have shown that CRP is not only a very good indicator of inflammation, it is also a good indicator of coronary artery disease when significantly increased. The increase in concentration occurs in a variety of tissue lesions in a non-specific manner, such as: infection, rheumatoid arthritis, myocardial infarction, malignancy, and the like.

49 amylase (AMY)

Serum amylase assay is mainly used to diagnose acute pancreatitis. Amylase activity is significantly increased during acute attacks. Urinary amylase will also increase 12-24 hours after onset. Some chronic pancreatic diseases, such as chronic pancreatitis, pancreatic tumors, and mumps, salivary glands, or glandular tube occlusion, serum amylase will also increase, and for various liver diseases such as hepatitis, cirrhosis, liver Abscess, liver cancer and cholecystitis, etc., amylase activity decreased.

50 lipase (LIPA or LPS)

Lipase activity was measured to reflect the imbalance of the pancreas. In acute pancreatitis, lipase activity is 2-50 times higher than the reference upper limit within 4-8 hours of abdominal pain, peaking at 24 hours, and decreasing within 8-14 days. Lipase activity is also elevated in chronic pancreatitis and pancreatic duct occlusion.

51 glycated hemoglobin (HbA1c)

The degree of control of diabetes was assessed, and the average blood glucose level was measured 1-2 months before the response. When the red blood cell survival period is shortened for any reason, the HbA1c% will decrease, even though the blood glucose level may be elevated at this time.