қң қ:
- ө ұң үң қ
- ө ұ қ ү қ қ.
қ ұқ ғ 3 қ ғ қ
қ ұқ ү ғ қ
қ
- ө ұң үң
- ө ұ қ ү қ қ ғ .
қ ғ
ү ғ
қң ұқ:
1. өң қ ңң ұ
2. ң ү ә ң ұ. ү.
3. өң қ ң ұ (, ), .
4. , . қ ң .
5. , ү, .
6. ң ұқ ә ұқ , .
7. Қ ң I ә II үң .
8. ң . ң .
9. Қ ң қ. ә ң .
қ қ ү ә:
қ қң ұқ , , ә ә
қ ә:
ұ, ә ә қ , .
қң
| қң ң | қ | |
| Ұқ ө. ү. қң қ , ө | 5 | |
| қң 1-5 ұқ , 1-2 | 45 | |
| Ү | 10 | |
| 6-9 ұқ | 35 | |
| 10 | ||
| қ қ, ғ | 5 |
ӘƲ˲ Ұ
| 1 . | ң ө қң құ. қ (+) қ (-) қ ә (0)- | |||||
| Қ қ | ||||||
| 2 . | қ қ қ ң ү , ң қ. |
Ә: ә ү қғ . қң әқ 1-2 ө . ғ ғ. қ қ ө қ ғ. қ. қ. 40 ң ә қ қ ң қ ( қ ә ө, , қғ ү ұғ). ә қң қ 1,0-1,5 10% , ә қ , қ ғ. қ қғ ң ғң ғ ү, қ .
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-6-.
- ң ә -6- қ .
Glycogenolysis is the breakdown of glycogen to glucose-1-phosphate and glucose.
- (, , ).
- ң өғ (, ққ, ) ө ү.
Gluconeogenesis is the generation of glucose from non-carbohydrate carbon substrates such as pyruvate, glycerol, and glucogenic amino acids.
- , , . I - -6- , ( ), II - α-1,4- , , , ( ), III - -1,6- , , ( ), IV - -1,4->1,6- ( ), V - ( -), VI - ( ) .
ң қ ң қғ ұққ . ң 1- ү , ү -6- ң қғ ( ), ң 2- ү , ү, ұқ , a-1, 4- қғ ( ) , ң 3- ү , ұқ , -1,6- қғ ( ) , ң 4- ү -1,4-> қғ ( ) , ң 5 ү ұқ қғ (- ) , ң 6- ү қғ ( ) ә ғ қ.
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Glycogenosis is a group of inherited diseases caused by inherited defects in the enzymes involved in the breakdown of glycogen. Type I Glycogenosis is defect in glucose-6-phosphatase activity of the liver, kidneys (Von Gierkes disease), Type II glycogenosis is defect in α-1,4-glucosidase activity of the liver, kidneys, muscle, myocardium (Pompes disease), type III glycogenosis is defect in amilo-1,6-glucosidase activity of the liver, muscles, and myocardial (Forbes disease), type IV glycogenosis is deficiency of amilo-1, 4 -> 1,6 - glucosyl transferase (Andersen disease), type V glycogenosis is defect in muscle glycogen phosphorylase (McArdl disease), type VI glycogenosis is deficiency of the liver phosphorylase (Hers' disease) and others.
3,4 5,6 /
қ ң қ ң (3,4 - 5,6 /).
Normoglycemia is normal blood glucose level (3.4 - 5.6 mmol / l)
6,1 /
қ ңң 6,1 / ғ .
Hyperglycemia is increased blood glucose level more than 6.1 mmol / L
3 /
қ ңң 3 / ө .
Hypoglycemia is decrease in blood glucose level less than 3 mmol / l
- , .
ғ қ ғ қ ұ
қ, қ ү қ ә қ. қ ә, қ ғ ң, ң ө ( ө ү).
Glucose tolerance test is laboratory method used for the diagnosis of impaired glucose tolerance.
- (9-10 /), .
ү ү ғ - қғ ө () 9 10 / ғ ү қ , ө, қ ө.
"Renal threshold for glucose is the maximal concentration of blood glucose (9 - 10 mmol / L), when glucose is not detected in the urine.
ң .
ү ү ө ң ңң (ң) ұ ү.
,
ү ү, ү ғ ғ ғ .
Glycosuria is the appearance of glucose in the urine
Renal glucosuria is due to impaired glucose reabsorption in the renal tubules
Extrarenal glucosuria is caused by hyperglycemia more than "renal threshold"
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- , / .
Қ ң () () .
Diabetes mellitus is a disease at the heart of which lies the absolute and / or relative insulin deficiency.
() - -
Ұқ ң (, ) - ғң - қғ .
(), , .
Ұқ () , ө, қ ә, ә ғ .
Pancreatic insulin deficiency (absolute) develops when there is damage to beta-cells of Langerhans islets
Extrapancreatic insulin deficiency (relative) develops when insulin is produced, but not effective.
() - , .
ө () ұ ң ө () ғ ң ң (ң) ө , ә ә қғқβ .
Insulin resistance is a condition in which the body's cells become resistant to the effects of insulin as a result of which glucose is not assimilated by insulin-dependent tissues and hyperglycemia develops.
I - , ( ), β-. HLA-.
Қ ң 1 ү қ ң ғ қ ү қ (қ ), β -ң құ ү ұ. L- қ () .
Type I diabetes mellitus is immune-mediated diabetes, the main pathogenetic factor of which is an inflammation in Langerhans islets (autoimmune insulinitis), leading to the destruction of β-cells. There is a clear association with HLA genes.
II - : β-.
Қ ң ү ұ ң қ , ң құ : ө ә -ң .
Type II Diabetes mellitus is the total collective name of heterogeneous disorders in the pathogenesis of which there are two major factors: insulin resistance and β-cell dysfunction.
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: → → →
қ әң (ң) : > > > .
қ қң ғ ң ө.
,
қ ғ ұқ ө қ, ө.
-
ң ғ ә қ ң ө ң ғ қ қ.
Diabetic syndrome is complex of diabetic symptoms: hyperglycemia→ glycosuria → polyuria → polydipsia
Polyuria - increased diuresis due to increased ultrafiltrate osmotic pressure
Polydipsia - thirst, increased fluid intake due to hyperosmolar hypohydration
Polyphagia - excessive use of food as a result of disorders of nutrient utilization at insulin deficiency
. ( 19,4 / ), .
қ қ . Қ ң - ү қ (19,4 / , ғ ғ), ә .
Ketoacidotic hyperglycemic coma develops most often in patients with type 1 diabetes mellitus. It is due to hyperglycemia (from 19.4 mmol / L or more), hyperketonemia and metabolic acidosis.
2 50 (, , , , , , ). , 55 /, .
қ Қ - ү 50- қ қ қ ғ ә ққ (құ, ө, ғ, ү, қ, , қғ) . ң ң қ ң қ ү . ұ 55 / ү, қ .
Hyperglycemic hyperosmolar coma develops in patients with type 2 diabetes over 50 years, when there are additional pathogenic effects of dewatering factors (vomiting, diarrhea, limiting fluid intake, burns, blood loss, polyuria, diuretics). The main stages of pathogenesis are dehydration and development of hyperosmolarity of plasma. Glucose levels can be up to 55 mmol / l, there is no pronounced hyperketonemia and ketonuria.
- : , -, , (),
қ ң қ ң ң ө - , ә (, ) қғ, .
Laktacidotic coma Pathogenetic factors are: decrease in activity of pyruvate dehydrogenase enzyme complex that converts pyruvate to acetyl-CoA, the usage of drugs that stimulate anaerobic glycolysis (biguanide), hypoxia
- - , ,
әң ң әң (, , ) қ.
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Non-enzymatic glycosylation of proteins is glucose binding to free amino groups of proteins: collagen, crystallins, hemoglobin
, , , , , , .
. ұ ғ, ғ ң , ә ө , ө ұғ, ү ғ, , , ғ ә қ ң қ.
Enzymatic glycosylation is increased conversion rate of glucose to sorbitol and mannitol, which leads to their accumulation within the cells and intercellular spaces of the retina, lens, renal glomeruli, endothelial cells, Schwann cells, or neurons.
- .
қң қ.
- ( ) . .
ұғ қ ң ү ұ қ қғ әң . ү ә ө ң қ қ.
Macrovasopathy is atherosclerotic vessels.
Microvasopathy is damage to vessels of microcirculation. It is due to metabolic disturbances in the vascular wall (glycosylation of proteins) and the development of vasculitis. Most often affects the kidneys and blood vessels of the retina.is characterized by basement membrane thickening because of increased glycosylation of base membrane proteins (collagen)
Of microangiopathy, due to metabolic disturbances in the vascular wall ( proteins) and the development of vasculitis. Most often affects the vessels of the kidneys and of the retina of the eye.
2.5 /. ( )
қ 2,5 / ө ғ. ң қ, ққ қ ( ).
Hypoglycemic coma develops when blood glucose is below 2.5 mmol / l. The main pathogenetic factor is the energy deficit of neurons (substrate hypoxia)
Ә:
1. Ә.ұұұ. . ; ʳ, 2007. . 130 - 139.
2. // . .., .. .. : - , 2010., 1, . 568-620
3. .. : . .: , 2009. - . 111-127.
4. . . // .. . : -. 2008. . 67-69
5. : / .. ... 2- . .: -, 2004. . 251-269
6. қ қ // Қ ғ ..ө, ғ .., .. .: , ҚҰ, 2007.- . 163 174
Қ
7. : : . . ... : ʳ, 2004. . 52-60
8. / .., .., .., .., ... .: -, 2002. . 228-238.
9. : . / .. .. .-: .-, 2006, . 271-293.
10. .. : : 2 . .: -, 2003. . 1. . 266-301.
11. .. . . : , 2000.
12. ., . . -,1998- 402.
Қ
. қң: қ қ // Қ ғ ..ө, ғ .., .. .: - , ҚҰ, 2007.- . 163-174
Ө
