סכרת נעורים 2012. איבחון וקלסיפיקציה של סכרת נעורים קטואצידוזיס: הגדרה וטיפול. סכרת נעורים: 2005. אבחון וקלסיפיקציה של סכרת נעורים Expert Committee on the Diagnosis and classification of Diabetes Mellitus Diabetes care, July 1997 National Diabetes Data Group (NDDG) - 1979 WHO - 1980-1985.
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סכרת נעורים: 2005
אבחון וקלסיפיקציה של סכרת נעורים
Expert Committee on the Diagnosis and classification of Diabetes Mellitus
Diabetes care, July 1997
National Diabetes Data Group (NDDG) - 1979
WHO - 1980-1985.
genetic defects of beta-cell function
Genetic defects in insulin action
Diseases of the exocrine pancreas
Drug- or chemical-induced
Unknown forms of immune-mediated diabetes
Other genetic syndromes sometimes associated with diabetes
1] Symptoms of diabetes plus causal plasma glucose levels > 200 mg%.
Casual defined as any time of the day without regard to time since last meal. The classic symptoms include polyuria, polydipsia, and unexplained weight loss.
2] FPG > 126 mg%. Fasting: no caloric intake for at least 8 h.
3] 2h PG>200 mg% during an OGTT: Glucose load of 75g.
In the absence of unequivocal hyperglycemia with acute metabolic decompensation, these criteria should be confirmed by repeat testing on a different day.
Type 1: b-cell destruction with tendency to ketoacidosis, d/t autoimmune process with autoantibodies or without (type 1 idiopathic)
Osmotic diuresis (glycosuria)NS 20cc/kg 1st hour
vomitingmaintenance + deficit
(Kussmaul breathing, fever)
InsulinopeniaInsulin 0.1 Unit/kg/hour
Insulin resistance (acidosis)
Water shift to ECFNS 1st hour
Pseudohyponatremia0.5 NS later
AcidosisK < 3.5 meq/L: 40 meq/L
pre renal azotemiaK 3.5-5 meq/L: 30 meq/L
K 5-5.5 meq/L: 20 meq/L
Phosphaturia½ KCL, ½ KPO4
Free fatty acids (lypolysis)Insulin
1] Mutations in hepatocyte nuclear factor (HNF)-1a, chromosome 12 (MODY 3)
2] Mutations in glucokinase, chromosome 7 (MODY 2)
3] Mutations in HNF-4a, chromosome 20 (MODY 1)
4] Point mutations in mitochondrial DNA (mainly position 3243 in tRNA of leucine gene, similar to MELAS syndrom)
5]Impaired conversion of proinsulin to insulin (IGT)
6] Mutant insulin molecule with impaired receptor binding
Glucokinase loss-of-function mutations:
Decreased G phosphorylation decreased Insulin secretion MODY 2.
Glucokinase gain-of-function mutations:
Hyperinsulinism: Glaser et al: NEJM 1998;338,226.
Autosomal dominant (3 generations)
In vitro study: increased affinity of glucokinase for G higher rate of glycolysis at low G concentrations
GSIR threshold: about 40 mg%
Sequels: T1DM at later age
Extended-family pedigree (6 generations)
Onset of DM: 35 y (range 17-67 )
Heterozygous individuals: 6/8 Rx of diet or OH
No signs of ketosis or severe insulin deficiency
Murations of the insulin receptor with subsequent insulin resistance (acanthosis nigricans, virilization, PCOS)