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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 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.


סימפטומים של סכרת נעורים

  • פוליאוריה

  • פולידיפסיה

  • אבדן משקל

  • פוליפאגיה (לעתים)

  • טשטוש ראיה (לפעמים)


Etiologic classification of diabetes
Etiologic classification of diabetes

  • Type 1 diabetes

  • Type 2 diabetes - may range from predominantly insulin resistance with relative insulin deficiency to vice versa.

  • Other specific type

    genetic defects of beta-cell function

    Genetic defects in insulin action

    Diseases of the exocrine pancreas

    Endocrinopathies

    Drug- or chemical-induced

    Infections

    Unknown forms of immune-mediated diabetes

    Other genetic syndromes sometimes associated with diabetes

  • Gestational diabetes mellitus (GDM)


Criteria for the diagnosis of dm
Criteria for the diagnosis of DM

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.

O r

2] FPG > 126 mg%. Fasting: no caloric intake for at least 8 h.

Or

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.


Impaired glucose tolerance fasting glucose
Impaired glucose tolerance & fasting glucose

  • IFG: > 100 mg% but < 126 mg% Near the level above which acute phase insulin secretion is lost in IV-GTT. Associated with a progressively greater risk of developing micro- & macrovascular complications.

  • IGT: 2h levels of BG after OGTT between 140 mg% to 200 mg%.

  • IGF & IGT are risk factors for future diabetes.

  • Associated with syndrome X (insulin resistance syn)


סיבוכים ארוכי טווח של סכרת (1)

  • Retinopathy: potential loss of vision

  • Nephropathy: potential renal failure

  • Peripheral neuropathy: Foot ulcer

    Amputation

    Charcot joints

  • Autonomic neuropathy: Gastrointestinal

    Genitourinary

    Cardiovascular

    Sexual dysfunction


סבוכים ארוכי טווח של סכרת (2)

  • Vascular disease: Cardiovascular

    Peripheral vascular

    Cerebrovascular

  • Hypertension

  • dislypidemia

  • Periodontal disease

  • Psychosocial dysfunction


Changes of the new classification
Changes of the new classification

  • Elimination of insulin dependent vs. insulin independent

  • Type 1 & type 2:

    Type 1: b-cell destruction with tendency to ketoacidosis, d/t autoimmune process with autoantibodies or without (type 1 idiopathic)

  • Elimination of malnutrition-related diabetes

  • Addition of impaired fasting glucose (IFG) to the entity of IGT.


Type 1 diabetes
Type 1 diabetes

  • Cellular-mediated immune destruction of the b-cells

  • HLA association (HLA class II): DQA, DQB, DRB

  • Autoantibodies: insulin autoantibodies (IAA) Islet cells autoantibodies (ICA) anti Glutmic acid decarboxylase (GAD65) antibodies to tyrosine phosphatase IA-2 & IA-2b

  • Young age/ lean habitus/ ketoacidosis/ autoimmune

  • Idiopathic diabetes

  • No autoimmunity, no HLA predisposition (but inherited)

  • Most are of African or Asian origin

  • Insulin requirement may come and go


Diabetic ketoacidosis
Diabetic ketoacidosis

DEFINITION

  • Blood glucose > 250 mg%

  • Ketonemia

  • pH < 7.30 and standard bicarbonate < 15 meq/L


Diabetic ketoacidosis 1
Diabetic ketoacidosis [1]

  • Dehydration

    Osmotic diuresis (glycosuria) NS 20cc/kg 1st hour

    vomiting maintenance + deficit

    Insensible loss

    (Kussmaul breathing, fever)

  • Hyperglycemia

    Insulinopenia Insulin 0.1 Unit/kg/hour

    Insulin resistance (acidosis)

    Counterregulatory hormones


Diabetic ketoacidosis 2
Diabetic ketoacidosis [2]

  • Hyponatremia

    Water shift to ECF NS 1st hour

    Pseudohyponatremia 0.5 NS later

  • Hyperkalemia

    Acidosis K < 3.5 meq/L: 40 meq/L

    pre renal azotemia K 3.5-5 meq/L: 30 meq/L

    K 5-5.5 meq/L: 20 meq/L

  • Hypophosphatemia

    Phosphaturia ½ KCL, ½ KPO4


Diabetic ketoacidosis 3
Diabetic ketoacidosis [3]

  • Acidosis

    Free fatty acids (lypolysis) Insulin

    Lactic acidosis Rehydration

  • Hyperlipidemia

  • Lypolysis Insulin


Genetic defects of b cell function
Genetic defects of b-cell function

  • Monogenetic defects: autosomal dominant pattern (MODY)

  • Onset: before 25 y, mild hyperglycemia

    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 ying yang interplay
GLUCOKINASE:YING & YANG INTERPLAY

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)

Val455Met mutation

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


Ipf1 pdx1 deficiency linked to mody4 stoffers et al nature genetics 1997 17 138
IPF1 (PDX1) deficiency linked to MODY4Stoffers et al: nature genetics 1997;17,138.

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


Genetic defects in insulin action
Genetic defects in insulin action

Murations of the insulin receptor with subsequent insulin resistance (acanthosis nigricans, virilization, PCOS)

  • Leprechaunism: characteristic facial features, fatal

  • Rabson-Mendelhall syndrome: abnormalities of teeth and nails, pineal gland hyperplasia

  • Lipoatrophic diabetes: a defect in the post-receptor signal transduction pathway.


Diseases of the exocrine pancreas
Diseases of the exocrine pancreas

  • Pancreatitis

  • Trauma \ pancreatectomy

  • Neoplasia

  • Cystic fibrosis

  • Hemochromatosis

  • Fibrocalculous pancreatopathy


Other genetic syndromes
Other genetic syndromes

  • Down’s syndrome (autoimmune diseases)

  • Kleinfelter syndrome

  • Turner syndrome

  • Wolfram’s syndrome (DIDMOD)


Enedocrinopathies
Enedocrinopathies

  • Acromegaly

  • Cushing syndrome

  • Glucagonoma

  • Pheormacytoma

  • Hyperthyroidism

  • Somatostatinoma

  • Aldosteronoma


Drug or chemical induced
Drug- or chemical-induced

  • Vacor (rat poison): permanently destroy b-cells

  • Pentamidine: permanently destroy b-cells

  • Nicotinic acid: impair insulin action

  • Glucocorticoids: impair insulin action

  • Interferon-a: induce antibodies’ positive diabetes


I n f e c ti o n s
I n f e c ti o n s

  • Congenital rubella

  • CMV

  • Coxsackie B virus

  • Adenovirus

  • Mumps


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