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Curs despre diagnoticul diabetului zaharat

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DIABETUL ZAHARAT

Diabetul zaharatDefiniieDiabetul zaharat = grup heterogen de afeciuni metabolice, caracterizate prin hiperglicemie cronic determinat de 2 cauze principale:defecte ale secreiei de insulininsulinorezisten ( sensibilitii la insulin)

Consecutiv hiperglicemiei apar perturbri ale metabolismului protidic, lipidic i hidroelectrolitic.

IstoricNicolae Paulescu 1921DefiniieInsulinorezistena =scderea sensibilitii la insulin = situaia n care este necesar o cantitate mai mare de insulin pentru a produce un efect biologic normalImportanFrecven crescutSeveritateCosturiEpidemiologieRomnia: 4% din populaia adult800.000 pacieni cu medicaietot atia necunoscuiTimi:23.000 pacieni nregistrai2.000 pacieni noi/anLume: frecven n cretere366 milioane n 2011 552 milioane n 2030The Diabetes Epidemic: Global Projections, 20102030

IDF. Diabetes Atlas 5th Ed. 2011Figures given are: number of people with diabetes in 2011 and predicted number of people that will have diabetes in 2030 according to IDF estimates. Percentage is the increase in diabetes from 2011 to 2030. World box acts as the legend.

The burden of diabetes is one of the greatest challenges of the 21st century, as seen in the global incidence and projections of diabetes epidemic worldwide.

366 million people have diabetes in 2011 and this is predicted to rise to 552 million by 2030.

Diabetes caused at least $465 billion in healthcare expenditure in 2011 11% of the total expenditure, and is expected to exceed $595 billion by 2030.

D I A B E S I T Y Severitatea diabetului zaharatDiabetul zaharatOrbire *Insuficien renal *

Amputaii*Sperana de via cu 5 - 10 aniBolile cardiovasculare de 2-4 X*Diabetul zaharat este prima cauz de insuficien renal, cazuri noi de orbire i amputaii netraumaticeAfectarea SN n 60% la 70% dintre pacieniA 5-a cauz de deces (dup infecii, BCV, cancere, accidente)Diabetes Statistics. October 1995 (updated 1997). NIDDK publication NIH 96-3926.Harris MI. In: Diabetes in America. 2nd ed. 1995:1-13.

CosturiPentru pacientPentru sistemele de asigurriSocialeStri ale homeostaziei glicemiceNormalDZCategorii de risc crescut (prediabet)Alterarea glicemiei a jeun (AGJ) = modificarea glicemiei bazale (MGB) [impaired fasting glucose (IFG)]Scderea toleranei la glucoz (STG) [impaired glucose tolerance (IGT)]AGJ + STGGlicemie a jeun (mg/dl)Glicemie la 2 ore (mg/dl)110 12670140200

DZSTGAGJNormalCategorii de risc crescutpentru diabet (prediabet)1. Alterarea glicemiei a jeun (AGJ)glicemia a jeun: 110 - 125 mg/dl 2. Scderea toleranei la glucoz (STG )glicemia a jeun < 110 mg/dl + glicemia la 2 h (TTGO): 140 - 199 mg/dl3. AGJ + STGglicemia a jeun 110-125 mg/dl + glicemia la 2 h (TTGO): 140 - 199 mg/dl

Clasificarea DZ (OMS 1999)1. Diabet zaharat tip 1 (5-10%)

2. Diabet zaharat tip 2 (90-95%)

3. Alte tipuri specifice de diabet zaharat (defecte genetice, boli pancreatice, endocrinopatii, medicamente, substane chimice etc.)

4. Diabetul zaharat gestaionalEtiopatogeniaDZ tip 1 DZ tip 2!!!

1. Predispoziia genetic

2. Factorii de mediu

3. Autoimunitatea

Distrucia celulelor Etiopatogenia DZ tip 1Etiopatogenia DZ tip 1

Proces autoimunIdiopatic Distrucia de celule Glicemiei Factori de mediuPredispoziia genetic secreiei de insulin

InsulitaEvoluia natural a DZ tip 1

Factori de riscNemodificabili

Predispoziia genetic

Vrsta

EtniaModificabili

Greutatea

SedentarismulEtiopatogenia DZ tip 2Etiopatogenia DZ tip 2

DeFronzo RA. Diabetes. 2009;58:773-795.Reproducere dup Primary Care, 26, Ramlo-Halsted BA, Edelman SV, The natural history of type 2 diabetes. Implications for clinical practice, 771789, 1999Model evolutiv pentru DZ tip 2 i complicaiile saleNivelul InsulineiRezistena la insulinProducia hepatic de glucozGlicemia postprandialGlicemia a jeunFuncia celulei betaEfect incretineProgresia Diabetului Zaharat de tip 2Toleran redus la glucoz Diagnosticul diabetuluiDiabet manifest47 ani Dezvoltarea complicaiilor macrovasculareDezvoltarea complicaiilor microvasculare21Development and Progression of Type 2 Diabetes

This conceptual diagram shows a proposed paradigm on the development and progression of pathophysiology in type 2 diabetes.1The horizontal axis in the figure shows the years before and after diagnosis of diabetes. Insulin resistance begins years before diagnosis.1 Insulin resistance rises during disease development and continues to rise during impaired glucose tolerance (IGT). Over time, insulin resistance remains stable during the progression of type 2 diabetes.1The insulin secretion rate increases to compensate for the decrease in insulin effectiveness due to insulin resistance. -cell function can decrease even as insulin secretion increases. At the time of diagnosis of type 2 diabetes and 6 years afterwards about 50% and 73% of -cell function has been lost, respectively.2 Over time, -cell compensatory function deteriorates and insulin secretion decreases. -cell function progressively fails.1,2Initially, fasting glucose is maintained in near-normal ranges. The pancreatic cells compensate by increasing insulin levels, leading to hyperinsulinemia. This compensation keeps glucose levels normalized for a time, but as cells begin to fail, IGT develops with mild postprandial hyperglycemia. As the disease progresses, the cells continue to fail, resulting in higher PPG levels. With continued loss of insulin secretory capacity, fasting glucose and hepatic glucose production increase.1Once cells cannot secrete sufficient insulin to maintain normal glycemia at the fasting or postprandial stage, type 2 diabetes (hyperglycemia) becomes evident.Insulin resistance and -cell dysfunction are established well before type 2 diabetes is diagnosed.1ReferencesRamlo-Halsted BA, Edelman SV. The natural history of type 2 diabetes. Implications for clinical practice. Prim Care. 1999;26:771789.Bell DSH. The case for combination therapy as first-line treatment for type 2 diabetic patients. Treat Endocrinol. 2006;5:131137.PurposeTo address the common misconception that an increase in insulin secretion (hyperinsulinemia) connotes an improvement in -cell function.TakeawayBoth insulin resistance and -cell dysfunction start earlyand well before diabetes is diagnosedleading to rises in fasting plasma glucose (FPG) and postprandial glucose (PPG) levels.Declinul progresiv al funciei celulei n DZ tip 2020406080100109876543210123456Years-Cell Function (% )Deficit de insulin: (DZ tip 1)- absolut(DZ tip 2)- relativ prelurii celulare de glucoz glicogenolizeiproteolizlipoliz gluconeogenezei hepaticeHIPERGLICEMIEFiziopatologia DZ Hiperglicemie marcat =foame energeticTablou clinic50% asimptomatici50% simptomaticipoliuriepolidipsiescdere ponderalastenie, scderea forei fizice i intelectualepolifagiesemnele complicaiilor infecioase i degenerativeInvestigaii paracliniceglicemia plasmatic (a jeun sau ntmpltoare)

HbA1c

TTGO

cetonuria

pentru depistarea complicaiilor cronice

glicozuriaDiagnosticglicemia plasmatic a jeun 126 mg/dl

glicemia plasmatic recoltat ntmpltor 200 mg/dl

TTGO (200 mg/dl la 2 h)

HbA1c 6,5% (VN: 5,6%; 5,7-6,4%: prediabet)

Exceptnd cazurile cu simptome tipice i hiperglicemie 200 mg/dl, testarea trebuie repetat!

DiagnosticGAJGPPTTGOHbA1cDiferenierea dintre DZ tip 1i 2 semne evidente, / N / Caracteristici DZ tip 1 DZ tip 2 Vrsta la debut de obicei 40 de ani Tendin la cetoz mare rar, dar posibil Tablou clinic frecvente dezechilibre variabil, rareori semne severe Greutate corporal frecvent obez Insulinemie(peptid C) deficit absolut, sever variat (hipo-, normo-sau hiperinsulinemie)Anticorpipancreatici da nu Tratament cu insulin indispensabil uneori (diabet insulinonecesitant) Asociere cu boliautoimunedanu