This document discusses the diagnosis and treatment of hyperglycemic crises in adult patients with diabetes mellitus. It addresses diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS), defining their diagnostic criteria and typical clinical presentations. For DKA, symptoms develop rapidly and include abdominal pain and Kussmaul breathing. For HHS, symptoms develop more gradually over days and include neurological changes with dehydration. Laboratory findings for both conditions include high blood glucose, electrolyte abnormalities, and metabolic acidosis. Treatment involves fluid resuscitation, insulin administration, electrolyte replacement, and identifying and treating any precipitating factors.
Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycaemia, dehydration, and acidosis producing derangements in intermediary metabolism.
Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycaemia, dehydration, and acidosis producing derangements in intermediary metabolism.
DKA is a life-threatening condition that develops when cells in the body are unable to get the glucose they need for energy because deficiency of the insulin.
Without enough insulin, the body begins to break down fat as fuel.
This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated.
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.
DKA is a life-threatening condition that develops when cells in the body are unable to get the glucose they need for energy because deficiency of the insulin.
Without enough insulin, the body begins to break down fat as fuel.
This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated.
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Crisis de hiperglicemia en pacientes adultos con diabetes
1. Crisis de hiperglicemia en pacientes adultos con Diabetes Mellitus MARIA ALEJANDRA ENRIQUEZ R I MEDICINA INTERNA FUSM
2. Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate. Crisis de hiperglicemia en DM
3. CRITERIOS DIAGNOSTICOS PARA CAD Y HHS Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
4. Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate. Crisis de Hiperglicemia en DMEpidemiologia
5. Patogenesis Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
6. Patogenesis Kitabchi, Abbas E; Epidemiology and pathogenesis of diabetic ketoacidosis and Hyperosmolar hiperglycemic state, Agosto 2009
7. Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
9. Factores precipitantes Data from: Kitabchi, AE, Umpierrez, GE, Murphy, MB, et al. Management of hyperglycemic crises in patients with diabetes mellitus (Technical Review). Diabetes Care 2001; 24:131
10. Factores precipitantes Data from: Kitabchi, AE, Umpierrez, GE, Murphy, MB, et al. Management of hyperglycemic crises in patients with diabetes mellitus (Technical Review). Diabetes Care 2001; 24:131
11. CAD desarrollo rápido, 24-horas, dolor abdominal y respiración Kussmaul HHS insidiosa, con poliuria, polidipsia y pérdida de peso, varios días antes de su ingreso. Sintomas neurológicos progresivos incluyendo letargo, signos focales, y obnubilación, progresar a coma en etapas posteriores Presentación Clínica Kitabchi Abbas, Clinical Features and Diagnosis of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults Enero 2010, Uptodate
12. Osmolaridad elevada causa alt. Neurológicas. >320 mmol/kg Osmolaridad efectiva= 2Na + glucemia/18 urea no induce cambios intracelulares en volumen o el gradiente osmótico de la membrana celular Diuresis osmótica, perdida de agua Na Y K. Osmolaridad normal, y sx neurológicos obliga a buscar otras causas Presentación clínica Kitabchi Abbas, treatment of diagnosis of Diabetic Ketoacidosis and Hyperosmolar Hyperglicemic state in adults Enero 2010, Uptodate
13. Dolor abdominal, En CAD 40%, en relación con severidad de acidosis Se relaciona con HCO3 5-15 Lento vaciamiento gástrico Desequilibrio H – Electrolítico Si persiste post a resolución de CAD buscar otras causas. Presentación clínica Kitabchi Abbas, Clinical Features And diagnosis of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic state in adults, Jan 2010, Uptodate.
15. Hallazgos de laboratorio Kitabchi Abbas, Clinical features and diagnosis of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
16. Hallazgos de laboratorio Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
17. La gravedad de acidosis metabólica depende La tasa de producción de cetoacidos. La duración de la producción cetoácido Tasa de excreción urinaria. ( depende funcion renal) El anión gap: Estimación de la cantidad de aniones no medidos en suero anion gap = Na sérico - (Cl + HCO3) Hallazgos de Laboratorio Kitabchi Abbas, Clinical Features and diagnosis of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Jan 2009, Uptodate.
18. Hallazgos de Laboratorio Kitabchi Abbas, Features and diagnosis of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Jan 2009, Uptodate.
19. Hallazgos de Laboratorio Kitabchi Abbas, Clinical Features and diagnosis of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Jan 2009, Uptodate.
22. Puede elevarse amilasa por producción en glan. salivaresKitabchi Abbas, Clinical Features and diagnosis of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Jan 2009, Uptodate.
23. Hallazgos de Laboratorio Kitabchi Abbas, Clinical Features and diadnosis of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Jan 2009, Uptodate.
24. Tratamiento Evaluación inicial examen físico deben centrarse en: Vía aérea, respiración y circulación (ABC) Estado mental Posibles factores precipitantes Estado de hidratación y volemia La evaluación inicial de laboratorio: Glucosa sérica Electrolitos (con cálculo del anión gap), Azoados Hemograma completo con diferencial Uroanálisis y cetonas en la orina con tira reactiva Osmolaridad de plasma Cetonas en suero Gases arteriales Electrocardiograma Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
25. Tratamiento Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
26. Tratamiento Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
27. Tratamiento Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
28. Tratamiento Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
29. Tratamiento Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
30. Tratamiento Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
31. Tratamiento Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct 2009, Uptodate.
32. Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Jan. 2009, Uptodate. Kitabchi Abbas, treatment of Diabetics Ketoacidosis and Hyperosmolar Hyperglicemic State in adults, Oct. 2009, Uptodate. Diabetes Care, American Diabetes Association, July 2009 Bibliografia