SIGNIFICANCE
OVERVIEW
WHAT IS DIABETES?
DEFINITION
MECHANISM
PREVELANCE
EPIDEMIOLOGY
CLASSIFICATION
GESTATIONAL DIABETES
RISK FACTORS
DIAGNOSIS
COMPLICATIONS
MEDICAL TEST
MEDICAL NUTRITIONAL THERAPY
HERBS FOR DIABETES
MYTHS AND FACTS
REFERENCES
Definition of diabetes - introduction - classification of diabetes - etiology of diabetes type 1 and type 2- risk factors for diabetes - diagnosis of diabetes - clinical manifestations of diabetes type 1 and type 2- investigations for diabetes - treatment of diabetes - non-pharmacological treatment and pharmacological treatment - pharmacotherapy of type 1 and type 2 - acute complications of diabetes and treatment
SIGNIFICANCE
OVERVIEW
WHAT IS DIABETES?
DEFINITION
MECHANISM
PREVELANCE
EPIDEMIOLOGY
CLASSIFICATION
GESTATIONAL DIABETES
RISK FACTORS
DIAGNOSIS
COMPLICATIONS
MEDICAL TEST
MEDICAL NUTRITIONAL THERAPY
HERBS FOR DIABETES
MYTHS AND FACTS
REFERENCES
Definition of diabetes - introduction - classification of diabetes - etiology of diabetes type 1 and type 2- risk factors for diabetes - diagnosis of diabetes - clinical manifestations of diabetes type 1 and type 2- investigations for diabetes - treatment of diabetes - non-pharmacological treatment and pharmacological treatment - pharmacotherapy of type 1 and type 2 - acute complications of diabetes and treatment
Diabetes Mellitus Complete (Introduction, Pathophysiology, Types, Diagnostic Tests, Treatment, Insulin, Prevention)
Table of Contents
Introduction
Normal Physiology
Pathophysiology
Types of Diabetes
Type 1 Diabetes
Type 2 Diabetes
Difference
Common Symptoms
How does diabetes transmit?
Diagnostic Tests for Checking Diabetes
Management of Diabetes
Treatment Strategies of Diabetes
Oral Hypoglycaemic Agents
Insulin & Insulin Analogues
Insulin preparation and Treatment
Prevention
Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
1. Microvascular (due to damage to small blood vessels).
2. Macrovascular (due to damage to larger blood vessels).
SGLT2 Inhibitors (Gliflozins): A New Class of Drugs to treat Type 2 Diabetes:Naina Mohamed, PhD
Sodium-Glucose Linked Transporter 2 (SGLT2) inhibitors such as Dapagliflozin (Farxiga), Canagliflozin (Invokana) and Empagliflozin (Jardiance) are a new class of oral drugs available to treat type 2 diabetes mellitus (Type 2 DM).
Diabetes Mellitus Complete (Introduction, Pathophysiology, Types, Diagnostic Tests, Treatment, Insulin, Prevention)
Table of Contents
Introduction
Normal Physiology
Pathophysiology
Types of Diabetes
Type 1 Diabetes
Type 2 Diabetes
Difference
Common Symptoms
How does diabetes transmit?
Diagnostic Tests for Checking Diabetes
Management of Diabetes
Treatment Strategies of Diabetes
Oral Hypoglycaemic Agents
Insulin & Insulin Analogues
Insulin preparation and Treatment
Prevention
Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
1. Microvascular (due to damage to small blood vessels).
2. Macrovascular (due to damage to larger blood vessels).
SGLT2 Inhibitors (Gliflozins): A New Class of Drugs to treat Type 2 Diabetes:Naina Mohamed, PhD
Sodium-Glucose Linked Transporter 2 (SGLT2) inhibitors such as Dapagliflozin (Farxiga), Canagliflozin (Invokana) and Empagliflozin (Jardiance) are a new class of oral drugs available to treat type 2 diabetes mellitus (Type 2 DM).
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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
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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
2. Objectives of the Lecture
Be able to define diabetes mellitus
Be able to classify diabetes mellitus
Be able to list predisposing factors
Be able to list clinical features of diabetes mellitus
Be able to list drugs used in treatment of diabetes
mellitus
Diabetes Mellitus: An Overview 229/03/2014
3. Outline
DM definition
DM epidemiology
Types of DM
Clinical features
Investigations
Treatment
Complications
29/03/2014 3Diabetes Mellitus: An Overview
4. What is Type 2 Diabetes Mellitus (T2DM)?
– Current ADA definition1
• T2DM is a metabolic disease characterized by
hyperglycemia, resulting from a combination of
resistance to insulin action and an inadequate insulin
secretory response
– T2DM involves 2 primary pathogenic processes:
• progressive decline in pancreatic islet function
(↓ insulin secretion and inadequately suppressed
glucagon secretion)2,3
• diminished tissue responses to insulin (insulin
resistance)2,4
Diabetes Mellitus: An Overview 429/03/2014
ADA=American Diabetes Association
1American Diabetes Association. Diabetes Care. 2006; 29 (Suppl 1): S43–S48; 2Weyer C, et al. J Clin Invest. 1999; 104: 787–794;
3Müller WA, et al. N Engl J Med. 1970; 283: 109–115; 4Ahrén B, Pacini G. Diabetes Obes Metab. 2005; 7: 2–8.
5. Epidemiology
More than 285 million (2010) people affected
worldwide
By 2030, some 566 million people are projected to
have diabetes.
3.2% (12.1million) from Africa in 2010
By 2030, 3.7% (23.9 million) from Africa 2010
Diabetes Mellitus: An Overview 529/03/2014
7. Classification of Diabetes
Type 1 diabetes
β-cell destruction
Type 2 diabetes
Progressive insulin secretory defect
Other specific types of diabetes
Genetic defects in β-cell function, insulin action
Diseases of the exocrine pancreas
Drug- or chemical-induced
Gestational diabetes mellitus
Diabetes Mellitus: An Overview 729/03/2014
8. TYPE 1 DM
Due to B-cell destruction.
Require insulin for survival.
Presence of certain autoantibodies.
Type 1A – presence of autoantibodies (anti-GAD, IA2, ICAA,
and anti-insulin antibodies).
Type 1B – absence of autoantibodies (idiopathic)
Diabetes Mellitus: An Overview 829/03/2014
9. Type 2 DM
Most common form of DM
Characterized by disorder in insulin action and insulin secretion or
both.
Specific etiology unknown
Insulin resistance
Progressive B-cell failure.
They are obese.
Diabetes Mellitus: An Overview 929/03/2014
10. Predisposing Factors
Obesity
Hypertension
Strong family history
Sedentary lifestyle
Lack of exercise
Alcoholism
Smoking
Western diet
Advancing age
Diabetogenic drugs
Low birth weight
Artificial or cow milk
formulae in neonates
Viruses
Migration
Diabetes Mellitus: An Overview 1029/03/2014
12. Gestational diabetes
Carbohydrate intolerance associated with
hyperglycemia of variable severity with the onset
or first recognition during pregnancy.
In early pregnancy, fasting and post prandial
glucose concentration are normally lower than in
non pregnant women
Diabetes Mellitus: An Overview 1229/03/2014
13. Risk of developing GDM
Old women
Previous history of glucose intolerance
History of babies large for gestational age
Diabetes Mellitus: An Overview 1329/03/2014
14. Underlying causes of Type 2 Diabetes
Diabetes Mellitus: An Overview 1429/03/2014
Obesity
Insulin
resistance
-cell
defect
Impaired
glucose
tolerance
Early
diabetes
Late
diabetes
Hyperinsulinaemia
Decreased insulin
secretion
-cell failure
Saltiel AR. J Clin Invest 2000;106:163–164.
ACE/CDR/05/20746/1
17. Testing for Diabetes in
Asymptomatic Patients
Consider testing overweight/obese adults (BMI ≥25 kg/m2)
with one or more additional risk factors
In those without risk factors, begin testing at age 45 years
If tests are normal
Repeat testing at least at 3-year intervals
Use A1C, FPG, or 2-h 75-g OGTT
In those with increased risk for future diabetes
Identify and, if appropriate, treat other CVD risk factors
Diabetes Mellitus: An Overview 1729/03/2014
18. Diagnostic Criteria
Fasting Glucose
mg/dL
2-h OGTT
mg/dL
Random Glucose
mg/dL
A1c
Normal <100 <140 <200 <5.7%
Prediabetes 100-125
(IFG)
140-199
(IGT)
5.7-6.4%
Diabetes ≥ 126 ≥ 200 ≥ 200 ≥ 6.5%
Diabetes Mellitus: An Overview 1829/03/2014
Note: In the absence of unequivocal hyperglycemia, result(s) should be
confirmed by repeat testing.
19. DIAGNOSTIC CRITERIA FOR GDM
ADA ADA WHO
75g oral
glucose
(Mg/dL)
100g oral
glucose
(Mg/dL)
75g oral
glucose
(Mg/dL)
Fasting 95 95 >/= 126
1 hour 180 180
2 hour 155 155
3 hour NA 140 >/= 140
Diabetes Mellitus: An Overview 1929/03/2014
22. Eyes
(retinopathy, glaucoma,
cataracts)
Brain and Cerebral
Circulation
(stroke, TIA)
Heart and Coronary
Circulation
(angina, MI, CHF)Kidneys
(nephropathy, ESRD)
Peripheral Nervous
System
(peripheral neuropathy) Peripheral Vascular Tree
(peripheral vascular disease,
gangrene, amputation)
Tissue Damage in Many Organ Systems Leads to
Serious Long-term Complications in T2DM
Diabetes Mellitus: An Overview 2229/03/2014
CHF=congestive heart failure; ESRD=end-stage renal disease; MI=myocardial infarction; TIA=transient ischemic attack; T2DM=type 2 diabetes mellitus
Adapted from International Diabetes Federation. Complications. Available at: www.eatlas.idf.org/complications Accessed February 17, 2009.
23. Chronic Complications
Affects many organ systems.
Vascular :
Microvascular
Macrovascular
Non vascular:
Gastroparesis
Sexual dysfunction
Skin changes
Diabetes Mellitus: An Overview 2329/03/2014
24. Mechanism of Complications
There are 3 major theories (not mutually
exclusive);
Formation of Advanced Glycosylation End Products (AGEs)
via the nonenzymatic glycosylation of cellular protein.
Increase glucose metabolism via the sorbitol pathway by
enzyme aldose reductase.
Increase formation of diacyglycerol leading to activation of
certain isoforms of protein kinase C (PKC).
Diabetes Mellitus: An Overview 2429/03/2014
27. Outline
Purpose of laboratory testing
Confirmation of diagnosis of DM
Assessment of severity and level of DM control
Identification of co-morbidities and complications
Effect of treatment
Self urine and blood glucose monitoring
Laboratory monitoring
29/03/2014 27Diabetes Mellitus: An Overview
28. Confirmation of diagnosis
FPG and 2hrPP
Urinalysis
HBA1c
Serum lipids
Serum electrolytes
Imaging studies
29/03/2014 28Diabetes Mellitus: An Overview
30. Aims of treatment
Reduce the symptoms of hyperglycaemia
Limit adverse effects of treatment
Maintain quality of life and psychological well-
being
Prevent or delay vascular complications of
diabetes
Diabetes Mellitus: An Overview 3029/03/2014
31. Basis of Treatment
Reducing insulin resistance
Replacing or augmenting insulin secretion
Reducing gluconeogenesis
Treating effects of lipolysis and reducing lipolysis
Diabetes Mellitus: An Overview 3129/03/2014
33. Glycemic Recommendations
Diabetes Mellitus: An Overview 3329/03/2014
*Individualize goals based on these values.
†Postprandial glucose measurements should be made 1–2 h after the
beginning of the meal, generally peak levels in patients with diabetes
Target Treatment
Goal
AACE/ACE 2011 ADA 2012
A1c ≤6.5% <7%
Fasting Glucose FPG <110 mg/dl Preprandial PG 70-
130mg/dl
Postprandial
Glucose
2-hr postprandial
<140mg/dl
Peak <180mg/dl
34. Blood Pressure and Lipid Goals
Blood pressure <130/80 mmHg†
Lipids
LDL cholesterol <100 mg/dL (<2.6
mmol/L)‡
Diabetes Mellitus: An Overview 3429/03/2014
†Based on patient characteristics and response to therapy, higher or lower
systolic blood pressure targets may be appropriate.
‡In individuals with overt CVD, a lower LDL cholesterol goal of <70 mg/dL
(1.8 mmol/L), using a high dose of statin, is an option.
35. Approach to Patient with DM
History
Physical examination
Laboratory assessment.
Diabetes Mellitus: An Overview 3529/03/2014
36. Management contd
Requires a multidisciplinary team:
Primary care provider
Endocrinologist/Diabetologist
Certified diabetic educator
Nutritionist
Diabetes Mellitus: An Overview 3629/03/2014
37. Management contd
When complication arises, the team will
include;
Neurologist
Nephrologists
Cardiologist
Vascular surgeon
Ophthalmologist
podiatrist
Diabetes Mellitus: An Overview 3729/03/2014
39. Non pharmacologic treatment
Education of patients:
Individualized or
group based
Done by various
health professionals
Repetitive,
interactive
Address causes,
course, treatment
Define target for DM
control
29/03/2014 Diabetes Mellitus: An Overview 39
41. Dietary Management of DM
Individualized, simple instructions
Aim to achieve ideal body weight and encourage
healthy eating habits and lifestyle modification
Calculate activity level and caloric requirements to
achieve above
Diet should be able to reduce hyperglycaemia,
glucotoxicity and lipotoxicity
Diabetes Mellitus: An Overview 4129/03/2014
42. The Ideal or Paleolithic Diet
50 -65% carbohydrate, complex carbohydrates
derived mainly from whole grains and legumes, low
glycaemic index
0.6g/kg body weight proteins (15-20%) derived from
game animals or fish, insects
15 -25% fat derived from vegetable and nut oils.
High fiber 25 – 30g daily
Diabetes Mellitus: An Overview 4229/03/2014
43. EXERCISE IN DIABETES
Dynamic or isotonic
Graduated & individualised
Regular with adequate warm up
Appropriate footcare
Precautions in OHA or insulin dose
Contraindicated in some conditions
29/03/2014 43Diabetes Mellitus: An Overview
44. Exercise Therapy
Benefits
Increase insulin sensitivity
Improved long term glycaemic control – lower HbA1c
Improved circulating lipid profile
Improved BP control
May promote redistribution of body fat ( reduce CVD
risk)
Health benefits – 3 days wkly
29/03/2014 44Diabetes Mellitus: An Overview
45. Individualized regimen
State of control
Stretching & warm-up
Aerobic level sustainable for 30mins
Cool down
Full evaluation before prescribing exercise
Complications/risks
Precautions for patient
29/03/2014 45Diabetes Mellitus: An Overview
48. Indications for Use of Insulin
All type 1DM patients
High risk type 2 DM patients
All pregnant diabetics not controlled with diet
All acutely or chronically ill persons with DM
All patients preparing for or just having surgery
All diabetics who have trauma, leg ulcers,
gangrene, moderately severe nephropathy,
myocardial infarction.
Any person who desires strict control
Diabetes Mellitus: An Overview 4829/03/2014
49. INSULIN DOSAGE
0.6-1.0 units/kg body weight (ideal body weight)
Divide this dose into tds if soluble insulin OR into bd if
70/30 insulin (humulin) used
Additional 0.3 units/kg body weight added if infection,
sepsis or DKA present
Insulin to be given 30 minutes premeals if 30:70 or
soluble insulin and 30-45 min premeal if Isophane or
Lente (Humulin N) insulin
Do not add insulin to N/Saline infusion
Do not give Humulin 30:70 or Isophane (Humulin
N)insulin I.V
Adjust insulin dose with blood sugar
Diabetes Mellitus: An Overview 4929/03/2014
50. Targets for Control
Absence of symptoms, well being
Ideal body weight, BMI 20-23, maximum waist 88cm
in females and 94 in males
Blood pressure 130/80mmHg
FBS 70 -90mg/dL
2hpp 70 – 140mg/dL
HbA1c 6 – 7%
Total cholesterol <5mmol(200mg)
No proteinuria
Diabetes Mellitus: An Overview 5029/03/2014
52. Pharmacology - Biguanides
Class Biguanides
Compound Metformin
Mechanism Activates AMP-kinase
Action(s) • Hepatic glucose production
• Intestinal glucose absorption
• Insulin action
Glucose
Lowering Effect
• Fasting
• Post Prandial
Advantages • No weight gain
• No hypoglycemia
• Reduction in cardiovascular events and mortality (UKPDS
f/u)
Disadvantages • Gastrointestinal side effects (diarrhea, abdominal
cramping)
• Lactic acidosis (rare)
• Vitamin B12 deficiency
• Contraindications: reduced kidney function
Cost Low
Diabetes Mellitus: An Overview29/03/201452
53. Pharmacology - SulfonylureasClass Sulfonylureas (2nd generation)
Compound • Glibenclamide/Glyburide
• Glipizide
• Gliclazide
• Glimepiride (3rd generation)
Mechanism Closes KATP channels on β-cell plasma membranes
Action(s) Insulin secretion
Advantages • Generally well tolerated
• Reduction in cardiovascular events and mortality (UKPDS f/u)
Disadvantages • Relatively glucose-independent stimulation of insulin
secretion: Hypoglycemia, including episodes necessitating
hospital admission and causing death
• Weight gain
• Primary and secondary failure
Cost Low
Diabetes Mellitus: An Overview29/03/201453
54. Pharmacology – Meglitinides
Class Meglitinides
Compound • Repaglinide (Prandin®)
• Nateglinide (Starlix®)
Mechanism Closes KATP channels on β-cell plasma membranes
Action(s) Insulin secretion
Advantages Accentuated effects around meal ingestion
Disadvantages • Hypoglycemia, weight gain
• Dosing frequency
Cost Medium
Diabetes Mellitus: An Overview29/03/201454
55. Pharmacology – Thiazolidinediones
(TZD)
Class Thiazolidinediones (Glitazones)
Compound Pioglitazone (Actos®)
Mechanism Activates the nuclear transcription factor PPAR-
Action(s) Peripheral insulin sensitivity
Advantages • No hypoglycemia
• HDL cholesterol
• Triglycerides
Disadvantages • Weight gain
• Edema
• Heart failure (CI with stage III and IV)
• Bone fractures
Cost High
Diabetes Mellitus: An Overview29/03/201455
56. Pharmacology – Thiazolidinediones
(TZD)
Class Thiazolidinediones (Glitazones)
Compound Rosiglitazone (Avandia®)
Mechanism Activates the nuclear transcription factor PPAR-
Action(s) Peripheral insulin sensitivity
Advantages No hypoglycemia
Disadvantages • LDL cholesterol
• Weight gain
• Edema
• Heart failure (CI with stages III and IV)
• Bone fractures
• Increased cardiovascular events (mixed evidence)
• FDA warnings on cardiovascular safety
Cost High
Diabetes Mellitus: An Overview29/03/201456
57. TZDs and the FDA
Rosiglitazone
Restricted by FDA – can only be used by patients currently
benefiting from therapy or do not get adequate DM
treatment from other agents and not willing to use
pioglitazone
1-800-AVANDIA
Pioglitazone
FDA alert – ongoing analysis of risk of bladder cancer
(with prolonged use >12 months)
Diabetes Mellitus: An Overview29/03/201457
58. Pharmacology – Alpha-Glucosidase
Inhibitors
Class α-Glucosidase inhibitors
Compound • Acarbose
• Miglitol
Mechanism Inhibits intestinal α-glucosidase
Action(s) Intestinal carbohydrate digestion and absorption
slowed
Advantages • Nonsystemic medication
• Postprandial glucose
Disadvantages • Gastrointestinal side effects (gas, flatulence,
diarrhea)
• Dosing frequency
Cost Medium
Diabetes Mellitus: An Overview29/03/201458
59. Pharmacology – Incretin Enhancers
Class DPP-4 inhibitors (incretin enhancers)
Compound • Sitagliptin (Januvia®)
• Vildagliptin (Galvus®)
• Saxagliptin (Onglza®)
• Linagliptin (Tradjenta®)
Mechanism Inhibits DPP-4 activity, prolongs survival of endogenously released
incretin hormones
Action(s) • Active GLP-1 concentration
• Insulin secretion
• Glucagon secretion
Advantages • No hypoglycemia
• Weight “neutrality”
Disadvantages • Occasional reports of urticaria/angioedema
• Cases of pancreatitis observed
• Long-term safety unknown (cancer ?)
Cost High
Diabetes Mellitus: An Overview29/03/201459
60. SGLT-2 Inhibitors
Sodium glucose cotransport 2 inhibitors
These are drugs which inhibit the reabsorption of
glucose in the distal tubules of the kidney
Idea for using these drugs emanated from people with
the rare familial glycosuria patients
Dapagliforzin, Canagliforzin are the first 2 in this group
Cause weight loss and reduce weight by glycosuria
Dapagliforzin failed FDA approval early last year
Canagliflorzin (Invokana) was approved by FDA in
March 2013
Side effects are nasal stuffiness and mild increase in UTI
29/03/2014
Diabetes Mellitus: An
Overview60
62. Pharmacology – Amylin Analog
Class Antihyperglycemic Synthetic Analog
Compound • Pramlintide (Symilin®)
Mechanism • Amylinomimetic
Action(s) • Glucagon secretion (glucose-dependent)
• Slows gastric emptying
• Satiety
Advantages • Potential weight loss
Disadvantages • Meal time injections
• Nausea
• Hypoglycemia in combination with insulin
Cost High
Diabetes Mellitus: An Overview
Lexi-Drugs Online [Internet]. Hudson (OH) : Lexi-Comp, Inc. 1978-2012[cited 2012
August 1].
29/03/201463
63. Pharmacology – Bile Acid
Sequestrants
Class Bile acid sequestrants
Compound Colesevelam (Welchol®)
Mechanism Binds bile acids/cholesterol
Action(s) Bile acids stimulate receptor on liver to produce
glucose
Results • Lowers fasting and post prandial glucose
Advantages • No hypoglycemia
• LDL cholesterol
Disadvantages • Constipation
• Triglycerides
• May interfere with absorption of other medications
Cost High
Diabetes Mellitus: An Overview29/03/201464
67. Definition
An acute metabolic complication of DM
Hyperglycaemia (>300mg/dL)
Acidosis , blood pH <7.3
Increased total blood ketones, > 5 mmol/L
In clinical practice it is suspected when there is
ketonuria++ in the face of hyperglycaemia
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68. Epidemiology of DKA
Few published Nigerian data
Europeans and Americans quote 10 – 30 cases
per 100, 000 population.
Commoner in females
Commoner in non-whites
Mortality higher in the elderly
Diabetes Mellitus: An Overview 6929/03/2014
69. Aetiopathogenesis/Pathophysiology
Insulin deficiency and glucagon excess leads to
excess acetyl-CoA
Acetyl CoA is converted to acetoacetate
Some acetoacetate is converted to other
ketones
These ketones require to be buffered and thus
bicarbonate is used up as pH drops
The respiratory centre is stimulated and
Kussmaul’s breathing occurs
Diabetes Mellitus: An Overview 7029/03/2014
70. Aetiopathogenesis/Pathophysiology
Urine becomes acidic, osmotic diuresis occurs
H and Na and K are lost in the urine together
with ketones
FFAs are increased due to lipolysis from
stimulation of lipoprotein lipase
A major role for initiating all the events is
elevation of counter-regulatory hormones
Diabetes Mellitus: An Overview 7129/03/2014
72. Clinical Features
Risk factors of
infection, trauma,
omission of
medication
Malaise
Weight loss
Polyuria, polydipsia,
Nausea, vomiting,
abdominal distension
Confusion, lethargy
Hypotension,
arhythmias
Severe dehydration
Acetone breath
Glycosuria and
ketonuria
Diabetes Mellitus: An Overview 7329/03/2014
73. Clinical Features contd
Deep coma and or seizures may occur
Acute abdomen may be present and confused
with surgical abdomen
Fluid loss is in range of 6 – 8 litres in adults
Diabetes Mellitus: An Overview 7429/03/2014
75. Investigations
Urinalysis
Ketostix
Electrolytes and urea
Haemogram incl WBC
Blood pH and ketones
ECG,
Urine and blood culture
Blood sugars
Diabetes Mellitus: An Overview 7629/03/2014
76. Treatment
Admit to emergency or ICU, NPO, resuscitate
Intravenous saline 6 – 8 litres in 24 hours in adults
Saline given 1 litre fast, then 1 litre in an hour, then
1 litre in 2hrs, then 1 litre 4 hourly
Soluble insulin 10 units IM or IV stat, then give 6
units hourly till RBS <250mg/dL
Sugars should drop at 50-70mg/dL per hour
If not dropping double the dose of insulin
Diabetes Mellitus: An Overview 7729/03/2014
77. Treatment (contd)
When RBS <250mg/dL change the IV fluids to
5% dextrose to run 1 pint 4 hourly and add KCl
20 – 40mmol per pint with soluble insulin 4-6
units per pint
When patient fully conscious and rehydrated
then change insulin to s/c t.d.s pre-meals at
dose of 0.2 – 0.3 units/kg body weight and allow
patient eat
Diabetes Mellitus: An Overview 7829/03/2014
78. Treatment 4
Antibiotics may be indicated if sepsis present but
it should be remembered that leucocytosis is a
regular feature of DKA
NG tube may be required if there is gastric
dilatation
Dysequillibrium syndrome is a complication of
excessive rapid lowering of blood sugar
Diabetes Mellitus: An Overview 7929/03/2014
79. Prognosis
This is good if treatment commenced early and
adequate monitoring of sugars, electrolytes and
fluid balance is done.
Diabetes Mellitus: An Overview 8029/03/2014
80. HYPEROSMOLAR
HYPERGLYCAEMIC STATE (HHS)
Definition
Epidemiology
Aetiopathogenesis/Pathophysiology
Clinical Features
Investigations
Treatment
Prognosis
Diabetes Mellitus: An Overview 8129/03/2014
81. Definition of HHS
Similar to DKA but:
Blood sugars in range of 600 – 2000mg/dL
No ketonuria or trace ketones
No anion gap or mild anion gap <10
Often have azotaemia, increased Na, K
Normal blood pH
Diabetes Mellitus: An Overview 8229/03/2014
82. Epidemiology
HHS is not as common as DKA
Commoner in elderly patients who are often
institutionalised or with cognitive impairment
Males slightly more commonly affected
Seen in type 2 DM
Rare in type 1 DM
Diabetes Mellitus: An Overview 8329/03/2014
83. Aetiopathogenesis
Patient is fairly insulin sensitive
There is still some circulating insulin sufficient to
suppress ketosis but insufficient to suppress
gluconeogenesis
Renal impairment couple with dehydration from
reduced fluid intake over a period
Often patient on diuretic
Hyperosmolarity ensues with thrombogenicity
Diabetes Mellitus: An Overview 8429/03/2014
84. Clinical features
Polyuria, polydipsia and then oliguria
Confusion or coma
Severe dehydration
No Kussmaul’s respiration
DVT or PE is common
Diabetes Mellitus: An Overview 8529/03/2014
85. Clinical Features
Severe dehydration, fluid deficit 8 – 10 litres
Altered sensorium, seizures, etc
Thromboembolic events eg DVT, PE, CVA, , MI,
etc
Vomiting and gastroparesis
Gastric erosions and haematemesis common
Diabetes Mellitus: An Overview 8629/03/2014
87. Treatment
Very similar to DKA treatment
Admit, NPO
Rehydrate with 6 – 10 litres of fluid preferably
half normal saline
Hourly soluble insulin 4-6 units after a stat
10units IV
Use heparin or enoxaparin to anticoagulate
Watch out for fluid overload if CKD present
Diabetes Mellitus: An Overview 8829/03/2014
88. Prognosis
Poorer than DKA, mortality being 50 – 90% in
most centres
Mortality may follow cerebral oedema, embolic
events or uraemia
Diabetes Mellitus: An Overview 8929/03/2014
89. Hypoglycaemia
Defined as low blood sugar
Blood sugars below 2.2mmol/L taken as
hypoglycaemia in general population
In DM patients the threshold for hypoglycaemia
is lower so coma may occur in blood sugars 50 –
80mg/dL and in those with rapid decline in blood
sugars
Diabetes Mellitus: An Overview 9029/03/2014
90. Definition
Thus Whipple’s triad often used to identify and
confirm hypoglycaemia in DM patient
Triad is made up of
- hypoglycaemic symptoms
- biochemically proven low blood sugar
- relief of symptoms after administration of sugar
or carbohydrate containing drink/meal
Diabetes Mellitus: An Overview 9129/03/2014
91. Aetiopathogenesis of Hypoglycaemia
Excess insulin whether from injections or
secretagogue
Inadequate calorie intake
Inadequate counter-regulatory response
Continued insulin secretion or insulin action
Diabetes Mellitus: An Overview 9229/03/2014
92. Risk factors for Hypoglycaemia
Skipping or postponing meals
Overdose of hypoglycaemic agents
Poor monitoring of blood sugars
Age – extremes of age, the very young and the
elderly
Alcohol and other substances that potentiate
hypoglycaemic drugs
Diabetes Mellitus: An Overview 9329/03/2014
94. Investigations
Blood sugars
Insulin assays
C-peptide
Liver, renal function tests
Diabetes Mellitus: An Overview 9529/03/2014
95. Treatment
Resuscitate with glucose containing soft drink, sugar
or glucose at home if conscious
Admit to hospital if unconscious or if first aid with
sugar at home not working
Resuscitate and give IV 10% glucose or diluted 50%
glucose via wide bore access
Give IM glucagon 1mg if available
Continue to monitor blood sugars, omit insulin or
OHAs patient was taking
Diabetes Mellitus: An Overview 9629/03/2014
96. Treatment contd
When conscious and alert encourage to eat
If delay in regaining consciousness KIV stroke,
MI, uraemia or other co-morbidities
Thus CT scan, ECG, E/U/C may be required
Prevent recurrence by drug dose adjustment
and patient education
Diabetes Mellitus: An Overview 9729/03/2014
97. Conclusion
Early detection and recognition of metabolic
complications is vital for full recovery
Self glucose monitoring will prevent these
conditions
Diabetes Mellitus: An Overview 9829/03/2014
The classification of diabetes includes four clinical classesType 1 diabetes (results from β-cell destruction, usually leading to absolute insulin deficiency)Type 2 diabetes (results from a progressive insulin secretory defect on the background of insulin resistance)Other specific types of diabetes due to other causes; e.g., genetic defects in β-cell function, genetic defects in insulin action, diseases of the exocrine pancreas (such as cystic fibrosis), and drug- or chemical-induced diabetes (such as in the treatment of HIV/AIDS or after organ transplantation)Gestational diabetes mellitus (GDM; diabetes diagnosed during pregnancy that is not clearly overt diabetes)Some patients cannot be clearly classified as having type 1 or type 2 diabetesClinical presentation and disease progression vary considerably in both types of diabetesOccasionally, patients who otherwise have type 2 diabetes may present with ketoacidosisSimilarly, patients with type 1 diabetes may have a late onset and slow (but relentless) progression despite having features of autoimmune diseaseSuch difficulties in diagnosis may occur in children, adolescents, and adultsThe true diagnosis may become more obvious over time
Recommendations for testing for diabetes in asymptomatic patients are summarized on this slide; testing should be considered in adults of any age with BMI ≥25 kg/m2 and one or more of the known risk factors for diabetesFor many illnesses, there is major distinction between screening and diagnostic testing; however, for diabetes, the same tests would be used for “screening” as for diagnosisA1C, fasting plasma glucose (FPG), or 2-hour oral glucose tolerance test (2-h OGTT) are appropriate to test for diabetesThe same assays used for testing for diabetes will also detect individuals with prediabetesIn adults, prediabetes and diabetes meet established criteria for conditions in which early detection is appropriate; both conditions are common, increasing in prevalence, and impose significant health burdensThere is a long presymptomatic phase before the diagnosis of type 2 diabetes is usually made; relatively simple tests are available to detect preclinical diseaseAdditionally, the duration of glycemic burden is a strong predictor of adverse outcomes, and effective interventions exist to prevent progression of prediabetes to diabetes (see Section IV. Prevention/Delay of Type 2 Diabetes) and to reduce risk of complications of diabetes (see Section VI. Prevention and Management of Diabetes Complications)
In 1997 and 2003, The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus1,2 recognized an intermediate group of individuals whose glucose levels, although not meeting criteria for diabetes, are nevertheless too high to be considered normalThis group was defined as having impaired fasting glucose (IFG) or impaired glucose tolerance (IGT)IFG: fasting plasma glucose (FPG) of 100–125 mg/dL (5.6–5.9 mmol/L)*IGT: 2-hour plasma glucose (2-h PG) on the 75-g oral glucose tolerance test (OGTT) of 140–199 mg/dL (7.8–11.0 mmol/L)Individuals with IFG and/or IGT have been referred to as having prediabetes, indicating a relatively high risk for future development of diabetesIFG and IGT should not be viewed as clinical entities in their own right but rather risk factors for diabetes as well as cardiovascular disease (CVD)IFG and IGT are associated with obesity (especially abdominal or visceral obesity), dyslipidemia with high triglycerides and/or low HDL cholesterol, and hypertensionIndividuals with an A1C of 5.7–6.4% should be informed of their increased risk for diabetes as well as CVD and counseled about effective strategies to lower their risks (see Section IV. Prevention/Delay of Type 2 Diabetes)*The World Health Organization (WHO) and a number of other diabetes organizations define the cutoff for IFG at 110 mg/dL (6.1 mmol/L)A1CIn 2009, an International Expert Committee that included representatives of the American Diabetes Association (ADA), the International Diabetes Federation (IDF), and the European Association for the Study of Diabetes (EASD) recommended the use of the A1C test to diagnose diabetes, with a threshold of ≥6.5%1, and ADA adopted this criterion in 20102The diagnostic test should be performed using a method certified by the National Glycohemoglobin Standardization Program (NGSP) and standardized or traceable to the Diabetes Control and Complications Trial (DCCT) reference assay3Point-of-care A1C assays, for which proficiency testing is not mandated, are not sufficiently accurate at this time to use for diagnostic purposes3The A1C has several advantages to the FPG and OGTT, including greater convenience (since fasting is not required), evidence to suggest greater preanalytical stability, and less day-to-day perturbations during periods of stress and illnessThese advantages must be balanced by greater cost, the limited availability of A1C testing in certain regions of the developing world, and the incomplete correlation between A1C and average glucose in certain individualsIn addition, HbA1C levels may vary with patients’ race/ethnicity4,5
Recommended glycemic goals for nonpregnant adults These recommendations are based on those for A1C values, with listed blood glucose levels that appear to correlate with achievement of an A1C of <7%The issue of preprandial versus postprandial self-monitoring of blood glucose (SMBG) is complex;2 in some epidemiological studies, elevated postchallenge two-hour oral glucose tolerance test (2-h OGTT) glucose values have been associated with increased cardiovascular risk independent of fasting plasma glucose (FPG)In diabetic subjects, some surrogate measures of vascular pathology, such as endothelial dysfunction, are negatively affected by postprandial hyperglycemia3Individualize based on duration of diabetes, age/life expectancy, comorbid conditions, known CVD or advanced macrovascular complications, hypoglycemia unawareness, individual patient concernsNOTE: A1c ≥6.5% are associated with an increased risk of blood vessel damage
2nd generation is more potent than 1st generation1st generation (tolbutamide, chlorpropamide, tolazamide)Glimepiride is most potent,
Insulin secretion is glucose dependentUse with sulfonylureas is duplicate therapy
Due to risks of MI restrict use of rosiglitazone to those currently using or those whose blood sugar is not controlled with any other meds and prefer not to use actosAvandia is available only through a restricted distribution program – prescriber would call 1800avandia
DPP4 enzyme is known to suppress some cancer growth