A 30-year-old man was brought to the emergency room unconscious. He was diagnosed with diabetes based on diagnostic criteria of an A1C of 6.5% or higher, fasting plasma glucose of 126 mg/dL or higher, or 2-hour plasma glucose of 200 mg/dL or higher during an oral glucose tolerance test. The document discusses the classification, management, and treatment goals of diabetes, including lifestyle modifications, medication (oral hypoglycemics, insulin, GLP-1 agonists), and screening and treatment of complications such as hypertension, dyslipidemia, and kidney disease.
Controlling blood sugar (glucose) levels is the major goal of diabetes treatment, in order to prevent complications of the disease.
Type 1 diabetes is managed with insulin as well as dietary changes and exercise.
Type 2 diabetes may be managed with non-insulin medications, insulin, weight reduction, or dietary changes.
Medications for type 2 diabetes are designed to
increase insulin output by the pancreas,
decrease the amount of glucose released from the liver,
increase the sensitivity (response) of cells to insulin,
decrease the absorption of carbohydrates from the intestine, and
slow emptying of the stomach, thereby delaying nutrient digestion and absorption in the small intestine.
Controlling blood sugar (glucose) levels is the major goal of diabetes treatment, in order to prevent complications of the disease.
Type 1 diabetes is managed with insulin as well as dietary changes and exercise.
Type 2 diabetes may be managed with non-insulin medications, insulin, weight reduction, or dietary changes.
Medications for type 2 diabetes are designed to
increase insulin output by the pancreas,
decrease the amount of glucose released from the liver,
increase the sensitivity (response) of cells to insulin,
decrease the absorption of carbohydrates from the intestine, and
slow emptying of the stomach, thereby delaying nutrient digestion and absorption in the small intestine.
Diabetic drugs is a very important topic for pg entrance.....so all about it has been discussed in detail as required for pg entrance....do make use of it...
COMPLICATIONS, MANAGEMENT AND TREATMENT APPROACH OF DIABETES MELLITUSAnas Indabawa
Diabetes describes a group of metabolic diseases in which the person has high blood glucose (blood sugar), either because insulin production is inadequate, or because the body's cells do not respond properly to insulin, or both. Mellitus is Latin for “sweet as honey”.
Pancreas is an elongated, tapered gland that is located behind the stomach and secretes digestive enzymes and the hormones insulin and glucagon.
The Pancreas secretes insulin and Glucagon directly into the blood stream.
It also secretes digestive enzymes into the pancreatic duct, which joins the common bile duct from the liver and drains into the small intestine.
Insulin and Glucagon have opposite effects on liver and other tissues for controlling blood-glucose levels.
GLP-1 receptor agonists (GLP-1RAs): cardiovascular actions and therapeutic po...OlgaGoryacheva4
My students Babisweta Swain, Abhishek Raj and Piyush Barwal had presented this topic in our 22nd Student Scientific Society Conference in the department of Propaedeutic of Internal Diseases No.2
What is diabetes mellitus, Epidemiology of diabetes, Diabetes diagnosis, Features of diabetes, WHO classification of Diabetes Mellitus, Complications of diabetes, Metabolic alterations of diabetes, Oral glucose tolerance test, WHO criteria of OGTT interpretation, Classification of diabetes mellitus, Gestational diabetes, Pre-diabetes, Insulin, Biosynthesis of insulin, Insulin actions, Hypoglycemia, Impaired fasting glucose, Insulin structure
Diabetic drugs is a very important topic for pg entrance.....so all about it has been discussed in detail as required for pg entrance....do make use of it...
COMPLICATIONS, MANAGEMENT AND TREATMENT APPROACH OF DIABETES MELLITUSAnas Indabawa
Diabetes describes a group of metabolic diseases in which the person has high blood glucose (blood sugar), either because insulin production is inadequate, or because the body's cells do not respond properly to insulin, or both. Mellitus is Latin for “sweet as honey”.
Pancreas is an elongated, tapered gland that is located behind the stomach and secretes digestive enzymes and the hormones insulin and glucagon.
The Pancreas secretes insulin and Glucagon directly into the blood stream.
It also secretes digestive enzymes into the pancreatic duct, which joins the common bile duct from the liver and drains into the small intestine.
Insulin and Glucagon have opposite effects on liver and other tissues for controlling blood-glucose levels.
GLP-1 receptor agonists (GLP-1RAs): cardiovascular actions and therapeutic po...OlgaGoryacheva4
My students Babisweta Swain, Abhishek Raj and Piyush Barwal had presented this topic in our 22nd Student Scientific Society Conference in the department of Propaedeutic of Internal Diseases No.2
What is diabetes mellitus, Epidemiology of diabetes, Diabetes diagnosis, Features of diabetes, WHO classification of Diabetes Mellitus, Complications of diabetes, Metabolic alterations of diabetes, Oral glucose tolerance test, WHO criteria of OGTT interpretation, Classification of diabetes mellitus, Gestational diabetes, Pre-diabetes, Insulin, Biosynthesis of insulin, Insulin actions, Hypoglycemia, Impaired fasting glucose, Insulin structure
Pediatric Type 2 Diabetes Mellitus. BY DR SAYED ISMAILSayed Ahmed
diabetes mellitus type 2 in children
pathophysiology of type 2 DM
manifestations of DM
Complications , investigation and management of type2 DM in children
Definition : Diabetes mellitus is a group of metabolic disorders characterized by hyperglycemia resulting from impaired insulin secretion, insulin action [ insulin resistance ] or both .
The chronic hyperglycemia in DM is associated with long term damage dysfunction and failure of various organs
Is based on etiology not on type of treatment or age of the patient.
Type I(Beta cell destruction-absolute insulin deficiency)
Immune mediated Idiopathic
Type II
predominant insulin resistant with relative insulin deficiency
predominant secretory defect with insulin resistance
Non-pharmacological Management of Diabetes Mellitus.pptxSamson Ojedokun
Diabetes mellitus DM, is a metabolic disorder of biomolecules characterized by chronic hyperglycemia due to defects in insulin synthesis or utilization or both
DM requires lifelong therapy. A multidisciplinary approach is needed to control glycemia, as well as to limit the development of its devastating complications and manage such complications when they do occur.
Increases cost of living and reduces life expectancy
This is a slide presentation for MBBS students. a brief overview of hemochromatosis, an iron overload condition. overview of hemochromatosis, pathophysiology, clinical features, approach, and management
Liver transplantation; notes of DM/DNB/SpecialistsPratap Tiwari
Liver transplantation; extensive notes of DM/DNB/Specialists. This was my notes for my exam compiled from several sources, credit goes to original authors. This is just for quick revision
This is a lecture note for 5th-semester MBBS students. Lecture notes on hepatology, liver disease, and liver abscess. Introduction to a liver abscess, pyogenic liver abscess, causes, approach and management of liver abscess.
This is a lecture note for 5th semester MBBS students. Lecture notes on hepatology, liver disease, alcoholic liver disease, alcohol-related liver disease, portal hypertension, hepatic encephalopathy, and acute liver failure. Introduction to acute liver failure, causes, approach, and management of acute liver failure .
This is a lecture note for 5th semester MBBS students. Lecture notes on hepatology, liver disease, alcoholic liver disease, alcohol-related liver disease, portal hypertension, and hepatic encephalopathy. Introduction to hepatic encephalopathy, causes, differentials, approach, and management of hepatic encephalopathy .
This is a lecture note for 5th semester MBBS students. Lecture notes on hepatology, liver disease, alcoholic liver disease, alcohol-related liver disease, alcoholic hepatitis, portal hypertension, ascites. Introduction to ascites and management of ascites.
This is a lecture note for 5th semester MBBS students. Lecture notes on hepatology, liver disease, alcoholic liver disease, alcohol-related liver disease, portal hypertension, ascites. Introduction to ascites and management of ascites.
brief lecture notes for 5th sem MBBS, on portal hypertension and varices. Introduction to portal hypertension and esophageal and gastric varices and management of variceal bleeding.
Chronic liver disease, lecture presentation for 5th sem MBBS students. Introduction to chronic liver disease, notes on liver fibrosis, alcoholic hepatitis, liver histology and overview.
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
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
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.
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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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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.
2. CASE SUMMARY
• A 30 yrs old M was brought in ERD in the state of unconsciousness.
(Note: Coma is a symptom, not a diagnosis.)
Pic taken from http://censorbugbear-reports.blogspot.com/2010/03/shocking-neglect-of-comatose-patient-at.html
3. RECAP OF PREVIOUS PARTS
• Causes of patient in state of coma
• Definition of terms related to consciousness
• Causes of Coma in a Diabetic Patient
• Insulin Synthesis/ Secretion
• Regulation of Glucose hemostasis
• Response of hypoglycemia in normal & DM
• Hypoglycemia & symptoms
• DKA /HHS
• Abnormal respiration patterns
4. DIABETES MELLITUS
• Diabetes mellitus is a clinical syndrome characterised by
hyperglycaemia caused by absolute or relative deficiency of
insulin.
5. DIAGNOSTIC CRITERIA
• A1C ≥6.5%
• OR
• Fasting plasma glucose (FPG) ≥126 mg/dL (7.0 mmol/L)
OR
• 2-hour plasma glucose ≥200 mg/dL (11.1 mmol/L) during an OGTT
OR
• A random plasma glucose ≥200 mg/dL (11.1 mmol/L), in patients with
classic symptoms of hyperglycemia or hyperglycemic crisis
6. PRE DIABETES
1. IFG: fasting plasma glucose (FPG) levels of 100–
125 mg/dL (5.6–6.9 mmol/L)*
2. IGT: 2-hour plasma glucose (2-h PG) in the 75-g oral
glucose tolerance test (OGTT) of 140–199 mg/dL
(7.8–11.0 mmol/L)
3. A1c: 5.7-6.4%
Note: In 1997 and 2003, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus recognized a
group of individuals whose glucose levels did not meet the criteria for DM, but were too high to be considered N.
These persons were defined as having IFG or IGT.
7. PREDIABETES
• Individuals with IFG and/or IGT have been referred to as
having pre-diabetes, indicating a relatively high risk for
future development of diabetes
• IFG and IGT are associated with obesity (especially
abdominal or visceral obesity), dyslipidemia with high
triglycerides and/or low HDL cholesterol, and
hypertension
• Note: WHO and a number of other diabetes organizations
define the cutoff for IFG at 110 mg/dL (6.1 mmol/L)
8.
9. SCREENING FOR AND DIAGNOSIS OF GDM
• Perform a 75-g OGTT, with plasma glucose measurement fasting and at 1
and 2 h, at 24–28 weeks of gestation in women not previously diagnosed
with overt diabetes.
• The OGTT should be performed in the morning after an overnight fast of at
least 8 h.
• The diagnosis of GDM is made when any of the following plasma glucose
values are exceeded:
1. Fasting: ≥92 mg/dL (5.1 mmol/L)
2. 1 h: ≥ 180 mg/dL (10.0 mmol/L)
3. 2 h: ≥ 153 mg/dL (8.5 mmol/L)
10. CLASSIFICATION OF DIABETES
1. Type 1 diabetes (due to β-cell destruction, usually leading to absolute
insulin deficiency)
2. Type 2 diabetes (due to a progressive insulin secretory defect on the
background of insulin resistance)
3. 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)
4. Gestational diabetes mellitus (GDM)(diabetes diagnosed during
pregnancy that is not clearly overt diabetes)
11. MANAGEMENT
• Dietary and lifestyle modification including exercise and
weight reduction if obese
• Manage hyperglycemia : OHA / Insulin therapy
• Management of complications of diabetes, including
treatment of HTN(<140/80) and dyslipidaemia.
• Patient Education / Vaccination (influenza,
pneumococcal , hepatitis b)
12. GOAL
• Attain individualized glycemic, blood pressure, and lipid goals.
General recommended goals from the ADA for these markers are
as follows:
• A1C < 7%.
• Blood pressure < 140/80 mmHg.
• LDL cholesterol < 100 mg/dL; triglycerides < 150 mg/dL;
• HDL cholesterol < 40 mg/dL for men; HDL cholesterol < 50
mg/dL for women.
• Achieve and maintain body weight goals.
13. ASPIRIN
• Consider aspirin therapy (75–162 mg/ day) as a primary
prevention strategy in those with type 1 or type 2 diabetes at
increased cardiovascular risk .
• This includes most men aged >50 years or women aged >60
years who have at least one additional major risk factor (family
history of CVD, hypertension, smoking, dyslipidemia, or
albuminuria).
14. STATIN
• Statin therapy should be added to lifestyle therapy,
regardless of baseline lipid levels, for diabetic patients:
1. with overt CVD
2. without CVD who are over the age of 40 years and
have one or more other CVD risk factors (family history
of CVD,hypertension, smoking, dyslipidemia,or
albuminuria).
15. ACE INHIBITOR
• An ACE inhibitor or ARB for the primary prevention of diabetic
kidney disease is not recommended in diabetic patients with
normal blood pressure and albumin excretion <30 mg/24 h. B
• Either ACE inhibitors or ARBs (but not both in combination) are
recommended for the treatment of the nonpregnant patient with
modestly elevated (30–299 mg/24 h) C or higher levels (.300
mg/24 h) of urinary albumin excretion. A
19. END OF SLIDES
References:
1. Harrison's Principles of Internal Medicine, 18th Edition
2. Davidson Practice of Medicine
3. Uptodate 20.3
4. Standards of Medical Care in Diabetesd 2014. American Diabetes Association. Diabetes
Care Volume 37, Supplement 1, January 2014
5. Medscape.com
6. Mercksmanual
Editor's Notes
Extra notes:
The precise mechanisms underlying gestational diabetes remain unknown.
The hallmark of GDM is increased insulin resistance. Pregnancy hormones and other factors are thought to interfere with the action of insulin as it binds to the insulin receptor.
Since insulin promotes the entry of glucose into most cells, insulin resistance prevents glucose from entering the cells properly. As a result, glucose remains in the bloodstream, where glucose levels rise .
Because glucose travels across the placenta (through diffusion facilitated by GLUT1 carrier), If the untreated gestational diabetes fetus is exposed to consistently higher glucose levels, this leads to an increased fetal levels of insulin (insulin itself cannot cross the placenta). The growth-stimulating effects of insulin can lead to excessive growth and a large body (macrosomia). After birth, the high glucose environment disappears, leaving these newborns with ongoing high insulin production and susceptibility to low blood glucose levels (hypoglycemia).
Women who have had gestational diabetes in a previous pregnancy should be offered early self-monitoring of blood glucose or an OGTT at 16–18 weeks, and a further OGTT at 28 weeks if the results are normal.