This document provides an overview of diabetes mellitus (DM) presented by Dr. Mukesh Kumar Samota. It begins with definitions and classifications of DM, then discusses epidemiology, genetics, pathophysiology, risk factors, approaches to patients, management, and complications. Type 2 DM is the main focus. It is characterized by insulin resistance and impaired insulin secretion. Worldwide prevalence is rising due to obesity, sedentary lifestyles, and aging populations. Management involves lifestyle changes, medications, monitoring, and preventing complications through screening and treatment.
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.
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).
Diabetes and various types have been discussed in detail as regard for Pg entrance and with various images, tables .....
Topics discussed: 1) introduction
2) types of diabetes
3) comp0lication of diabetes
4) DKA
5) NKHOC
6) Diabetic nephropathy
7) skin diseases in diabetes
Chronic kidney disease (CKD) means your kidneys are damaged and can't filter blood the way they should. The disease is called “chronic” because the damage to your kidneys happens slowly over a long period of time.
Diabetes mellitus -INTRODUCTION,TYPES OF DIABETES MELLITUSvarinder kumar
INTRODUCTION
TYPES OF DIABETES MELLITUS
DIAGNOSE TEST FOR DIABETES MELLITUS
MECHANISM OF ACTION OF INSULIN (IDDM)
HERBAL DRUG TREATMENT FOR DIABETES
LIFESTYLE FOR TYPE 1 AND TYPE 2 DM
NEW ANTI DIABETIC DRUGS
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.
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).
Diabetes and various types have been discussed in detail as regard for Pg entrance and with various images, tables .....
Topics discussed: 1) introduction
2) types of diabetes
3) comp0lication of diabetes
4) DKA
5) NKHOC
6) Diabetic nephropathy
7) skin diseases in diabetes
Chronic kidney disease (CKD) means your kidneys are damaged and can't filter blood the way they should. The disease is called “chronic” because the damage to your kidneys happens slowly over a long period of time.
Diabetes mellitus -INTRODUCTION,TYPES OF DIABETES MELLITUSvarinder kumar
INTRODUCTION
TYPES OF DIABETES MELLITUS
DIAGNOSE TEST FOR DIABETES MELLITUS
MECHANISM OF ACTION OF INSULIN (IDDM)
HERBAL DRUG TREATMENT FOR DIABETES
LIFESTYLE FOR TYPE 1 AND TYPE 2 DM
NEW ANTI DIABETIC DRUGS
Diabetes Mellitus is a group of disorders characterized by high levels of blood glucose in the body which is a result from the defects caused by insulin production, insulin action and sometimes both.
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
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
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
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
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
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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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.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
- 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
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NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
2. SCHEME OF PRESENTATRION :
1.INTRODUCTION AND DEFINITION OF DM
2.EPIDEMIOLOGY
3.GENETIC CONSIDERATION
4.PATHOPHYSIOLOGY
5. RISK FACTORS
6.APPROACH TO PATIENT
7.MANAGMENT
8NON PHARMACOLOGICAL
9 PHARMACOLOGICAL
10PREVENTION AND SCREENING
11.COMPLICATIONS
12.MANAGMENT OF COMPLICATIONS
3. INTRODUCTION:
Diabetes mellitus (DM) refers to a group of common
metabolic disorders that share the phenotype of
hyperglycemia.
Caused by a complex interaction of genetics and
environmental factors.
Depending on the etiology of the DM, factors
contributing to hyperglycemia include reduced insulin
secretion, decreased glucose utilization, and increased
glucose production
4. TYPE 2 DM
Type 2 DM is a heterogeneous group of disorders
characterized by variable degrees of insulin resistance,
impaired insulin secretion, and increased glucose
production.
Distinct genetic and metabolic defects in insulin action
and/or secretion give rise to the common phenotype of
hyperglycemia in type 2 DM
5. EPIDEMIOLOGY
The worldwide prevalence of DM has risen dramatically over the
past two decades
Prevalence of type 2 DM is rising much more rapidly, presumably
because of increasing obesity, reduced activity levels as countries
become more industrialized, and the aging of the population
In 2013, the prevalence of diabetes in individuals from age 20–79
ranged from 23 to 37%
The countries with the greatest number of individuals with
diabetes in 2013 are China (98.4 million), India (65.1 million),
United States (24.4 million), Brazil (11.9 million)
6. The prevalence is similar in men and women
throughout most age ranges
Diabetes is a major cause of mortality
Diabetes was listed as the seventh leading cause
of death in 2010
A recent estimate suggested that diabetes was
responsible for almost 5.1 million deaths or 8% of
deaths worldwide in 2013
7. GENETIC CONSIDERATIONS :
Type 2 DM has a strong genetic component.
The concordance of type 2 DM in identical twins is between 70
and 90%.
Individuals with a parent with type 2 DM have an increased risk
of diabetes; if both parents have type 2 DM, the risk
approaches 40%
The disease is polygenic and multifactorial, because in addition
to genetic susceptibility, environmental factors (such as obesity,
nutrition, and physical activity) modulate the phenotype
9. PATHOPHYSIOLOGY
Type 2 DM is characterized by impaired insulin secretion due to B
cell dysfunction, insulin resistance at peripheral receptors that
leads to excessive hepatic glucose production, and abnormal fat
metabolism.
In the early stages of the disorder, glucose tolerance remains near-
normal, despite insulin resistance, because the pancreatic beta
cells compensate by increasing insulin output
As insulin resistance and compensatory hyperinsulinemia
progress, the pancreatic islets in certain individuals are unable to
sustain the hyperinsulinemic state.
10. Then develops IGT, characterized by elevations in
postprandial glucose,
A further decline in insulin secretion and an increase in
hepatic glucose production lead to overt diabetes with
fasting hyperglycemia.
Ultimately, beta cell failure ensues.
Although both insulin resistance and impaired insulin
secretion contribute to the pathogenesis of type 2 DM,
the relative contribution of each varies from individual
to individual.
11. 1. METABOLIC ABNORMALITIES
A. ABNORMAL MUSCLE AND FAT METABOLISM
Insulin resistance --->> impairs glucose utilization by insulin-sensitive tissues
and increases hepatic glucose output; both effects contribute to the
hyperglycemia.
Insulin receptor levels and tyrosine kinase activity in skeletal muscle are
reduced
“Postreceptor” defects in insulin-regulated
phosphorylation/dephosphorylation
Accumulation of lipid within skeletal myocytes, which may impair
mitochondrial oxidative phosphorylation and reduce insulin-stimulated
mitochondrial ATP production.
Obesity The increased adipocyte mass leads to increased levels of
circulating free fatty acids and other fat cell products (nonesterified free
fatty acids, retinolbinding protein 4, leptin, TNF-α, resistin, IL-6, and
adiponectin
12. B.IMPAIRED INSULIN SECRETION
A second genetic defect— superimposed upon insulin
resistance—leads to beta cell failure.
Beta cell mass is decreased by approximately 50% in
individuals with longstanding type 2 DM.
Islet amyloid polypeptide or amylin, co-secreted by the
beta cell, forms the amyloid fibrillar deposit found in
the islets of individuals with long-standing type 2 DM.
“Glucose toxicity” and “lipotoxicity”) and dietary fat
may also worsen islet function
13. C.INCREASED HEPATIC GLUCOSE AND LIPID PRODUCTION
Insulin resistance in the liver reflects the failure of
hyperinsulinemia to suppress gluconeogenesis, which results in
fasting hyperglycemia and decreased glycogen storage by the
liver in the postprandial state.
Adipose tissue->> lipolysis and free fatty acid flux from
adipocytes are increased, leading to increased lipid (very-low-
density lipoprotein [VLDL] and triglyceride) synthesis in
hepatocytes
leads to dyslipidemia] (elevated triglycerides, reduced high-
density lipoprotein [HDL], and increased small dense low-
density lipoprotein [LDL] particles
14. APPROACH TO THE PATIENT
HISTORY:-
Attention should be directed to symptoms related to
diabetes (acute and chronic) and classifying the type
of diabetes by proper history and GPE.
DM and its complications produce a wide range of
symptoms and signs; those secondary to acute
hyperglycemia may occur at any stage of the disease,
whereas those related to chronic hyperglycemia begin
to appear during the second decade of hyperglycemia
15. SIGN AND SYMPTOMS
Polydipsia.
Polyuria.
Weight gain/lose
Fatigue.
Weakness.
Blurry vision.
Frequent superficial infections (vaginitis, fungal skin
infections).
Slow healing of skin lesions after minor trauma.
Metabolic derangements relate mostly to hyperglycemia
(osmotic diuresis) and to the catabolic state of the patient
(urinary loss of glucose and calories, muscle breakdown
due to protein degradation and decreased protein
synthesis).
16. PAST HISTRORY: -
In a patient with established DM, the initial assessment should also
include special emphasis on
Prior diabetes care.
Type of therapy-OHA/insulin
Prior HbA1c levels.
Self-monitoring blood glucose results.
Frequency of hypoglycemia.
Presence of DM-specific complications.
Assessment of the patient’s knowledge about diabetes, exercise, and
nutrition.
Presence of DM-related comorbidities and complications should be
sought
1) Cardiovascular disease,
2) Hypertension,
3) Dyslipidaemia,
4) CKD,
5) Ophthalmopathy ,
6) CVA).
17. FAMILY HISTORY:
History of DM in 1st degree and sibling of patients
should obtained in detailed as
History of HTN,DYSLPIDEAMIA,OBESITY,CAD , PTB
PERSONAL HISTORY:
Diet/nourishment/change in weight
Smoking/tobacco
Alcohal use
Menstrual /obstetrics history in female
18. OCCUPATIONAL HISTORY:
PHYSICAL EXAMINATION
Complete physical examination
Built and nourishment
Weight/height/BMI/WC/HC/WHR
Facial examination- symmetry/pallor /cyanosis/icterus/ teeth/gum/
Peripheral pulses and blood pressure in all for limbs
LAP
Examination neck for swelling/LAP/scar marks/dilated veins/JVP/ neck circumference
Chest and abdomen for shape/symmetry/scar marks/dilated vein/hernia/visible
pulsation/insulin injection site/organomegaly
Examination of hand for clubbing/cyanosis/nail changes.
Groin and genital
Legs for assessment of blood flow/oedema/scar marks/ulcer/dilated veins/ look for the
presence of foot deformities such as hammer or claw toes / Charcot foot; and identify
sites of potential ulceration/nail care
19. SYSTEMIC EXAMINATIONS:
Skin and mucus membrane for skin changes/uleration
Eye: fundus/retinal/corneal/examination
Cvs examinations
Respiratory system
CNS:
sensation (vibratory sensation [128-MHz tuning fork at the
base of the great toe].
The ability to sense touch with a monofilament [5.07, 10-g
monofilament].
Pinprick sensation.
Testing for ankle reflexes.
Vibration perception threshold using a biothesiometer),
Ankle reflexes.
21. B. OTHER RELEVANT INVESTIGATIONS:
HbA1c
Cbc
Lipid profile
Urine albumin and sugar
Thyroid function test
Serum insulin ,glucagon
C-peptide level
Ecg,2 D echocardiography.
Serum electrolytes.
LFT/RFT
Chest xray.
C-reactive protein
Islet cell autoantibodies ICAs(GAD, insulin, IA-2/ICA-512, and ZnT-8
serve as a marker of the autoimmune process of type 1 DM)
UPT in case of female.
22. MANAGEMENT AND THERAPIES
OVERALL GOALS
The goals of therapy for type 1 or type 2 diabetes
mellitus (DM) are to
(1) eliminate symptoms related to hyperglycaemia.
(2) reduce or eliminate the long-term micro vascular
and macro vascular complications of DM .
(3) allow the patient to achieve as normal a lifestyle as
possible.
23. COMPREHENSIVE MEDICAL CARE FOR PATIENTS WITH DIABETES
Optimal and individualized glycaemic control
Self-monitoring of blood glucose (individualized frequency)
HbA1c testing (2–4 times/year)
Patient education in diabetes management (annual);
diabetes-self management education and support
Medical nutrition therapy and education (annual)
Eye examination (annual or biannual)
Foot examination (1–2 times/year by physician; daily by
patient)
Screening for diabetic nephropathy (annual)
Blood pressure measurement (quarterly)
Lipid profile and serum creatinine (estimate GFR)
(annual)
The ADA recommends annual screening for distal symmetric
neuropathy beginning with the initial diagnosis of diabetes and annual
screening for autonomic neuropathy at the time of diagnosis of type 2
DM.
Influenza/pneumococcal/hepatitis B immunizations
Consider antiplatelet therapy
24. PREVENTION
Type 2 DM is preceded by a period of IGT or IFG, and a
number of lifestyle modifications and pharmacologic agents
prevent or delay the onset of DM
patients who had increased risk of diabetes should be reduce
body weight and increase physical activity as well as being
screened for cardiovascular disease
The ADA has suggested that metformin be considered in
individuals with both IFG and IGT who are at very high risk
for progression to diabetes (age <60 years, BMI ≥35 kg/m2,
family history of diabetes in first-degree relative, and women
with a history of GDM).
Individuals with IFG, IGT, or an HbA1c of 5.7–6.4% should be
monitored annually to determine if diagnostic criteria for
diabetes are present.
26. PATIENT EDUCATION ABOUT DM, NUTRITION, AND
EXERCISE:
The patient with type 1 or type 2 DM should receive
education about
Nutrition.
Exercise.
care of diabetes during illness.
medications to lower the plasma glucose.
27. NUTRITIONAL RECOMMENDATIONS FOR ADULTS WITH DIABETES OR
PREDIABETESA
A. Weight loss diet (in prediabetes and type 2 DM) /minimize weight gain (or T1DM)
Hypo caloric diet that is low-carbohydrate and modest weight lose(5-7%)
B. Fat in diet (optimal % of diet is not known; should be individualized)
Minimal trans fat consumption
Mediterranean-style diet rich in monounsaturated fatty acids may be
better
C. Carbohydrate in diet (optimal % of diet is not known; should be individualized)
Monitor carbohydrate intake in regard to calories
Sucrose-containing foods may be consumed with adjustments in insulin
dose, but minimize intake
Amount of carbohydrate determined by estimating grams of carbohydrate
in diet (type 1 DM)
Use glycaemic index to predict how consumption of a particular food
may affect blood glucose
Fructose preferred over sucrose or starch
D. Protein in diet (optimal % of diet is not known; should be individualized)
E. Other components
•Dietary fiber, vegetable, fruits, whole grains, dairy products, and
sodium intake as advised for general population
•Nonnutrient sweeteners
•Routine supplements of vitamins, antioxidants, or trace elements not
advised
28. EXERCISE:
Exercise has multiple positive benefits including
i. cardiovascular risk reduction,
ii. reduced blood pressure,
iii. maintenance of muscle mass,
iv. reduction in body fat, and weight loss.
For individuals with type 1 or type 2 DM, exercise is also useful
for lowering plasma glucose (during and following exercise) and
increasing insulin sensitivity.
In patients with diabetes, the ADA recommends 150 min/week
(distributed over at least 3 days) of moderate aerobic physical
activity with no gaps longer than 2 days..
Untreated proliferative retinopathy is a relative contraindication
to vigorous exercise, because this may lead to vitreous
haemorrhage or retinal detachment.
33. INSULIN SECRETAGOGUES:
agents that affect the atp-sensitive k+ channel
SULFONYLUREAS:
First-generation :chlorpropamide, tolazamide, tolbutamide
Second-generation:
Glibenclamide (Glyburide) 2.5 -15mg (1-2)
Glipizide 5-20 mg (1-2)
Gliclazide 40-240mg [1-2]
Glimepirid1-6mg[1-2]
More rapid onset of action
Better coverage of the postprandial glucose rise,
Shorter half-life of some agents may require more than once-
a-day dosing.
Reduce both fasting and postprandial glucose and should be
initiated at low doses
34. Sulfonylureas increase insulin acutely and thus
should be taken shortly before a meal; with
chronic therapy, though, the insulin release is
more sustained
S/E hypoglycemia
Weight gain
Contraindications :Renal/liver disease
36. GLUCAGON LIKE PEPTIDE-1 (GLP-1) : INCRETIN
secreted by L cells located in the distal GI tract (ileum and colon) in
response to ingested glucose.
Releases insulin by binding to its specific receptor (GLP-1R)
Slow gastric emptying
Supress appetite
Decrese glucagon
Weight loss
MOA: It is positively coupled to increase in intracellular cAMP and
Ca2+levels in β cells.
Exenatide: analouge of glp1
Liraglutide : synthetic
Daluglutide
Parentral use [sc]
S/E: increase risk of hypoglycemia
C/I: renal disease
Agents that also slow GI motility;
Medullary carcinoma of thyroid
37. DIPEPTIDYL PEPTIDASE IV INHIBITORS[DPP 𝟒]
Inhibit degradation of native incretins
Prolong endogenous GLP-1 action and insulin secration
Prefrential effect on PP glucose
Weight gain.
Eg Sitagliptin 100 mg daily PO
Vildagliptin 50 mg[1-2]
Alogliptin, Anagliptin, Gemigliptin, linagliptin,
saxagliptin, sitagliptin, teneligliptin, vildagliptin
Well tolerated, do not cause hypoglycemia
C/I: Reduced dose with renal disease;
Associated with increase heart failure risk;
Possible association with ACE inhibitor– induced
angioedema
38. INSULIN SENSITIZERS
BIGUANIDES : Metformin
Mechanism of Action : Metformin activates AMP-
dependent protein kinase
It reduces hepatic glucose production
Improves peripheral glucose utilization
It reduces fasting plasma glucose (FPG) and insulin levels.
Improves the lipid profile, and promotes modest weight
loss.
side effects :diarrhea, anorexia, nausea, metallic taste
The major toxicity :lactic acidosis,. Vitamin B12 levels
decrease
Contraindications: renal insufficiency (glomerular filtration
rate [GFR] <60 mL/min), any form of acidosis, unstable
congestive heart failure (CHF), liver disease, or severe
hypoxemia.
39. THIAZOLIDINEDIONES:
MOA: ↓ Insulin resistance to the PPAR Y[peroxisome
proliferative activated receptor –y],
↑ glucose utilization
Rosiglitazone: asso with s/e MI CHF, STROKE
pioglitazone; may have risk of blader cancer
Improve glucose entry to fat tissue
Hepatic gluconeogenesis decrease
FA and lipolysis decrease
Decrease TG
Lower insulin requirements
S/E: hepatotoxity,Peripheral edema, CHF, weight gain,
fractures, macular edema
C/I :CHF, liver disease
40. DECREASE GLUCOSE PRODUCTIONS
Α-GLUCOSIDASE INHIBITORS:
MOA: ↓ GI glucose absorption PP by inhibiting enzyme
oligosaccharidese that cleavage oligosaccharides into simple
suger
Reduce postprandial glycemia
Acarbose 50-100 mg. TDS PO
Miglitol 25-100 mg TDS PO
voglibose 200-300 microgm TDS PO
These itself never cause hypoglycemia but can cause with insulin
secretagogues
S/E diarrheal
Flatulence
Abd distension
C/I:
IBD/Renal/liver disease
41. MISCELLANEOUS ANTIDIABETIC DRUGS
AMYLIN ANALOGUE: It is produced by pancreatic B
cell and acts in the brain to
• Reduse glucagon secration from A cells
• Delayed gastric emptying
• Retard glucose absorption
• Promote satiety
PRAMLINITIDE
reduce postprandial glycemic excursions in type 1 and
type 2 diabetic patients taking insulin.
In type 2 DM, pramlintide is started as a 60-μg SC
injection before each meal and may be titrated up to a
maximum of 120 μg
The major side effects are nausea and vomiting
42. SODIUM-GLUCOSE CO-TRANSPORTER 2 INHIBITORS
(SLGT2)
MOA:
lower the blood glucose by selectively inhibiting this co-
transporter, which is expressed almost exclusively in the
proximal, convoluted tubule in the kidney.
This inhibits glucose reabsorption, lowers the renal threshold
for glucose, and leads to increased urinary glucose excretion.
Due to the increased urinary glucose, urinary or vaginal
infections are more common, and the diuretic effect can lead
to reduced intravascular volume.
As part of the FDA approval of canagliflozin in 2013,
postmarketing studies for cardiovascular outcomes and for
monitoring bladder and urinary cancer risk are under way
43. Bile acid–binding resins:
The bile acid–binding resin colesevelam has been
approved for the treatment of type 2 DM (already
approved for treatment of hypercholesterolemia).
Because bile acid–binding resins are minimally
absorbed into the systemic circulation, how bile acid–
binding resins lower blood glucose is not known.
Bromocriptine:
• A formulation of the dopamine receptor agonist
bromocriptine (Cycloset) has been approved by the
FDA for the treatment of type 2 DM.
However, its role in the treatment of type 2 DM is
uncertain
44. INSULIN THERAPY IN TYPE 2 DM
Insulin should be considered as the initial therapy in
type 2 DM, particularly in
lean individuals
those with severe weight loss
In individuals with underlying renal or hepatic disease
that precludes oral glucose-lowering agents,
In individuals who are hospitalized or acutely ill.
Insulin therapy is ultimately required by a substantial
number of individuals with type 2 DM because of the
progressive nature of the disorder and the relative
insulin deficiency that develops in patients with long-
standing diabet
45. Insulin is usually initiated in a single dose of long-
acting insulin (0.3–0.4 U/kg per day), given in the
evening (NPH) or just before bedtime (NPH, glargine,
detemir).
The insulin dose may then be adjusted in 10%
increments as dictated by SMBG results.
Both morning and bedtime long-acting insulin may be
used in combination with oral glucose-lowering
agents.
Initially, basal insulin may be sufficient, but often
prandial insulin coverage with multiple insulin
injections is needed as diabetes progresses
46.
47. INSULIN DEGLUDEC
An ultralong-acting basal Insulin analogue being developed
by Novo Nordisk under the brand name Tresiba.
One amino acid is deleted and conjugated to
hexadecanedioic acid via gamma-L-glutamyl spacer at the
amino acid lysine at position B29.
Lysine at the B29 position allows for the formation of multi-
hexamers in subcutaneous tissues
Results in slow insulin release into the systemic circulation.
Duration of action up to 40 hour. administered via
subcutaneous injection.
49. The level of hyperglycemia and the patient’s
individualized goal should influence the initial choice
of therapy.
Assuming that maximal benefit of MNT and increased
physical activity has been realized, patients with mild
to moderate hyperglycemia (FPG 200–250 mg/dL)
often respond well to a single, oral glucose-lowering
agent. Patients with more severe hyperglycemia (FPG
250 mg/dL) stepwise approach that starts with a single
agent and adds a second agent to achieve the glycemic
target can be used.
Insulin can be used as initial therapy in individuals
with severe hyperglycemia (FPG 250–300 mg/dL) or in
those who are symptomatic from the hyperglycemia.
50. COMBINATION THERAPY WITH GLUCOSE-LOWERING
AGENTS
A number of combinations of therapeutic agents are
successful in type 2 DM
Mechanisms of action of the first and second agents
should be different, the effect on glycemic control is
usually additive
Titration of single agent to a maximum dose and then
addition of a second agent is used to achieve glycemic
control
If adequate control is not achieved with the
combination of two agents (based on reassessment of
the HbA1c every 3 months), a third oral agent or basal
insulin should be added
51. EMERGING THERAPIES
Bariatric surgery for obese individuals with type 2 DM
has shown considerable promise, sometimes with
dramatic resolution of the diabetes or major
reductions in the needed dose of glucose-lowering
therapies
Several large, unblinded clinical trials have
demonstrated a much greater efficacy of bariatric
surgery compared to medical management in the
treatment of type 2 DM; the durability of the diabetes
reversal or improvement is uncertain
The ADA clinical guidelines state that bariatric surgery
should be considered in individuals with DM and a
body mass index >35 kg/m2