This document provides an overview of blood glucose regulation and diabetes. It begins with definitions of key terms like blood sugar, normal glucose levels, and hyperglycemia and hypoglycemia. The document then discusses the history of diabetes research and discoveries. It explains the normal physiology of glucose regulation including the roles of insulin, glucagon, and other hormones. It also covers alterations in blood glucose levels and the public health impacts of diabetes.
Glucose is the main sugar found in the blood. The body get glucose from the food we eat.
This sugar is an important source of energy and provides nutrients to the body’s organs, muscles and nervous system.
Blood sugar concentration, or glucose level, refers to the amount of glucose present in the blood of a human.
Detail information about Oral Glucose Tolerance Test.
Here we discuss about the type, indications, contra-indications, precautions, Medication avoiding, Nursing care plan, Risks of OGTT & explain the technique, procedures of doing the test. Thus OGTT is a very important test in medical field. Upgrade your knowledge by reading this. Thanks.
Glucose is the main sugar found in the blood. The body get glucose from the food we eat.
This sugar is an important source of energy and provides nutrients to the body’s organs, muscles and nervous system.
Blood sugar concentration, or glucose level, refers to the amount of glucose present in the blood of a human.
Detail information about Oral Glucose Tolerance Test.
Here we discuss about the type, indications, contra-indications, precautions, Medication avoiding, Nursing care plan, Risks of OGTT & explain the technique, procedures of doing the test. Thus OGTT is a very important test in medical field. Upgrade your knowledge by reading this. Thanks.
Glucose tolerance test- Indications, contraindications, preparation of a patient, precautions, types of GTT, normal curve, diabetic curve, renal glycosuria, lag curve, Criteria for diagnosis of DM
Insulin and glucagon help maintain blood sugar levels. Glucagon helps prevent blood sugar from dropping, while insulin stops it from rising too high. Insulin and glucagon work together in a balance and play a vital role in regulating a person's blood sugar levels. Glucagon breaks down glycogen to glucose in the liver.
Glycosylated Hemoglobin, also called Glycated Hemoglobin, Hemoglobin A1c, or HbA1c, refers to hemoglobin which is bound to glucose. Glycosylated Hemoglobin Test is performed to measure the percentage of glycosylated hemoglobin in blood which reflects the average blood glucose over a period of past two to three months (8 - 12 weeks).
For more information, visit
https://www.1mg.com/labs/test/glycosylated-hemoglobin-1611
Blood glucose regulation, glucose homeostasis, factors regulating and under S...Mohit Adhikary
The slides explain about blood glucose regulation, glucose homeostasis, factors regulating and under Special Circumstances. Factors regulating Blood glucose level include the hormonal and non-hormonal.
Hormonal Regulation of blood Glucose - Part-III.pptxABHIJIT BHOYAR
Regulation of blood glucose is largely done through the endocrine hormones of the pancreas, a beautiful balance of hormones achieved through a negative feedback loop. The main hormones of the pancreas that affect blood glucose include insulin, glucagon, somatostatin, and amylin.
Glucose tolerance test- Indications, contraindications, preparation of a patient, precautions, types of GTT, normal curve, diabetic curve, renal glycosuria, lag curve, Criteria for diagnosis of DM
Insulin and glucagon help maintain blood sugar levels. Glucagon helps prevent blood sugar from dropping, while insulin stops it from rising too high. Insulin and glucagon work together in a balance and play a vital role in regulating a person's blood sugar levels. Glucagon breaks down glycogen to glucose in the liver.
Glycosylated Hemoglobin, also called Glycated Hemoglobin, Hemoglobin A1c, or HbA1c, refers to hemoglobin which is bound to glucose. Glycosylated Hemoglobin Test is performed to measure the percentage of glycosylated hemoglobin in blood which reflects the average blood glucose over a period of past two to three months (8 - 12 weeks).
For more information, visit
https://www.1mg.com/labs/test/glycosylated-hemoglobin-1611
Blood glucose regulation, glucose homeostasis, factors regulating and under S...Mohit Adhikary
The slides explain about blood glucose regulation, glucose homeostasis, factors regulating and under Special Circumstances. Factors regulating Blood glucose level include the hormonal and non-hormonal.
Hormonal Regulation of blood Glucose - Part-III.pptxABHIJIT BHOYAR
Regulation of blood glucose is largely done through the endocrine hormones of the pancreas, a beautiful balance of hormones achieved through a negative feedback loop. The main hormones of the pancreas that affect blood glucose include insulin, glucagon, somatostatin, and amylin.
A blood glucose test measures the amount of a type of sugar, called glucose, in your blood. Glucose comes from carbohydrate, Protein and Lipid. It is the main source of energy used by the body. Insulin is a hormone that helps your body's cells use the glucose. Insulin is produced in the pancreas and released into the blood when the amount of glucose in the blood rises.
Buy Accu chek active glucometer,test strips and other branded glucose meter in Diabeticpick.com. Shop for best diabetic products online, get free shipping.
blood glucose homeostasis and the role of tissues and hormones, roles of Insulin and glucagon in regulating blood glucose, regulation of glucose metabolism during exercise, insulin receptor and its mechanism
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
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
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.
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.
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!
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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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.
3. Introduction
History & Basic considerations
Normal Physiology
Mechanisms of Blood Sugar Regulation
Hormonal Role
Alteration of blood glucose levels
Diabetes Mellitus
Public Health Scenario
Conclusion & References
Previous year questions
4. Blood sugar concentration, or glucose level, refers to
the amount of glucose present in the blood of a human.
Normally, in mammals the blood glucose level is
maintained at a reference range between about 3.6 and
5.8 mM (mmol/l).
It is tightly regulated as a part of metabolic
homeostasis.
5. 1552 BC: Ebers Papyrus in ancient Egypt. First known written
description of diabetes.
1st Century AD: Arateus — “Melting down of flesh and limbs
into urine.”
1776: Matthew Dobson conducts experiments showing sugar
in blood and urine of diabetics.
Mid 1800s: Claude Bernard studies the function of the
pancreas and liver, and their roles in homeostasis.
1869: Paul Langerhans identifies cells of unknown function in
the pancreas. These cells later are named “Islets of
Langerhans.”
6. 1889: Pancreatectomized dog develops fatal diabetes.
1921: Insulin “discovered” — effectively treated
pancreatectomized dog.
1922: First human treated with insulin. Eli Lilly begins mass
production.
1923: Banting and Macleod win Nobel Prize for work with
insulin.
1983: Biosynthetic insulin produced.
2001: Human genome sequence completed.
7. Blood sugar/Glucose concentration:
The amount of Glucose ( in mg) in 1 dl of the human
blood. Measured as mg/ dl or mg %.
Normal Blood Glucose
Fasting state : 60 to 100 mg%
Postprandial : 100 to 140 mg %
8. Hyperglycemia:
It is a condition in which an excessive amount
of glucose circulates in the blood plasma. This is
generally a blood sugar level higher than
11.1 mmol/l (200 mg/dl).
Hypoglycemia:
It is a condition in which blood sugar (or
blood glucose) concentrations fall below a level
necessary to properly support the body's need for energy
and stability throughout its cells.
11. CELL GROWTH AND ENERGY
METABOLISM
TCA Cycle
Kreb’s Cycle
Proteins
Amino acids
Fats
Fatty acids
Carbohydrates
Glucose Pyruvate
ATP
12.
13. In normal persons, blood glucose level is controlled within a
narrow range.
In the early morning after overnight fasting, the blood
glucose level is low ranging between 70 and 110 mg/dL of
blood.
Between first and second hour after meals (postprandial), the
blood glucose level rises to 100 to 140 mg/dL.
Glucose level in blood is brought back to normal at the end of
second hour after the meals.
14. Blood glucose regulating mechanism is operated through liver
and muscle by the influence of the pancreatic hormones –
insulin and glucagon.
Many other hormones are also involved in the regulation of
blood glucose level.
Among all the hormones, insulin is the only hormone that
reduces the blood glucose level and it is called the anti-
diabetogenic hormone.
The hormones which increase blood glucose level are called
diabetogenic hormones or anti-insulin hormones.
15. Regulation of blood glucose (sugar) level is very
essential because:
Glucose is the only nutrient that is utilized for energy
by many tissues such as
I. brain tissues,
II. retina
III. germinal epithelium of the gonads.
16. Liver serves as an important glucose buffer system.
When blood glucose level increases after a meal, the excess
glucose is converted into glycogen and stored in liver.
Afterwards, when blood glucose level falls, the glycogen in
liver is converted into glucose and released into the blood.
The storage of glycogen and release of glucose from liver are
mainly regulated by insulin and glucagon.
17.
18. There are two types of mutually antagonistic metabolic
hormones affecting blood glucose levels:
1. Catabolic hormones (such as glucagon, growth
hormone, cortisol and catecholamines) which increase
blood glucose;
2. Anabolic hormone (insulin), which decreases blood
glucose.
19. The pancreas detects the change in blood glucose
concentration and releases the appropriate hormone:
20.
21.
22. Glucagon binding to its' receptors on the surface of liver cells
triggers an increase in cAMP production leading to an
increased rate of glycogenolysis by activating glycogen
phosphorylase via the PKA-mediated cascade.
This is the same response hepatocytes have to epinephrine
release.
The resultant increased levels of G6P in hepatocytes is
hydrolyzed to free glucose, by glucose-6-phosphatase, which
then diffuses to the blood.
23. The glucose enters extrahepatic cells where it is re-
phosphorylated by hexokinase.
Since muscle and brain cells lack glucose-6-phosphatase,
the glucose-6-phosphate product of hexokinase is retained
and oxidized by these tissues.
24. Insulin stimulates extrahepatic uptake of glucose from the
blood and inhibits glycogenolysis in extrahepatic cells and
conversely stimulates glycogen synthesis.
As the glucose enters hepatocytes it binds to and inhibits
glycogen phosphorylase activity.
The binding of free glucose stimulates the
de_phosphorylation of phosphorylase thereby, inactivating
it.
25. When blood glucose levels are low, the liver does not compete
with other tissues for glucose since the extra-hepatic uptake of
glucose is stimulated in response to insulin.
Conversely, when blood glucose levels are high extra-hepatic
needs are satisfied and the liver takes up glucose for
conversion into glycogen for future needs.
Under conditions of high blood glucose, liver glucose levels
will be high and the activity of glucokinase will be elevated.
The G6P produced by glucokinase is rapidly converted to G1P
by phosphoglucomutase, where it can then be incorporated
into glycogen.
26. Glucagon secretion increases during exercise to promote
liver glycogen breakdown (glycogenolysis)
Epinephrine and Norepinephrine further increase
glycogenolysis
Cortisol levels also increase during exercise for protein
catabolism for later gluconeogenesis.
Thyroxine promotes glucose catabolism
27. Glucose uptake is enhanced by insulin.
Exercise may enhance insulin’s binding to
receptors on the muscle fiber.
Up-regulation (receptors) occurs with insulin after
4 weeks of exercise to increase its sensitivity
(diabetic importance).
28. Hormone
Tissue of
Origin
Metabolic Effect
Effect on
Blood
Glucose
Insulin
Pancreatic
β-cells
1) Enhances entry of glucose into cells;
2) Enhances storage of glucose as glycogen, or
conversion to fatty acids;
3) Enhances synthesis of fatty acids and
proteins;
4) Suppresses breakdown of proteins into
amino acids, of adipose tissue into free fatty
acids.
Lowers
Somatosta
tin Pancreatic
D- Cells
1) Suppresses glucagon release from α cells
(acts locally);
2) Suppresses release of Insulin, Pituitary
tropic hormones, gastrin and secretin
Raises
Glucagon
Pancreatic
α-cells
1) Enhances release of glucose from glycogen;
2) Enhances synthesis of glucose from amino
acids
Raises
29. Epinephrine Adrenal
medulla
1) Enhances release of glucose from glycogen;
2) Enhances release of fatty acids from
adipose tissue.
Raises
cortisol Adrenal
cortex
1) Enhances gluconeogenesis;
2) Antagonizes Insulin.
Raises
ACTH Anterior
pituitary
1) Enhances release of cortisol;
2) Enhances release of fatty acids from adipose
tissue.
3) Inhibiting uptake by extrahepatic tissues.
Raises
Growth
hormone
Anterior
Pituitary
1)Antagonizes Insulin,
2) Inhibiting uptake by extrahepatic tissues. Raises
thyroxine Thyroid 1) Enhances release of glucose from glycogen;
2) Enhances absorption of sugars from
intestine
Raises
30. Insulin is small protein, with a molecular weight of about 6000
Daltons.
It is composed of two chains held together by disulfide bonds.
The amino acid sequence is highly conserved, and insulin from
one mammal almost certainly is biologically active in another.
Many diabetic patients are treated with insulin extracted from
pig pancreas.
31. Insulin is synthesized in beta cells in the pancreas.
The insulin mRNA is translated as a single chain precursor
called preproinsulin, and removal of its signal peptide during
insertion into the endoplasmic reticulum generates proinsulin.
33. Major source of net endogenous glucose production.
Accomplished by gluconeogenesis and glycogenolysis
when glucose is low
And of glycogen synthesis when glucose is high.
Can oxidize glucose for energy and convert it to fat
which can be incorporated into VLDL for transport.
34.
35. Can convert glucose to glycogen.
Can convert glucose to pyruvate through glycolysis - further
metabolized to lactate or transaminated to alanine or
channeled into the TCA cycle.
In the fasting state, can utilize FA for fuel and mobilize
amino acids by proteolysis for transport to the liver for
gluconeogenesis.
Can break down glycogen
But cannot liberate free glucose into the circulation.
36.
37. Can store glucose by conversion to fatty acids and combine
these with VLDL to make triglycerides.
In the fasting state can use fatty acids for fuel by beta
oxidation.
40. Converts glucose to CO2 and H2O.
Can use ketones during starvation.
Is not capable of gluconeogenesis.
Has no glycogen stores.
Brain is the major glucose consumer
Consumes 120 to 150 g of glucose per day
Glucose is virtually the sole fuel for brain.
41. Brain does not have any fuel stores like glycogen.
Can’t metabolize fatty acids as fuel
Requires oxygen always to burn its glucose
Can not live on anaerobic pathways
One of most fastidious and voracious of all organs
Oxygen and glucose supply can not be interrupted
42. Based on the level of blood sugar in the body, two
major types of disorders occur:
1. Hyperglycemia
2. Hypoglycemia
43. A condition in which an excessive amount of glucose
circulates in the blood plasma (>10 mmol/L or 180 mg/dl).
Temporary hyperglycemia is often benign and asymptomatic.
Blood glucose levels can rise well above normal for short
periods without producing any permanent effects or symptoms.
44. However, chronic hyperglycemia at levels more than slightly
above normal can produce a very wide variety of serious
complications over a period of years, including kidney
damage, neurological damage, cardiovascular damage,
damage to the retina etc.
Exerts high osmotic pressure in extracellular fluid, causing
cellular dehydration
Excess of glucose begins to be lost from the body in the urine:
GLYCOSURIA.
45.
46.
47. Diabetes mellitus is a metabolic disorder characterized by
high blood glucose level, associated with other
manifestations.
‘Diabetes’ means ‘polyuria’ and ‘mellitus’ means ‘honey’.
The name ‘diabetes mellitus’ was coined by Thomas Willis,
who discovered sweetness of urine from diabetics in 1675.
In most of the cases, diabetes mellitus develops due to
deficiency of insulin.
48. There are several forms of diabetes mellitus, which occur due
to different causes.
Diabetes may be primary or secondary.
Primary diabetes is unrelated to another disease.
Secondary diabetes occurs due to damage or disease of
pancreas by another disease or factor.
Recent classification divides primary diabetes mellitus into
two types, Type I and Type II.
49. Type I diabetes mellitus is due to deficiency of insulin because
of destruction of β-cells in Islets Of Langerhans.
This type of diabetes mellitus may occur at any age of life.
But, it usually occurs before 40 years of age and the persons
affected by this require insulin injection.
So it is also called Insulin-dependent Diabetes Mellitus
(IDDM).
When it develops at infancy or childhood, it is called juvenile
diabetes.
50. Type I diabetes mellitus develops rapidly and progresses
at a rapid phase.
It is not associated with obesity, but may be associated
with acidosis or ketosis.
Causes of type I diabetes mellitus:
1. Degeneration of β-cells in the islets of Langerhans of
pancreas
2. Destruction of β-cells by viral infection
3. Congenital disorder of β-cells
4. Destruction of β-cells during autoimmune diseases.
5. It is due to the development of antibodies against β-
cells
51. Latent autoimmune diabetes in adults (LADA):
1. LADA or slow onset diabetes has slow onset and slow
progress than IDDM and it occurs in later life after 35 years.
2. It may be difficult to distinguish LADA from type II diabetes
mellitus, since pancreas takes longer period to stop secreting
insulin.
Maturity onset diabetes in young individuals (MODY): It is
a rare inherited form of diabetes mellitus that occurs before 25
years. It is due to hereditary defects in insulin secretion.
52. Type II diabetes mellitus is due to insulin resistance (failure of
insulin receptors to give response to insulin).
So, the body is unable to use insulin.
About 90% of diabetic patients have type II diabetes mellitus.
It usually occurs after 40 years.
Only some forms of Type II diabetes require insulin. In most
cases, it can be controlled by oral hypoglycemic drugs.
So it is also called Non Insulin Dependent Diabetes Mellitus
(NIDDM).
53. Type II diabetes mellitus may or may not be associated with
ketosis, but often it is associated with obesity.
Causes for type II diabetes mellitus:
In this type of diabetes, the structure and function of β-cells
and blood level of insulin are normal.
But insulin receptors may be less, absent or abnormal,
resulting in insulin resistance.
54. Common causes of insulin resistance are:
1. Genetic disorders (significant factors causing type II
diabetes mellitus)
2. Lifestyle changes such as bad eating habits and
physical inactivity, leading to obesity
3. Stress.
55. Other forms :
Gestational diabetes:
It occurs during pregnancy.
It is due to many factors such as hormones secreted
during pregnancy, obesity and lifestyle before and during
pregnancy.
Usually, diabetes disappears after delivery of the child.
However, the woman has high risk of development of
type II diabetes later.
56. Pre-diabetes:
It is also called chemical, subclinical, latent or borderline
diabetes.
It is the stage between normal condition and diabetes.
The person does not show overt (observable) symptoms
of diabetes but there is an increase in blood glucose level.
Though pre-diabetes is reversible, the affected persons
are at a high risk of developing type II diabetes mellitus.
57.
58. Secondary diabetes mellitus is rare and only about 2% of
diabetic patients have secondary diabetes.
It may be temporary or may become permanent due to the
underlying cause.
Endocrine disorders such as gigantism, acromegaly and
Cushing’s syndrome.
Hyperglycemia in these conditions causes excess stimulation
of β-cells.
Constant and excess stimulation, in turn causes burning out
and degeneration of β-cells.
The β-cell exhaustion leads to permanent diabetes mellitus.
59. Damage of pancreas due to disorders such as chronic
pancreatitis, cystic fibrosis and hemochromatosis (high iron
content in body causing damage of organs).
Pancreatectomy (surgical removal)
Liver diseases such as hepatitis C and fatty liver
Autoimmune diseases such as celiac disease
Excessive use of drugs like antihypertensive drugs (beta
blockers and diuretics), steroids, oral contraceptives,
chemotherapy drugs, etc.
Excessive intake of alcohol and opiates.
60. Various manifestations of diabetes mellitus develop because of
three major setbacks of insulin deficiency.
1. Increased blood glucose level (300 to 400 mg/dL) due to
reduced utilization by tissue
2. Mobilization of fats from adipose tissue for energy
purpose, leading to elevated fatty acid content in blood. This
causes deposition of fat on the wall of arteries and
development of atherosclerosis.
3. Depletion of proteins from the tissues.
61. Glucosuria is the loss of glucose in urine.
Normally, glucose does not appear in urine. When
glucose level rises above 180 mg/dL in blood,
glucose appears in urine.
It is the renal threshold level for glucose.
62. Osmotic diuresis is the diuresis
caused by osmotic effects.
Excess glucose in the renal tubules develops osmotic
effect.
Osmotic effect decreases the reabsorption of water from
renal tubules, resulting in diuresis.
It leads to polyuria and polydipsia.
63. Loss of strength is called asthenia. Body becomes very weak
because of this.
Asthenia occurs due to protein depletion, which is caused by
lack of insulin.
Lack of insulin causes decrease in protein synthesis and
increase in protein breakdown, resulting in protein depletion.
Protein depletion also occurs due to the utilization of proteins
for energy in the absence of glucose utilization.
64. During insulin deficiency, glucose cannot be utilized by the
peripheral tissues for energy.
So, a large amount of fat is broken down to release energy.
It causes the formation of excess ketoacids, leading to
acidosis.
One more reason for acidosis is that the ketoacids are excreted
in combination with sodium ions through urine (ketonuria).
Sodium is exchanged for hydrogen ions, which diffuse from
the renal tubules into ECF adding to acidosis.
65. In cases of severe ketoacidosis, acetone is expired in the
expiratory air, giving the characteristic acetone or fruity
breath odor.
It is a life-threatening condition of severe diabetes.
66. Kussmaul breathing is the increase in rate and depth of
respiration caused by severe acidosis.
67. Osmotic diuresis leads to dehydration, which
causes circulatory shock. It occurs only in severe
diabetes.
68. Due to Kussmaul breathing, large amount of carbondioxide is
lost during expiration.
It leads to drastic reduction in the concentration of bicarbonate
ions causing severe acidosis and coma.
It occurs in severe cases of diabetes mellitus.
Increase in the blood glucose level develops hyperosmolarity
of plasma which also leads to coma. It is called hyperosmolar
coma.
69. Prolonged hyperglycemia in diabetes mellitus causes
dysfunction and injury of many tissues, resulting in some
complications.
Development of these complications is directly proportional to
the degree and duration of hyperglycemia.
However, the patients with well controlled diabetes can
postpone the onset or reduce the rate of progression of these
complications.
70. Initially, the untreated chronic hyperglycemia affects the
blood vessels, resulting in vascular complications like
atherosclerosis.
Vascular complications are responsible for the development of
most of the complications of diabetes such as:
Complications contd.
71. Cardiovascular complications like:
i. Hypertension
ii. Myocardial infarction
Degenerative changes in retina called diabetic retinopathy.
Degenerative changes in kidney known as diabetic
nephropathy
Degeneration of autonomic and peripheral nerves called
diabetic neuropathy.
Complications contd.
72. Due to the systemic effects of diabetes mellitus, various
oral manifestations occur:
Gingivitis & periodontitis
Periradicular osteolytic inflammatory lesions
(abscesses, granulomas,etc)
Loss of teeth
Xerostomia and altered salivary composition
Lesions of oral mucosa and tongue.
73. Thickening of blood vessels
is a complication of diabetes
that may increase risk for gum
disease.
Blood vessels deliver oxygen
and nourishment to body
tissues, including the mouth,
and carry away the tissues'
waste products.
Diabetes causes blood vessels
to thicken, which slows the
flow of nutrients and the
removal of harmful wastes.
This can weaken the
resistance of gum and bone
tissue to infection.
74.
75. Diagnosis of diabetes mellitus includes the determination
of:
1. Fasting blood glucose
2. Postprandial blood glucose
3. Glucose tolerance test (GTT)
4. Glycosylated (glycated) hemoglobin.
76. Determination of glycosylated hemoglobin is commonly
done to monitor the glycemic control of the persons
already diagnosed with diabetes mellitus.
Abnormal response in diagnostic tests:
Abnormal response in diagnostic tests occurs in conditions
like pre-diabetes.
There is an increased fasting blood glucose level or
impaired (decreased) glucose tolerance.
77. The glycemic index or glycaemic index (GI) is a number
associated with a particular type of food that indicates the
food’s effect on a person’s blood glucose (also called blood
sugar) level.
The number typically ranges between 50 and 100, where 100
represents the standard, an equivalent amount of pure glucose.
The glycemic index is usually applied in the context of the
quantity of the food and the amount of carbohydrate in the
food that is actually consumed.
78. Foods with carbohydrates that break down quickly during
digestion and release glucose rapidly into the bloodstream
tend to have a high GI.
Foods with carbohydrates that break down more slowly,
releasing glucose more gradually into the bloodstream, tend to
have a low GI.
Fruits like watermelon and ripe bananas have high glycemic
index whereas strawberries have low glycemic index.
79.
80.
81.
82. Type I diabetes mellitus:
Type I diabetes mellitus is treated by exogenous
insulin.
Since insulin is a polypeptide, it is degraded in GI
tract if taken orally.
So, it is generally administered by subcutaneous
injection.
83. Type II diabetes mellitus:
Type II diabetes mellitus is treated by oral hypoglycemic
drugs.
Patients with longstanding severe diabetes mellitus may
require a combination of oral hypoglycemic drugs with
insulin to control the hyperglycemia.
84. Oral hypoglycemic drugs are classified into three
types.
Insulin secretagogues:
These drugs decrease the blood glucose level by
stimulating insulin secretion from β-cells.
Sulfonylureas (tolbutamide, gluburide, glipizide, etc.)
are the commonly available insulin secretagogues.
85. Insulin sensitizers:
These drugs decrease the blood glucose level by
facilitating the insulin action in the target tissues.
Examples are biguanides (metformin) and
thiazolidinediones (pioglitazone and rosiglitazone)
86. Alpha glucosidase inhibitors:
These drugs control blood glucose level by inhibiting
α-glucosidase.
This intestinal enzyme is responsible for the conversion of
dietary and other complex carbohydrates into glucose and
other monosaccharides, which can be absorbed from
intestine.
Examples of α-glucosidase inhibitors are acarbose and
meglitol.
87. Hyperinsulinism is the hypersecretion of insulin.
Cause:
Hyperinsulinism occurs due to the tumor of β-cells in the
Islets of Langerhans.
Signs and Symptoms:
Hypoglycemia
Blood glucose level falls below 50 mg/dL.
88. Manifestations of central nervous system
Manifestations of central nervous system occur when the
blood glucose level decreases. All the manifestations are
together called neuroglycopenic symptoms.
Initially, the activity of neurons increases, resulting in
nervousness, tremor all over the body and sweating.
If not treated immediately, it leads to clonic convulsions and
unconsciousness. Slowly, the convulsions cease and coma
occurs due to the damage of neurons.
89. The main objective is to maintain blood glucose levels
as close to normal as possible.
To minimize the risk of an intra-operative emergency,
clinicians need to consider some issues before
initiating dental treatment.
Medical history:
Glucose levels
Frequency of hypoglycemic episodes
Medication, dosage and times.
Consultation
90. Scheduling of visits
Morning appt. (endogeneous cortisol)
Do not coincide with peak activity.
Diet
Ensure that the patient has eaten normally and taken
medications as usual.
Blood glucose monitoring
Measured before beginning. (<70 mg/dL)
91. Prophylactic antibiotics
Established infection
Pre-operation contamination wound
Major surgery
During treatment
The most complication of DM occur is hypoglycemia
episode.
Hyperglycemia
After treatment
Infection control
Dietary intake
Medications : salicylates increase insulin secretion and
sensitivity avoid aspirin.
92. Initial signs : mood changes, decreased spontaneity,
hunger and weakness.
Followed by sweating, incoherence, tachycardia.
Consequenced in unconsiousness, hypotention,
hypothermia, seizures, coma, even death.
93. 15 grams of fast-acting oral carbonhydrate.
Measurement of blood sugar levels.
Loss of conscious, 25-30ml 50% dextrose solution iv.
over 3 min period.
Glucagon 1mg.
94. Severe hyperglycemia
A prolonged onset
Ketoacidosis may develop with nausea, vomiting,
abdominal pain and acetone odor.
Difficult to different hypo- or hyper-glycemia.
Hyperglycemia need medication intervention and
insulin administration.
While emergency, give glucose first !
Small amount is unlikely to cause significant harm.
95.
96.
97. There is a group of individuals (Type 1 1/2 diabetes), who
present like typical NIDDM, but have some of the
immunological and clinical features of IDDM.
Comparative studies in the area of cytokine production, T
cell reactivity and autoantibody clustering between classic
Type 1 diabetes and Type 1 1/2 diabetes patients are needed
as are studies with the animal model of Type 1 1/2 diabetes,
Psammomys obesus.
Ref: Type 1 1/2 diabetes: myth or reality? Juneja r, palmer jp.
Autoimmunity. 1999;29(1):65-83.
98. The conventional laboratory methods employed to detect
blood glucose are time consuming and require elaborative
equipments.
The advent of blood glucose monitors allows the clinician to
detect blood glucose at chair side.
Studies suggest a significant correlation was found between
gingival crevicular blood glucose levels and capillary finger
stick blood glucose levels in diabetics and non- diabetics.
The result suggests that Gingival Crevicular blood is an
efficient diagnostic tool for estimation of blood glucose levels
in patients with or without diabetes mellitus.
Ref: Estimation of Blood Glucose levels from GCF in patients with or without Diabetes Mellitus Tajinder
Bansal, Ruchika Bansal, Deepa Jatti, Jithender Reddy Kubbi, Irfana Khursheed J Adv Med Dent Scie Res
2014;2(3):4-9.
99. Prediabetes is the medical stage in which not all of the
symptoms required to label a person as diabetic are present, but
blood sugar is abnormally high. This stage is often referred to as
the "grey area.“
Impaired fasting glycaemia
Impaired glucose tolerance
The American College of Endocrinology (ACE) and
the American Association of Clinical Endocrinologists (AACE)
have developed lifestyle intervention guidelines for preventing
the onset of type 2 diabetes.
100.
101. Diabetes is part of a larger global epidemic of non communicable
diseases.
It has become a major public health challenge globally.
This disease affects 6.6% (285 million people) of the world’s
population in the 20--‐79 years age group.
According to the International Diabetic Federation (IDF), this
number is expected to grow to 380 million by 2025.
The IDF published findings revealing that in 2007, the country with
the largest numbers of people with diabetes is India (40.9 million),
followed by China (39.8 million), the United States (19.2 million),
Russia (9.6 million) and Germany (7.4 million).
102. The International Diabetes Federation (IDF) is an
umbrella organisation of over 200 national diabetes
associations in over 160 countries.
It represents the interests of the growing number of
people with diabetes and those at risk.
The Federation has been leading the global diabetes
community since 1950.
IDF’s mission is to promote diabetes care, prevention
and a cure worldwide.
103. India is home to forty million people with diabetes—nearly 15
percent of the global diabetes burden and projections show
that this will increase to seventy million by 2025.
Diabetes disproportionately affects people of working ages
and accounts for US$2.2 billion in annual health care costs in
India alone.
Ref: National programme on prevention and control of diabetes in India: Need to
focus. Ramesh Verma, Pardeep Khanna, Bharti. Australasian Medical Journal
[AMJ 2012, 5, 6, 310--‐315]
104. The “National Diabetes control program” was launched on a
pilot basis during the VIIth Five Year Plan in some districts of
Tamil Nadu, Karnataka and Jammu & Kashmir.
Due to paucity of funds in subsequent years this programme
could not be expanded further in remaining states.
However, during 1995--‐96, a sum of 12 lakh rupees was
allocated for the programme and subsequently in 1997--‐98 an
allocation of one core was made.
105. National diabetes prevalence is 4.3 percent in India.
Prevalence is higher among people living in cities compared to
rural areas, those in the South compared to the North, and those
of high socioeconomic status (SES) compared to low SES.
During 1971–2000, urban diabetes prevalence rose from 1.2
percent to 12.1 percent.
However, studies show that diabetes has risen rapidly in rural
areas, with a threefold increase (from 2.4 percent to 6.4
percent) in rural southern India over a fourteen-year period.
Ref: Finding A Policy Solution To India’s Diabetes Epidemic.
by Karen Siegel, K.M. Venkat Narayan, and Sanjay Kinra
106. The Ministry of Health spearheaded a national consultation in
2005 to “identify action pathways and partnerships for
implementing the Global Strategy in the context of India.”
The pilot phase of the National Program on Diabetes, CVD,
and Stroke (NPCDS) was launched in seven states in January
2008.
No national awareness survey has been performed, but a
recent study in Chennai found that awareness of diabetes as a
public health priority and knowledge of diabetes prevention is
poor, especially among women and people with little
education.
107. Although India accounts for approximately 15 percent of the
global burden of diabetes, it contributes 1 percent of the
world’s diabetes research.
There are few data on the quality of diabetes care, no national
monitoring system for processes and outcomes of care, and no
translational research to turn knowledge into action.
Only two national diabetes surveys have been conducted since
1975.
The Integrated Disease Surveillance (IDS) program,
launched in 2004, analyzes population wide chronic disease
risk factors, but it needs improvement.
108. More recently National Heart, Lung, and Blood Institute
(NHLBI) Chronic Disease Initiative and the International
Diabetes Federation (IDF) BRIDGES Initiative provide
potential for Indian researchers to work with policymakers and
uncover practical, country-specific solutions.
Ref: Ministry of Health and FamilyWelfare, “Pilot Phase of the National
Programme for Prevention and Control of Diabetes, Cardio-Vascular Diseases,
and Stroke Launched,” Press Release, 4 January 2008,
109. Sanofi, IDF and PHFI partner to fight diabetes among children
in India:
Sanofi (EURONEXT: SAN and NYSE: SNY), the International
Diabetes Federation (IDF) and Public Health Foundation of India
(PHFI) announced their first joint public health initiative in India,
KiDS (Kids and Diabetes in Schools).
For children with Type 1 diabetes, the project aims to encourage a
safe and supportive school environment to manage their diabetes and
avoid discrimination.
In addition, the program will raise awareness on diabetes (Type 1 and
Type 2) and benefits of healthy nutrition and exercise habits among
school children.
110. The Consultative Section on Diabetes Education (DECS) of
the International Diabetes Federation (IDF) was established
in 1994.
One of DECS’ functions is to conduct and/or stimulate the
development of programmes and activities relevant to
diabetes education worldwide.
112. Comprehensive Course in Diabetes Management by the
Endocrinology & Metabolism Research Institute of Tehran
University of Medical Sciences (Iran).
Intensive Training Course for Diabetes Educators by
the Philippine Center for Diabetes Education Foundation,
Inc. (Philippines)
MSc, Postgraduate Diploma and Postgraduate Certificate in
Diabetes by the University of Leicester (UK)
Masters (MSc) in Diabetes by the University of South Wales
(UK)
Postgraduate Diabetes Diploma by the Cardiff University
(UK)
113.
114. Essentials of medical physiology by Y.Sembuligam.(6th edition)
Glucose Homeostasis-Counter Regulation by Dr.Sarma.R.V.S.N
M.D., Consultant Physician and Chest Specialist
https://en.wikipedia.org/wiki/Blood_sugar_regulation?oldid=66461
8652
Understanding the processes behind the regulation of blood
glucose by Pat James, PhD; Roger McFadden, MSc. 20th April
2004 Vol 100 No 16 www.nursingtimes.net.
National programme on prevention and control of diabetes in
India: Need to focus. Ramesh Verma, Pardeep Khanna, Bharti.
Australasian Medical Journal [AMJ 2012, 5, 6, 310--‐315].
115. Ministry of Health and FamilyWelfare, “Pilot Phase of the
National Programme for Prevention and Control of
Diabetes, Cardio-Vascular Diseases, and Stroke Launched,”
Press Release, 4 January 2008.
Finding A Policy Solution To India’s Diabetes Epidemic. by
Karen Siegel, K.M. Venkat Narayan, and Sanjay Kinra
http://content.healthaffairs.org/content/27/4/1077.full.html
Sanofi, IDF and PHFI partner to fight diabetes among
children in India :
http://www.idf.org/diabetesatlas/5e/Update2012
116. National Program for Prevention and Control of Diabetes,
CVD and Stroke in India: Dr Sudhir Gupta Chief Medical
Officer (Non Communicable Diseases), Directorate General
of Health Services, Ministry of Health & Family Welfare, New
Delhi, India.
Recent developments in diabetes control and prevention in
India by H.T.Pandve, P.S.Chawla, K.Fernandez, S.A.Singru:
Int J Diab Dev Ctries, July-September 2010,Vol.30, Issue 3
Normal Regulation of Blood Glucose The Important Roles of
Insulin and Glucagon: Diabetes and Hypoglycemia by
James Norman M D, FACS, FACE
117. Ref: Type 1 1/2 diabetes: myth or reality? Juneja
r, palmer jp. Autoimmunity. 1999;29(1):65-83.
Ref: Estimation of Blood Glucose levels from GCF in
patients with or without Diabetes Mellitus Tajinder
Bansal, Ruchika Bansal, Deepa Jatti, Jithender Reddy
Kubbi, Irfana Khursheed J Adv Med Dent Scie Res
2014;2(3):4-9.
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