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.
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.
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.
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.
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.
Lipoprotein metabolism - (transport of lipids in the Blood)Ashok Katta
This presentation explains metabolism of lipoproteins (Chylomicron, VLDL, LDL, HDL) in very simple way. The presentation contains lots of animation to explain metabolism of individual lipoproteins.
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.
Lipoprotein metabolism - (transport of lipids in the Blood)Ashok Katta
This presentation explains metabolism of lipoproteins (Chylomicron, VLDL, LDL, HDL) in very simple way. The presentation contains lots of animation to explain metabolism of individual lipoproteins.
Control of blood glucose concentration.pptxHalaAlabdullah
MAYBE I USED SLIDES GO POWERPOINT AND SOME APPLICATION LIKE BITESIZE
SOURCE FROM Cambridge IGCSE Biology Coursebook
CREATED BY HALA GRADE 9
Very easy to understand it and very helpful
trust me
Diabetes mellitus refers to a group of diseases that affect how the body uses blood sugar (glucose). Glucose is an important source of energy for the cells that make up the muscles and tissues. It's also the brain's main source of fuel.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Title: Sense of 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
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
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.
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
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
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.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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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.
Couples presenting to the infertility clinic- Do they really have infertility...
Regulation of blood sugar
1. REGULATION OF BLOOD SUGAR
PRESENTED BY:- Dr SWATI
DEPARTMENT OF PUBLIC HEALTH DENTISTRY 1
2. • INTRODUCTION
• BASIC CONSIDERATION
• NORMAL BLOOD GLUCOSE LEVEL
• NECESSITY OF REGULATION OF BLOOD GLUCOSE LEVEL
• ROLE OF LIVER
• HORMONAL REGULATION
• ROLE OF PANCREAS
• GLUCAGON
• INSULIN
• REGULATION OF GLUCOSE METABOLISM DURING EXERCISE
• INSULIN SYNTHESIS AND SECRETION
• HYPERGLYCEMIA
• DIABETES MELLITUS
• HYPERINSULINISM
• MANAGEMENT IN DENTAL CLINIC
• PUBLIC HEALTH SCENARIO
• REFERENCES
CONTENTS
2
3. • 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.
• The absorption, storage and production of glucose is
regulated constantly by complex process involving the
small intestine, liver and pancreas.
INTRODUCTION
3
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.
4
5. • Glucose enters the blood stream after a person has taken
carbohydrates. The endocrine system helps keep the
bloodstream’s glucose levels in check using the pancreas.
• This organ produces the hormone INSULIN, releasing it
after a person consumes protein or carbohydrates.
• The insulin sends excess glucose in the liver as glycogen.
5
6. 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 %
BASIC CONSIDERATIONS
6
7. 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.
7
9. • 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.
NORMAL BLOOD GLUCOSE LEVEL
9
10. • 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.
10
11. • 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.
NECESSITY OF REGULATION OF
BLOOD GLUCOSE LEVEL
11
12. • 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.
ROLE OF LIVER
12
13. There are two types of mutually antagonists metabolic hormones
affecting blood glucose levels:
1. Catabolic hormone : (such as glucagon, growth hormone,
cortisol and catecholamines) which increase blood glucose
2. Anabolic hormone: (insulin) which decreases blood glucose.
Glucose Insulin Glycogenesis Glucose
Glucose glucagon glycogenolysis glucose
v
HORMONAL REGULATION
13
17. • Glucagon is the mobilizer of glucose. Normal fasting
glucagon concentration is 100-150pg/ml.
ACTIONS
1. Stimulates glycogenolysis- Glucagon increases the
breakdown of liver glycogen to glucose, producing a rapid
rise in blood glucose within a few minutes:
• By inhibiting glycogen synthetase
• By activating CAMP(cyclic adinosine monophosphate)
formation.
2. Promotes gluconeogenesis- Glucagon promotes formation
of glucose from lactate, pyruvate, glycerol and amino
acids producing a slower but more sustained rise in blood
glucose lasting for hours and days.
17
GLUCAGON
18. 3. Glucagon is a powerful lipolytic agent. It acts via
stimulating a lipase in adipose tissue which releases Free
Fatty Acid and glycerol into the circulation.
3. In large doses, glucagon increases force of contraction of
the heart by increasing Cyclic Adenosine Monophosphate
(CAMP).
4. It stimulates the secretion of Insulin and Pancreatic
somatostatin.
18
19. • 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
dephosphorylation of phosphorylase thereby, inactivating
it.
INSULIN
19
20. • 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.
20
21. • 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.
21
22. • 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.
REGULATION OF GLUCOSE
METABOLISM DURING EXERCISE
22
23. • Thyroxine promotes glucose catabolism
• 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).
23
24. • 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.
INSULIN SYNTHESIS AND
SECRETION
24
25. • 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.
25
26. • 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.
HYPERGLYCEMIA
26
27. • 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.
27
28. • 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.
DIABETES MELLITUS
28
29. • 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.
CLASSIFICATION
29
30. • 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.
Type I diabetes mellitus
30
31. • 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
31
32. • 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.
OTHER FORMS OF TYPE 1 DIABETES
MELLITUS
32
33. • 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).
TYPE II DIABETES MELLITUS
33
34. • 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:
i. In this type of diabetes, the structure and function of β-
cells and blood level of insulin are normal.
i. But insulin receptors may be less, absent or abnormal,
resulting in insulin resistance.
34
35. • Common causes of insulin resistance are:
i. Genetic disorders (significant factors causing type II
diabetes mellitus)
ii. Lifestyle changes such as bad eating habits and physical
inactivity, leading to obesity
iii. Stress.
35
36. 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.
TYPE II DIABETES MELLITUS
36
37. 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.
37
38. • 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.
SECONDARY DIABETES MELLITUS
38
39. • 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.
39
40. • 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
CAUSES OF SECONDARY DIABETES MELLITUS
40
41. • Excessive use of drugs like antihypertensive drugs (beta
blockers and diuretics), steroids, oral contraceptives,
chemotherapy drugs, etc.
• Excessive intake of alcohol and opiates
41
42. • 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.
SIGNS AND SYMPTOMS
42
43. • 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.
COMPLICATIONS OF DIABETES
MELLITUS
43
44. • 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 contraindicated
44
45. • 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.
45
46. • Due to the systemic effects of diabetes mellitus, various oral
manifestations occur:
a) Gingivitis & periodontitis
b) Periradicular osteolytic inflammatory lesions (abscesses,
granulomas,etc)
c) Loss of teeth
d) Xerostomia and altered salivary composition
e) Lesions of oral mucosa and tongue.
ORAL MANIFESTATION
46
47. • 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.
GINGIVITIS AND PERIODONTITIS
47
49. • 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.
DIAGNOSTIC TEST FOR DIABETES
MELLITUS
49
50. • 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.
50
51. 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.
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.
TREATMENT FOR DIABETES MELLITUS
51
52. 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.
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)
52
53. 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.
53
54. • Hyperinsulinism is the hypersecretion of insulin.
• Cause: 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.
HYPERINSULINISM
54
55. 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.
55
56. • 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
MANAGEMENT IN DENTAL CLINIC
56
57. 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)
57
58. 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. 58
59. • Mood changes, decreased spontaneity, hunger and
weakness.
• Followed by sweating, incoherence, tachycardia
• Consequenced in unconsciousness , hypotention,
hypothermia, seizures, coma even death.
• 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.
INITIAL SIGNS
EMERGENCY MANAGEMENT
59
60. 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.
60
61. • 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).
PUBLIC HEALTH SCENARIO
61
62. REFERENCES
1. katiyar vk. regulation of blood glucose level in diabetes mellitus using
palatable diet composition. australas phys eng sci med. 2003
sep;26(3):132-9
2. Sembulingam K and Prema sembulingam. Essentials of medical
physiology.Jaypee Brothers Medical Publishers (P) Ltd 2012; 6th edition
3. Bannerjee RK, et al: Regulation of fasted blood glucose by resistin.
Science 2004;303:1195.
4. william f. ganong .Review of medical physiology. McGraw hill
publication ;23rd edition:pg315-336
5. Robert k murray:harper’s illustrated biochemistry 28th edition