SIGNIFICANCE
OVERVIEW
WHAT IS DIABETES?
DEFINITION
MECHANISM
PREVELANCE
EPIDEMIOLOGY
CLASSIFICATION
GESTATIONAL DIABETES
RISK FACTORS
DIAGNOSIS
COMPLICATIONS
MEDICAL TEST
MEDICAL NUTRITIONAL THERAPY
HERBS FOR DIABETES
MYTHS AND FACTS
REFERENCES
The term ‘diabetes’ means excessive urination and the word ‘mellitus’ means honey.
Diabetes mellitus is a lifelong condition caused by a lack, or insufficiency of insulin. Insulin is a hormone – a substance of vital importance that is made by your pancreas. Insulin acts like a key to open the doors into your cells, letting sugar (glucose) in. In diabetes, the pancreas makes too little insulin to enable all the sugar in your blood to get into your muscle and other cells to produce energy. If sugar can’t get into the cells to be used, it builds up in the bloodstream. Therefore, diabetes is characterized by high blood sugar (glucose) levels.
SIGNIFICANCE
OVERVIEW
WHAT IS DIABETES?
DEFINITION
MECHANISM
PREVELANCE
EPIDEMIOLOGY
CLASSIFICATION
GESTATIONAL DIABETES
RISK FACTORS
DIAGNOSIS
COMPLICATIONS
MEDICAL TEST
MEDICAL NUTRITIONAL THERAPY
HERBS FOR DIABETES
MYTHS AND FACTS
REFERENCES
The term ‘diabetes’ means excessive urination and the word ‘mellitus’ means honey.
Diabetes mellitus is a lifelong condition caused by a lack, or insufficiency of insulin. Insulin is a hormone – a substance of vital importance that is made by your pancreas. Insulin acts like a key to open the doors into your cells, letting sugar (glucose) in. In diabetes, the pancreas makes too little insulin to enable all the sugar in your blood to get into your muscle and other cells to produce energy. If sugar can’t get into the cells to be used, it builds up in the bloodstream. Therefore, diabetes is characterized by high blood sugar (glucose) levels.
Learning objectives:
Understand the definition, causes, symptoms, risk factors of type 1 Diabetes.
Understand the definition, causes, symptoms, risk factors of type 2 Diabetes.
Understand the definition, causes, symptoms of Gestational Diabetes.
Diabetes Mellitus Complete (Introduction, Pathophysiology, Types, Diagnostic Tests, Treatment, Insulin, Prevention)
Table of Contents
Introduction
Normal Physiology
Pathophysiology
Types of Diabetes
Type 1 Diabetes
Type 2 Diabetes
Difference
Common Symptoms
How does diabetes transmit?
Diagnostic Tests for Checking Diabetes
Management of Diabetes
Treatment Strategies of Diabetes
Oral Hypoglycaemic Agents
Insulin & Insulin Analogues
Insulin preparation and Treatment
Prevention
This presentation is about the introduction to Diabetes Mellitus. This lifestyle disease has become common in the current generation. This presentation is about diabetes, its classification, the definition of DM, individual types with causes, events, changes, symptoms and treatments.
Definition of diabetes - introduction - classification of diabetes - etiology of diabetes type 1 and type 2- risk factors for diabetes - diagnosis of diabetes - clinical manifestations of diabetes type 1 and type 2- investigations for diabetes - treatment of diabetes - non-pharmacological treatment and pharmacological treatment - pharmacotherapy of type 1 and type 2 - acute complications of diabetes and treatment
Learning objectives:
Understand the definition, causes, symptoms, risk factors of type 1 Diabetes.
Understand the definition, causes, symptoms, risk factors of type 2 Diabetes.
Understand the definition, causes, symptoms of Gestational Diabetes.
Diabetes Mellitus Complete (Introduction, Pathophysiology, Types, Diagnostic Tests, Treatment, Insulin, Prevention)
Table of Contents
Introduction
Normal Physiology
Pathophysiology
Types of Diabetes
Type 1 Diabetes
Type 2 Diabetes
Difference
Common Symptoms
How does diabetes transmit?
Diagnostic Tests for Checking Diabetes
Management of Diabetes
Treatment Strategies of Diabetes
Oral Hypoglycaemic Agents
Insulin & Insulin Analogues
Insulin preparation and Treatment
Prevention
This presentation is about the introduction to Diabetes Mellitus. This lifestyle disease has become common in the current generation. This presentation is about diabetes, its classification, the definition of DM, individual types with causes, events, changes, symptoms and treatments.
Definition of diabetes - introduction - classification of diabetes - etiology of diabetes type 1 and type 2- risk factors for diabetes - diagnosis of diabetes - clinical manifestations of diabetes type 1 and type 2- investigations for diabetes - treatment of diabetes - non-pharmacological treatment and pharmacological treatment - pharmacotherapy of type 1 and type 2 - acute complications of diabetes and treatment
Diabetes mellitus (DM) is a group of diseases characterized by high levels of blood glucose resulting from defects in insulin production, insulin action, or both.
The term diabetes mellitus describes a metabolic disorder of multiple aetiology characterized by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both.
The effects of diabetes mellitus include long–term damage, dysfunction and failure of various organs.
Diabetes mellitus refers to a group of diseases that affect how your body uses blood sugar (glucose). Glucose is vital to your health because it's an important source of energy for the cells that make up your muscles and tissues. It's also your brain's main source of fuel.
With diabetes, your body doesn’t make enough insulin or can’t use it as well as it should. When there isn’t enough insulin or cells stop responding to insulin, too much blood sugar stays in your bloodstream. Over time, that can cause serious health problems, such as heart disease, vision loss, and kidney disease.
Diabetes Mellitus type 1 major comorbidity now days.
Insulin injection being the major treatment Diabetes Mellitus.
Some other drugs used to treat the Diabetes Mellitus are Tablet Metformin 500 mg and other hypoglycemic drugs.
Diabetes Mellitus and Hypertension how they are interlinked.
Diabetes is a disease that occurs when your blood glucose, also called blood sugar, is too high. Blood glucose is your main source of energy and comes from the food you eat. Insulin, a hormone made by the pancreas, helps glucose from food get into your cells to be used for energy. Sometimes your body doesn’t make enough—or any—insulin or doesn’t use insulin well. Glucose then stays in your blood and doesn’t reach your cells.
Diabetes mellitus (DM) is a group of diseases characterized by high levels of blood glucose resulting from defects in insulin production, insulin action, or both.
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
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
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.
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
2. DIABETES MELLITUS
Diabetes mellitus is a chronic disorder of
carbohydrate, protein and fat metabolism resulting
from insulin deficiency or abnormality in the use of
insulin
It results from defects in insulin secretion, insulin
sensitivity, or both.
7. Types
Type 1 Diabetes Mellitus
Type 2 Diabetes Mellitus
Gestational Diabetes
Other types:
LADA (Latent Autoimmune Diabetes in
Adults)
MODY (maturity-onset diabetes of youth)
Secondary Diabetes Mellitus
8. TYPE 1 Diabetes Mellitus
Was previously called insulin-dependent diabetes
mellitus (IDDM) or juvenile-onset diabetes.
Type 1 diabetes develops when the body’s immune system
destroys pancreatic beta cells, the only cells in the body
that make the hormone insulin that regulates blood
glucose.
This form of diabetes usually strikes children and young
adults, although disease onset can occur at any age.
Type 1 diabetes may account for 5% to 10% of all
diagnosed cases of diabetes.
Risk factors for type 1 diabetes may include autoimmune,
genetic, and environmental factors.
9. TYPE 2 DM
Was previously called non-insulin-dependent
diabetes mellitus (NIDDM) or adult-onset diabetes.
Type 2 diabetes may account for about 90% to 95% of
all diagnosed cases of diabetes.
It usually begins as insulin resistance, a disorder in
which the cells do not use insulin properly. As the
need for insulin rises, the pancreas gradually loses its
ability to produce insulin.
10. cont….
Type 2 diabetes is associated with older age, obesity,
family history of diabetes, history of gestational
diabetes, impaired glucose metabolism, physical
inactivity, and race/ethnicity.
Type 2 diabetes is increasingly being diagnosed in
children and adolescents.
13. Gestational diabetes
A form of glucose intolerance that is diagnosed in
some women during pregnancy.
During pregnancy, gestational diabetes requires
treatment to normalize maternal blood glucose levels
to avoid complications in the infant.
After pregnancy, 5% to 10% of women with
gestational diabetes are found to have type 2 diabetes.
Women who have had gestational diabetes have a
20% to 50% chance of developing diabetes in the next
5-10 years.
14. Other types of DM
Other specific types of diabetes result from specific
genetic conditions (such as maturity-onset diabetes of
youth), surgery, drugs, malnutrition, infections, and
other illnesses.
Such types of diabetes may account for 1% to 5% of all
diagnosed cases of diabetes.
LADA (Latent Autoimmune Diabetes in
Adults)
MODY (maturity-onset diabetes of youth)
Secondary Diabetes Mellitus
15. LADA Latent Autoimmune Diabetes in Adults (LADA) is a form of
autoimmune (type 1 diabetes) which is diagnosed in
individuals who are older than the usual age of onset of type 1
diabetes.
About 80% of adults apparently with recently diagnosed Type
2 diabetes but with GAD auto-antibodies (i.e. LADA)
progress to insulin requirement within 6 years.
The potential value of identifying this group at high risk of
progression to insulin dependence includes:
the avoidance of using metformin treatment
the early introduction of insulin therapy
16. MODY (maturity-onset diabetes of youth)
MODY – Maturity Onset Diabetes of the Young
MODY is a monogenic form of diabetes with an
autosomal dominant mode of inheritance:
Mutations in any one of several transcription factors or in
the enzyme glucokinase lead to insufficient insulin release
from pancreatic ß-cells, causing MODY.
Different subtypes of MODY are identified based on the
mutated gene.
Originally, diagnosis of MODY was based on presence of
non-ketotic hyperglycemia in adolescents or young
adults in conjunction with a family history of diabetes.
18. Drug induced hyperglycemia:
Atypical Antipsychotics - Alter receptor binding characteristics,
leading to increased insulin resistance.
Beta-blockers - Inhibit insulin secretion.
Calcium Channel Blockers - Inhibits secretion of insulin by
interfering with cytosolic calcium release.
Corticosteroids - Cause peripheral insulin resistance and
gluconeogensis.
Fluoroquinolones - Inhibits insulin secretion by blocking ATP
sensitive potassium channels.
Naicin - They cause increased insulin resistance due to increased
free fatty acid mobilization.
Phenothiazines - Inhibit insulin secretion.
Protease Inhibitors - Inhibit the conversion of proinsulin to insulin.
Thiazide Diuretics - Inhibit insulin secretion due to hypokalemia.
They also cause increased insulin resistance due to increased free
fatty acid mobilization
21. EPIDEMIOLOGY
Globally, an estimated 422 millon adults are living with
diabetes mellitus, according to the latest 2016 data
from WHO.
Increases in the overall diabetes prevalence rates
largely reflect an increase risk factors for type 2,
notably greater longevity and being overweight or
obese.
22. ETIOLOGY
Chronic hyperglycaemia with disturbances of
carbohydrate
Fat and protein metabolism resulting from defects in
insulin secretion
Insulin action
The effects of diabetes mellitus include long–term
damage, dysfunction and failure of various organs.
25. Signs & Symptoms
Increased thirst (polydipsia)
Frequent urination (polyuria)
Hunger (polyphagia)
Fatigue
Blurred vision
Numbness or tingling in the feet or hands
Unexplained weight loss
Increase blood sugar/glucose level
26. Management
Dietary management:
Don’t skip meals
Measure food accurately, do not estimate
Less added fat, fewer fatty foods and low
cholesterol.
Advise use of complex carbohydrates to help
stabilize blood sugar. Meal should include
more fibre and starch and fewer simple or
refined sugars.
Avoid concentrated sweets, high in sugar
(jellies, jams, cakes, ice creams)
27. cont….
If taking insulin, eat extra food before periods of
vigorous exercise.
Keep weight at normal level, obese diabetics should be
on a strict weight control program and should lose
weight.