- Insulin is a hormone produced by the pancreas that regulates carbohydrate and fat metabolism. It enables glucose absorption from the blood into liver, muscle, and fat cells.
- Diabetes occurs when the body does not produce enough insulin or the cells ignore insulin signals, resulting in high blood glucose levels. Long term complications include damage to organs like the eyes, kidneys, heart, and nerves.
- Insulin binds to receptors on cells and triggers processes that promote glucose and fat uptake and storage while inhibiting glucose and fat release. It has many effects including stimulating glycogen, protein, and lipid synthesis while inhibiting gluconeogenesis, glycogenolysis and lipolysis.
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
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
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
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
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
A complete knowledge about Diabetes Mellitus and its types including Type 1 Diabetes, Type 2 diabetes, gestational diabetes, pancreatic diabetes & monogenic diabetes along with clinical features, investigations and management
It also includes diabetic emergencies like Diabetic Ketoacidosis, Hyperglycaemic hyperosmolar state & hypoglycaemia.
It contains long term complications like neuropathy, nephropathy and retinopathy.
Lastly Diabetic Insipidus is also discussed here.
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.
Diabetes Mellitus
Introduction
Pathophysiology
Types of Diabetes Mellitus
Type 1, 2 and
gestational diabetes
rescent research in Type 1 diabetes
Risk factors and causes
Complications short term and long term of diabetes
Management
Treatment with Insulin
Diabetic drugs
Healthy Diet
Exercises prescription
aerobic exercises,
resistance exercises and
flexibility
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.
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
A complete knowledge about Diabetes Mellitus and its types including Type 1 Diabetes, Type 2 diabetes, gestational diabetes, pancreatic diabetes & monogenic diabetes along with clinical features, investigations and management
It also includes diabetic emergencies like Diabetic Ketoacidosis, Hyperglycaemic hyperosmolar state & hypoglycaemia.
It contains long term complications like neuropathy, nephropathy and retinopathy.
Lastly Diabetic Insipidus is also discussed here.
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.
Diabetes Mellitus
Introduction
Pathophysiology
Types of Diabetes Mellitus
Type 1, 2 and
gestational diabetes
rescent research in Type 1 diabetes
Risk factors and causes
Complications short term and long term of diabetes
Management
Treatment with Insulin
Diabetic drugs
Healthy Diet
Exercises prescription
aerobic exercises,
resistance exercises and
flexibility
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.
Pancreatic hormone - Endocrinology for biochemistryASHA SIVAJI
Pancreatic hormone - In this you will know about synthesis, metabolism, mode of action, biological actions, regulation and disorders related with insulin,Glucagon, Pancreatic somatostatin and pancreatic polypeptide.
Insulin is a peptide hormone, produced by beta cells of the pancreas, and is central to regulating carbohydrate and fat metabolism in the body. Insulin causes cells in the liver, skeletal muscles, and fat tissue to absorb glucose from the blood. In the liver and skeletal muscles, glucose is stored as glycogen, and in fat cells (adipocytes) it is stored as triglycerides.
Hormones of pancreas (The Guyton and Hall physiology Maryam Fida (o-1827))Maryam Fida
Pancreas is composed of two major types of tissues.
1. The Acini: which secrete digestive juices into the duodenum.
2. The islets of Langerhans: Contain three major types of cells INSULINMetabolized by the enzyme Insulinase (present mainly in the liver, kidneys and muscles).
Insulin is a small protein, it is composed of two amino acid chains connected to each otherby disulfide linkages. When the two amino acid chainsare split apart, the functional activity of the insulinmolecule is lost.
Insulin is synthesized in the beta cells.
Diabetes Mellitus
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.
These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Excess of hyperglycemic hormones (glucagon, ete. ) obesity: ; cause relative insulin deficiency the β cells Tag behind
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.
These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Insulin is synthesized in the β cells of pancreatic islets as a single chain peptide Preproinsulin (110 AA) from whic
Advances in current medication and new therapeutic approaches in epilepsySelf-employed researcher
Epilepsy is one of the most complicated neurological disorders associated with a brain disorder in which, after an initial
physiological insult, the networks of neurons regroup and communicate abnormally that can be defined as the neuronal hyper -
synchronizayion. The affected part of brain defines the patient’s abnormality behavior. Unlike the younger patients, who can
become seizure free after the age of 16-18, older patients are hardly able to overcome the seizures, especially once the type of
seizure developed to generalize tonic-clonic phase. Globally, epilepsy is considered as a disease which is originated from the
disorder of electrical function of the brain and estimated to effect approximately 50 million people worldwide.
Pharmacoresistance, drug interactions, drug tolerability, and various adverse effects are among the common problems
associated with the treatments of epilepsy with antiepileptic drugs (AEDs). Although, approximately 70% of the patient's
exhibit seizures that can be controlled with most AEDs, the remaining 30% of the patients fail to respond to treatment with
AEDs. Thus, looking for alternatives such as traditional treatment methods like utilizing medicinal plants, ketogenic diet, and
the Atkins diet as well as self-physical therapy like relaxation and yoga, are all positive options that can be considered as
a replacement and supportive therapy methods for the medications which are used in seizure control of epilepsy. Medicinal
plants are more commonly used by folk for making infusions administered as herbal teas for the pain relief and maintaining
good health. Investigating the active components of a plant extract, isolating and identifying their structure and
pharmacological effects, and finally utilizing them as a new agent from nature with fewer side effects and high economic value
is a widely interesting topic in the field of ethnopharmacology. In addition to AEDs, which are currently used, the suggested
alternative therapies are also able minimize the seizures of epilepsy but the surgical intervention still remains as the last option
in the treatment of epilepsy.
Phytochemical Profile and in vitro and in vivo Anticonvulsant and Antioxidant...Self-employed researcher
This study presents the phytochemical profile and in vitro and in
vivo anticonvulsant and antioxidant activities of Epilobium hirsutum, which
has been traditionally used in the treatment of epilepsy by local people of
Turkey. In vitro studies revealed that the extract contained a pronounced
amount of phenolics (206.3±0.9 mg Gallic acid Eq/g extract) and exhibited
significant levels of antioxidant (FRAP; 6226 µmol Fe2+/g extract, ORAC;
6593 µmol Trolox Eq/g extract, DPPH; IC50:33.8 ug/mL and metal chelation;
IC50:114 ug/mL) and anticonvulsant (AChE; IC50:71.2 ug/mL, BChE; IC50:92.5
ug/mL, GABA-T; IC50:94.7 ug/mL) activities. In vivo studies shown that the
the extract exhibited high anticonvulsant activities. In addition, the extracts
regulated the behavior, locomotion, and mental activities of the mice tested.
Biochemical evaluation of the brain tissue revealed that the extract inhibited
the production of MDA and stimulated the increase of antioxidant enzyme
levels, which suggest the possible antioxidative role of the extract that worked
as neuroprotective agents by scarfing the free radicals produced through PTZ
seizure inducer and attenuate convulsions. Moreover the extract regulated
serum biochemical parameters, total antioxidants, total oxidant, and ischemia modified albumin levels. Chromatographic studies were revealed that gallic
acid principally might be the major contributor of anticonvulsant and
antioxidant activities with the additive contributions of fatty acids and mineral
compounds. Findings obtained from this study partially justified the traditional
use of Epilobium hirsutum in the treatment of epilepsy and suggest potential
use of the extract as an industrial or pharmaceutical agent.
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.
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
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
- 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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
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
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.
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
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.
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.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
2. • Diabetes mellitus derived from Greek word for fountain
and the latin word from honey.
• when hyperglycemia increase it lead to polyuria,
ploydipsia, ketonuria, and weigth loss. Over time can lead
to hypertension, heart disease, renal failur, blindness
neurophathy, stroke.
3. INTRODUCTION:
Insulin is a peptide hormone, produced by beta cells
of the pancreas, and is central to regulating
carbohydrate and fat metabolism in the body. Insulin
causes cells in the liver, skeletal muscles, and fat
tissue to absorb glucose from the blood. In the liver
and skeletal muscles, glucose is stored as glycogen,
and in fat cells (adipocytes) it is stored as
triglycerides. When control of insulin levels fails,
diabetes mellitus can result. As a consequence,
insulin is used medically to treat some forms of
diabetes mellitus.
6. Insulin
The insulin plays an important role in storing the
excess energy. In the case of excess
carbohydrates, it causes them to be stored as
glycogen mainly in the liver and muscles.
All the excess carbohydrates that cannot be stored
as glycogen are converted under the stimulus of
insulin into fats and stored in the adipose tissue.
7. Insulin
In the case of proteins, insulin has a direct effect in
promoting amino acid uptake by cells and
conversion of these amino acids into protein.
In addition, it inhibits the breakdown of the
proteins that are already in the cells.
Anabolic
8.
9. STRUCTURE OF INSULIN
v Human insulin consists of 51aa in
two chains connected by 2 disulfide
bridges (a single gene product
cleaved into 2 chains during post-
translational modification).
v T1/2~5-10 minutes, degraded by
Glutathione-insulin
transhydrogenase (insulinase)
which cleaves the disulfide links.
v Bovine insulin differs by 3aa,
pork insulin differs by 1aa.
v Insulin is stored in a complex
with Zn2+ions.
10. BIOSYNTHESIS OF INSULIN:
Insulin is synthesized as
proinsulin in pancreatic β-
cells. It contains a signal
peptide which directs the
nascent polypeptide chain to
the rough endoplasmic
reticulum. Then it is cleaved
as the polypeptide is
translocated into lumen of
the RER, forming proinsulin.
Proinsulin is transported to
the trans-Golgi network
(TGN) where immature
granules are formed.
Proinsulin undergoes
maturation into active
insulin through action of
cellular endopeptidases
known as prohormone
convertases (PC1 and PC2),
as well as the exoprotease
carboxypeptidase E. The
endopeptidases cleave at 2
positions, releasing a
fragment called the C-
peptide, and leaving 2
peptide chains, the B- and A
- chains, linked by 2
disulfide bonds. The
cleavage sites are each
located after a pair of basic
residues and after cleavage
these 2 pairs of basic
residues are removed by
the carboxypeptidase. The C
-peptide is the central
portion of proinsulin, and
the primary sequence of
proinsulin goes in the order
"B-C-A”
The resulting mature insulin
is packaged inside mature
granules waiting for
metabolic signals (such as
leucine, arginine, glucose
and mannose) and vagal
nerve stimulation to be
exocytosed from the cell into
11. EFFECT OF INSULIN ON GLUCOSE UPTAKE AND
METABOLISM
Insulin binds
to its
receptor
Starts many
protein
activation
cascades
glycogen
synthesis
These include
translocation of
Glut-4 transporter
to the plasma
membrane and
influx of glucose
glycolysis triglyceride
12. Insulin release
qwhen Glucose get bind to
the receptor and cause.
qThis lead to increase ATP
which close ATP
depended K+ channel and
open Ca+ valtage ligant by
depolarization of the
membrane.
qAs the concentration of
Ca+ increase in to
intracelular
Cause insulin resale from
the granules
13. MOA
Insulin acts on specific receptors located on the cell
membrane of practically every cell, but their density
depends on the cell type: liver and fat cells are very
rich.
The insulin receptor is a combination of four subunits
held together by disulfide linkages:
Two alpha subunits that lie entirely outside the cell
membrane
Two beta subunits that penetrate through the
membrane, protruding into the cell cytoplasm
14.
15. metoblism
Insulin binds with alpha
↓
beta unit autophosphorylated
↓
tyrosine kinase
↓
phosphorylation of multiple other intracellular
enzymes including a group called
insulin-receptor substrates (IRS)
16. MECHANISM OF ACTION of the receptor :
v The insulin receptor is a receptor
tyrosine kinase (RTK) . Consisting of 2
extracellular α and 2 transmembrane β
subunits linked together by disulfide
bonds, orienting across the cell
membrane as a heterodimer
v It is oriented across the cell membrane
as a heterodimer.
v The α subunits carry insulin binding
sites, while the β subunits have tyrosine
kinase activity.
17. MECHANISM OF ACTION:
qAfter insulin bend to the
receptor by Alpha subunit and
influence B sub unit to cause
mutation and phosphorlation of
tyrosin kinase to the active form
which direcated to the
cytoplasmic protien of (IRS) inslin
receptor substrate
qIRS bind to other active kinase
(phosphatidylionsitol-3- kinase as
reasult transation of Glucose
transport
(GLUT4) to the cell membran and
result increase glucose up take
18.
19. DEGRADATION OF INSULIN:
The internalized receptor-insulin complex is
either degraded intercellularly or returned
back to the surface from where the insulin is
released extracellularly. The relative
preponderance of these two processes differs
among different tissues: maximum
degradation occurs in liver, least in vascular
endothelium.
20. FATE OF INSULIN
▲ Insulin is distributed only extracellularly. It is a peptide; gets
degraded in the g.i.t. if given orally.
▲ Injected insulin or that released from the pancreas is metabolized
primarily in liver and to a smaller extent in kidney and muscles.
▲ Nearly half of the insulin entering portal vein from pancreas is
inactivated in the first passage through liver.
▲ Thus, normally liver is exposed to a much higher concentration (4-8
fold) of insulin than other tissues.
▲ During biotransformation the disulfide bonds are reduced- A and B
chains are separated. These are further broken down to the constituent
amino acids
22. Diabetes
• People who do not produce the necessary amount
of insulin have diabetes. There are two general
types of diabetes.
– The most severe type, known as Type I or
juvenile-onset diabetes, is when the body does
not produce any insulin. Due to immune
response,ketoacidosis more comman
–Type II diabetics produce some insulin, but it is
either not enough or their cells do not respond
normally to insulin. This usually occurs in obese
or middle aged and older people.
–Gestation diabitese :in pregnancy (metformin)
–Prediabetes : (FPG 100-125) LEAD TO TYPEII
23. Diabetes complication
Short complication
• Hyperglacymia
• Hypoglacymia
Long complication
• Macrovascular :-
(hypertention – heart falier and
stock)
• Microvascular Damage
v Retinopathy
v Nephropathy
v Sensory and motor neuropathy
v Autonomic
neuropathy(Gastroparesis)
v Amputation secondary infection
v Erectile dysfunction
24. Carbohydrate Metabolism – Muscle
Immediately after a high-carbohydrate meal, the glucose that is absorbed
into the blood causes rapid secretion of insulin
The normal resting muscle membrane is only slightly permeable to glucose,
except when the muscle fiber is stimulated by insulin – so during much of the
day, muscle tissue depends not on glucose for its energy but on fatty acids
Moderate or heavy exercise – exercising muscle fibers become more
permeable to glucose even in the absence of insulin
Few hours after a meal because of insulin – Glucose stored as muscle
GLYCOGEN – used during anaerobic exercise
25. Carbohydrate Metabolism - Liver
Glucose absorbed after a meal to be stored almost immediately in the liver
in the form of glycogen - Between meals – liver glycogen – glucose.
1. Insulin inactivates liver phosphorylase - enzyme that causes liver
glycogen to split into glucose. This prevents breakdown of the glycogen
that has been stored in the liver cells.
2. It increases the activity of the enzyme glucokinase, which is one of the
enzymes that causes the initial phosphorylation of glucose after it diffuses
into the liver cells - phosphorylated glucose cannot diffuse back through
the cell membrane.
26. Carbohydrate Metabolism - Liver
3. Insulin also increases the activities of the enzymes that
promote glycogen synthesis, including glycogen synthase -
polymerization of the monosaccharide units to form the
glycogen
4. Enzyme glucose phosphatase inhibited
5. Glycolysis (oxidation of glucose) is increased in muscle &
liver by activating enzyme phosphofructokinase
27. Carbohydrate Metabolism - Liver
Glucose Is Released from the Liver Between Meals
1. The decreasing blood glucose causes the pancreas to decrease its insulin
secretion.
2. Stopping further synthesis of glycogen in the liver and preventing
further uptake of glucose by the liver from the blood.
3. The lack of insulin along with increase of glucagon, activates the
enzyme phosphorylase, which causes the splitting of glycogen into glucose
phosphate.
4. The enzyme glucose phosphatase, becomes activated by the insulin lack
and causes the phosphate radical to split away from the glucose
28. Carbohydrate Metabolism
When the quantity of glucose entering the liver cells is more than can
be stored as glycogen, insulin promotes the conversion of all this
excess glucose into fatty acids – triglycerides in VLDL - adipose tissue
and deposited as fat
Insulin also inhibits gluconeogenesis & glycogenolysis. Thus inhibiting
glucose production
Insulin decreases the release of amino acids from muscle and other
extrahepatic tissues and in turn the availability of these necessary
precursors required for gluconeogenesis
29. Fat Metabolism - Liver
Insulin increases the utilization of glucose by most of the body’s tissues
– fat sparer.
Promotes fatty acid synthesis in liver from excess glucose
1. Insulin increases the transport of glucose into the liver cells –
extra glucose via glycolytic pathway – pyruvate – acetyl CoA –
fatty acids
2. Energy from glucose via citric acid cycle - excess of citrate and
isocitrate ions - activates acetyl CoA carboxylase – acetyl CoA to
form malonyl CoA
30. Fat Metabolism – Adipose Tissue
Fat storage in adipose tissue
1. Fatty acids (triglycerides) are then transported from the
liver by way of the blood lipoproteins to the adipose cells.
2. Insulin activates lipoprotein lipase - splits the triglycerides
again into fatty acids, a requirement for them to be absorbed
into the adipose cells - again converted to triglycerides and
stored
31. Fat Metabolism – Adipose Tissue
- Insulin promotes glucose transport through the cell membrane
into the fat cells - large quantities of alpha glycerol phosphate
- supplies the glycerol that combines with fatty acids to form
the triglycerides
- Insulin inhibits the action of hormone-sensitive lipase – no
hydrolysis of the triglycerides stored in the fat cells - release
of fatty acids from the adipose tissue into the circulating blood
is inhibited
32. Fat Metabolism
Insulin deficiency - free fatty acid becomes the main energy
substrate used by essentially all tissues of the body besides the
brain – ketoacidosis – coma, death
The excess of fatty acids in the plasma also promotes liver
conversion of some of the fatty acids into phospholipids and
cholesterol - atherosclerosis
33. Protein Metabolism and Growth
1. Insulin stimulates transport of many of the amino acids into the
cells
2. Insulin increases the rate of transcription of selected DNA genetic
sequences
3. Insulin increases the translation of mRNA
4. Insulin inhibits the catabolism of proteins
5. In the liver, insulin depresses the rate of gluconeogenesis - conserves
the amino acids in the protein stores of the body
Insulin deficiency – enhanced urea excretion in the urine - protein wasting
– weakness
Insulin and Growth Hormone Interact Synergistically to Promote
Growth
35. Effects of insulin on various tissues
Adipose issue
Increased glucose entry
Increased fatty acid synthesis
Increased glycerol phosphate synthesis
Increased triglyceride deposition
Activation of lipoprotein lipase
Inhibition of hormone-sensitive lipase
Increased K+ uptake
Muscle
Increased glucose entry
Increased glycogen synthesis
Increased amino acid uptake
Increased protein synthesis in ribosomes
Decreased protein catabolism
Decreased release of gluconeogenic amino acids
Increased K+ uptake
36. Effects of insulin on various tissues
Liver
Decreased ketogenesis
Increased protein synthesis
Increased lipid synthesis
Decreased gluconeogenesis
Increased glycogen synthesis
General
Increased cell growth
37. Insulin also increase in the secretion of HCL
by parietal cells in the stomach via vagus
nerve
Insulin test is done to check whether
vagotomy is complete or not, as in case of
treatment of peptic ulcer
38.
39. Fasting level of blood glucose of 80 to 90 mg/100
ml, the rate of insulin secretion is minimal — 25
ng/kg of body weight per minute
41. DIABETES MELLITUS
Insulin is effective in all
forms of diabetes mellitus
and is a must for type 1
cases, as well as for post
pancreatectomy diabetes
and gestational diabetes.
Many type 2 cases can be
controlled.
Insulin therapy is generally
started with regular insulin
given s.c. before each major
meal. The requirement is
assessed by testing urine or
blood glucose levels .
DIABETIC KETOACIDOSIS
(DIABETIC COMA)
Regular insulin is used
to rapidly correct the
metabolic
abnormalities.
Usually within 4-6 hours
blood glucose reaches 300
mg/dl. Then the rate of
infusion is reduced to 2-3
U/hr
HYPEROSMOLAR
(NONKINETIC
HYPERGLYCAEMIC COMA)
This usually occurs in
elderly type 2 cases. The
cause is obscure.
The general principles of
treatment are the same as
for ketoacidotic coma, except
that faster fluid replacement
is to be instituted as alkali is
usually not required.
CONCLUSION: