it is presented by a MEDICAL STUDENT AT UNIVERSITY OF RWANDA
topic is about pathophysiology mechanisms of glypcerglycemia in causing microvascular complications. it will help medical student to know deep in cascade how high concentration ogf glucose is converted into other substances to affect blood vessels.
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
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 aim of sharing this material to help students and provide delayed information regarding topic.You all are most welcome for you suggestion to make i more easy, graspable and attractive.(easy to learn in creative way)
A review of the investigation and management of diabetic ketoacidosis in newly diagnosed type I diabetes. Patient details have been changed and anonymised to protect the identity of the individual.
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 aim of sharing this material to help students and provide delayed information regarding topic.You all are most welcome for you suggestion to make i more easy, graspable and attractive.(easy to learn in creative way)
pathology and Complications of type 2 diabetes mellitusAiswarya Thomas
explains in detail abou various complications of diabetes mellitus and its pathophysiology. Described about the peripheral, microvascular, macrovascular comlpication
GLYCOGEN STORAGE DISEASE , GSD , Von Gierke DiseaseRAHUL KATARIA
Detailed presentation about glycogen storage disease.
description about all types of GSDs like .
1. GSD I
2.GSD III
3. GSD IV
4. GSD VI
5. GSD IX
6. GSD 0
pathology and Complications of type 2 diabetes mellitusAiswarya Thomas
explains in detail abou various complications of diabetes mellitus and its pathophysiology. Described about the peripheral, microvascular, macrovascular comlpication
GLYCOGEN STORAGE DISEASE , GSD , Von Gierke DiseaseRAHUL KATARIA
Detailed presentation about glycogen storage disease.
description about all types of GSDs like .
1. GSD I
2.GSD III
3. GSD IV
4. GSD VI
5. GSD IX
6. GSD 0
CARBOHYDRATE METABOLISM : GLYCOLYSIS
Glycolysis is the first step in the breakdown of glucose to extract energy for cellular metabolism. Glycolysis consists of an energy-requiring phase followed by an energy-releasing phase.
What is glycolysis?
Glycolysis is a series of reactions that extract energy from glucose by splitting it into two three-carbon molecules called pyruvates. Glycolysis is an ancient metabolic pathway, meaning that it evolved long ago, and it is found in the great majority of organisms alive today^{2,3}
2,3
start superscript, 2, comma, 3, end superscript.
In organisms that perform cellular respiration, glycolysis is the first stage of this process. However, glycolysis doesn’t require oxygen, and many anaerobic organisms—organisms that do not use oxygen—also have this pathway.
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.
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.
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.
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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
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.
- 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
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.
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.
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.
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. Consistent with clinical evidence defining the critical role of
hyperglycemia in microvascular disease.
Data indicate that high intracellular levels of glucose in cells
that cannot down-regulate glucose entry:
endothelium,
glomeruli
nerve cells
3. result in microvascular damage via four
distinct, diabetes-specific pathways that were
sequentially discovered
(1) increased polyol pathway flux
(2) increased formation of advanced glycation end-
product (AGE),
(3) activation of protein kinase C (PKC)
(4) increased hexosamine pathway flux.
4.
5. Overproduction of reactive oxygen species (ROS) in response
to high glucose is thought to:
inhibit glyceraldehyde-3-phosphate dehydrogenase
(GAPDH), thus
increasing the concentration of upstream glycolytic
metabolites that are shunted into alternative pathways.
6. Among these are:
(1) conversion of glucose to sorbitol depletes NADPH, thus
preventing the regeneration of ROS scavengers;
7. (2) conversion of fructose-6-phosphate to uridine
diphosphateN-acetylglucosamine (UDP-GLcNAc) leads to
protein modifications that alter gene expression;
8. (3) glyceraldehyde-3 phosphate is metabolized to
form diacylglycerol (DAG), which in turn activates protein
kinase C (PKC), resulting in altered vascular hemodynamics
9. (4) carbonyls formed by multiple mechanisms, including
oxidation of glyceraldehyde-3 phosphate to form
methylglyoxal, react irreversibly with proteins to form
dysfunctional products (advanced glycosylated end-products,
AGE) that cause intracellular and extracellular vascular
changes.
10. It has been extensively studied in diabetic nerve cells and is also present in
endothelial cells.
Many cells contain aldose reductase, an enzyme that converts
toxic aldehydes to their respective alcohols (polyol pathway).
Aldose reductase has a low affinity for glucose, in case of intercellular
hyperglycemia, this pathway can account for up to one-third of glucose
flux, converting glucose to sorbitol.
11. excess sorbitol was originally thought to cause osmotic damage,
more recent data instead suggest that the real culprit is the
consumption of NADPH during glucose reduction.
NADPH is required to regenerate reduced glutathione (GSH), a
thiol that detoxifies reactive oxygen species, NADPH
consumption prevents the clearance of damaging free radicals.
12. Increased shunting of glucose through the hexosamine
pathway via diversion of the glycolytic intermediate,
fructose- 6-phosphate, is also postulated to play a role in
microvascular disease.
13. The hexosamine pathway contributes
to insulin resistance,
producing substrates that, when covalently linked to
transcription factors, stimulate the expression of proteins,
such as transforming growth factor and plasminogen
activator inhibitor, that enhance microvascular damage.
14. Dicarbonyl formation from direct auto-oxidation of
glucose also contributes to AGE formation
Intracellular endothelial hyperglycemia stimulates
glycolysis and, with this, an increase in the de novo
synthesis of diacylglycerol (DAG) from the glycolytic
intermediate, glyceraldehyde-3-phosphate
DAG, in turn, activates several isoforms of protein
kinase C (PKC) that are present in these cells.
15. This inappropriate activation of PKC alters blood
flow and changes endothelial permeability, in part via
effects on nitric oxide pathways, and also contributes to
thickening of the extracellular matrix.
16. The formation of irreversibly glycated proteins called (AGEs) also causes
microvascular damage in diabetes.
When present in high concentrations:
glucose can react reversibly and nonenzymatically with protein amino groups to
form an unstable intermediate, a Schiff base,
which then undergoes an internal rearrangement to form a more stable glycated
protein, also known as an early glycosylation product (Amadori
product) such as hemoglobin A1c
17. Such a reaction accounts for the formation of glycated HbA, also
known as HbA1c.
In diabetics, elevated glucose leads to increased glycation of
HbA within red blood cells. Because red blood cells circulate
for120 days, measurement of HbA1c in diabetic patients serves
as an index of glycemic control over the preceding months.
18. Early glycosylation products can undergo a further series of
chemical reactions and rearrangements, often involving the
formation of reactive carbonyl intermediates, leading to the
irreversible formation of AGE.
19. Via 3 major pathways:
(1) intracellular AGE formation from proteins involved in transcription
alters endothelial gene expression
(2) irreversible cross linking of AGE adducts formed from matrix proteins
results in vascular thickening and stiffness
(3) binding of extracellular AGE adducts to AGE receptors (RAGE) on
macrophages and endothelium stimulates NF-κB-regulated inflammatory
cascades and resultant vascular dysfunction.
20.
21. The formation of advanced glycosylation end-products (AGEs) occurs via
multiple pathways:
1)The reversible formation of glycated proteins (Amadori products),
such as hemoglobin A1c, through a complex series of chemical reactions, or
2) the direct oxidation of glucose and its metabolites (eg,
glyceraldehyde-3 phosphate, G3P), result in the production of reactive
dicarbonyls.
These moieties react irreversibly with proteins to form AGE.
22. More recent information suggests that increased flux through
these four pathways is induced by a common factor
overproduction of mitochondrial-derived reactive oxygen
species generated by increased flux of glucose through the
TCA cycle
The end result of these changes in the microvasculature is:
1)an increase in protein accumulation in vessel walls,
23. 2) endothelial cell dysfunction,
3) loss of endothelial cells, and,
4) occlusion.
24. Evidence suggests that all four of these pathways may actually
be linked by a common mechanistic element:
Hyperglycemia induced oxidative stress.
In particular, the increase in electron donors that results from
shunting glucose through the tricarboxylic acid cycle
increases mitochondrial membrane potential by pumping
proteins across the mitochondrial inner membrane.
25. This increased potential prolongs the half-life of superoxide
generating enzymes, thus increasing the conversion of O2 to O2–.
These increased reactive oxygen species lead:
to inhibition of the glycolytic enzyme, glyceraldehyde-3phosphate
dehydrogenase (GADPH), and
a resultant increase in upstream metabolites that can now be
preferentially diverted into the four mechanistic pathways
26. Gary D. H., Stephen J. M.Pathophysiology of diseases- An
introduction to clinical medicine, seventh edition. Chapter 18
Disorders of the Endocrine Pancreas, pg 534-538.