Minimal Change Disease (MCD), also known as Minimal Change Nephropathy, is a kidney disorder characterized by diffuse effacement and loss of foot processes in the glomeruli seen on electron microscopy. It is the most common cause of nephrotic syndrome in children aged 1-7 years and accounts for about 90% of cases. Boys are more commonly affected than girls. MCD is thought to be caused by an abnormal immune response involving T-cells and cytokines that damages the glomerular filtration barrier. This results in proteinuria but no significant pathology on light microscopy. The clinical features include nephrotic syndrome. The prognosis is generally good as over 90% will respond to corticosteroid therapy
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Brief explanation of each *refer harrison textbook for details causes of TIN
Acute interstitial nephritis
Chronic interstitial nephritis
Reflux nephropathy
Papillary necrosis
Sickle-cell nephropathy
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
Brief explanation of each *refer harrison textbook for details causes of TIN
Acute interstitial nephritis
Chronic interstitial nephritis
Reflux nephropathy
Papillary necrosis
Sickle-cell nephropathy
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
Pharmacoeconomics is a branch of health economics which compares the value of one drug or a drug therapy to another.
By understanding the principles, methods, and application of pharmacoeconomics, healthcare professionals will be prepared to make better decisions regarding the use of pharmaceutical products and services.
This is my first presentation friends, it was my project and I selected this topic and this was my presentation, I hope it will be informative for all of you.
I am in T.Y.B.pharmacy, MGV's College of Pharmacy, Nashik.
If there is any mistake or any problem in this presentation, please let me know......, thank you.
most of the glomerular diseases , either primary or secondary..touching all the aspects including light microscopy, electron microscopy and immunoflourescence.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Hemophagocytic lymphohistiocytosis (hlh), Langerhans cell histiocytosis dr vi...Vijitha A S
Hemophagocytic lymphohistiocytosis (hlh)
Langerhans cell histiocytosis,Benign proliferation of mature histiocytes and uncontrolled phagocytosis of the platelet, erythrocytes, lymphocytes, and their hematopoietic precursors in the bonemarrow & other tissues
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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.
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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
- 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
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.
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.
1. Minimal Change Disease/
Minimal Change Nephropathy
• Minimal change disease (MCD), also
known as
• Minimal Change Nephropathy
• lipoid nephrosis
• nil lesions or
• nil disease.
2. Minimal Change Disease/
Minimal Change Nephropathy
• Minimal change disease (MCD), also
known as
• Minimal Change Nephropathy
• lipoid nephrosis
• nil lesions or
• nil disease.
3. MCD
It refers to a histopathologic lesion in
the glomerulus that almost
always is associated with
nephrotic syndrome.
4. Lipoid Nephrosis
• The term lipoid nephrosis was used to
describe the finding of lipids in the
renal tubular cells
• as well as lipid-laden proximal tubular cells
or macrophages known as oval fat
bodies
in the urine.
5. Epidemiology
• Age: 1-7y (90%) & >80y
• Adults (10-15%)
• Teenager: 50% NS due to MCD
• Sex: Boys> Girls
• Association with Autoimmune disorders
• Association with Hematologic malignancies
6. Epidemiology
• Minimal Change Disease is most common in
very young children but can occur in older
children and adults (10-15%). It is by far the
most common cause of nephrotic syndrome
(NS) in children between the ages of 1 and 7,
accounting for the majority (about 90%) of
these diagnoses.
8. Epidemiology of MCD
Among children less than 10 years of age, boys
seem to be more likely to develop minimal
change disease than girls. Minimal change
disease is being seen with increasing
frequency in adults over the age of 80.
9. Epidemiology
• People with one or more autoimmune
disorders are at increased risk of developing
minimal change disease.
• Having minimal change disease also increases
the chances of developing other autoimmune
disorders.
10. Epidemiology of Lipoid Nephrosis
• MCD is associated with malignancies,
particularly hematologic malignancies,
such as Hodgkin’s disease, non-Hodgkin
lymphomas, or leukemias.
• Colorectal cancer-associated MCD is
uncommon and has been reported in only a
few cases to date.
11. Causes- Idiopathic
The cause is unknown, but the disease may
occur after or be related to:
• Allergic reaction (autoimmune etiology)
• Medication such as NSAID
• Tumors (Hematologic tumors)
• Vaccinations
• Viral infections (Such as EBV)
12. Pathology -Idiopathic
The pathology of minimal change disease is
unclear and is currently considered idiopathic
.
The pathology does not appear to involve
complement, immunoglobulins, or immune
complex deposition.
13. Factors which may involve in the Pathogenesis of MCD
• 1. Disorder of T-cell- secretion of cytokines.
• 2. Circulating T cell factor- Hemopexin
• 3. Endothelin 1
• 4. Nephrin
• 5. Dysferlin
• 6. CD 80
• 7.CTLA-4
• 8.PTPRO/ GLEPP1
• 9.HLA-DR 7
• 10. Synaptopodin
14. Mechanism of Nephrotic syndrome
• Rather, an altered cell-mediated immunologic
response the abnormal secretion of lymphokines
(cytokines13,12,4,18) by T cells (T lymphocytes)is
thought to reduce the production of anions in the
glomerular basement membrane, thereby
increasing the glomerular permeability to
serum albumin through a reduction of
electrostatic repulsion.
15. Mechanism of foot processes effacement
It is postulated that MCD is a disorder of T cells,
which release a cytokine (IL-12,4,13,18) that
injures the glomerular epithelial foot processes
podocytes swell up & foot processes effaced. This,
in turn, leads to a decreased synthesis of
polyanions.
Polyanion: a molecule or chemical complex having
negative charges at several sites
16. Pathology (Pathophysiology)
A circulating T-cell factor/permeability factor
(Hemopexin) causes podocyte cytoskeleton
disorganization leading to increased
glomerular capillary permeability and/or
changes (neutralize negative charges of
heparan sulfate) in glomerular basement
membrane heparan sulfate
glycosaminoglycans resulting in
proteinuria.
17. Pathology
•The loss of anionic charges
is also thought to favor
foot process fusion
(effacement).
19. Hemopexin- beta-1B- glycoprotein
• Hemopexin also known as beta-1B-
glycoprotein is a protein that in humans is
encoded by the HPX gene and belongs to
hemopexin family of proteins
20. ARF- Endothelin-1
• In patients who develop acute renal failure,
endothelin 1 (This peptide is a potent vasoconstrictor
and is produced by vascular endothelial cells). expression is
greater in the glomeruli, vessels, and tubules
than in the nonacute renal failure group.
21. Congenital Nephrotic Syndrome & Nephrin
• The glomerular epithelial cells (podocytes)
and the slit diaphragm connecting the
podocyte foot processes play a primary role
in the development of proteinuria.
• Nephrin is a major component of the slit
diaphragm.
22. Congenital Nephrotic
syndrome & Nephrin
• The slit diaphragm is often missing in
MC nephrotic syndrome (MCD) kidneys.
The role of nephrin and the slit diaphragm in
MCD is not known. However, genetic variants
of a glomerular filter protein may play a role
in some patients with MCD.
23. Congenital Nephrotic syndrome & Nephrin
• Nephrin is a protein necessary for the proper
functioning of the renal filtration barrier.
Nephrin is a protein that is a structural
component of the slit diaphragm.
• A defect in the gene for nephrin, NPHS1, is
associated with
congenital nephrotic syndrome and causes
massive amounts of protein to be leaked into
the urine, or proteinuria.
24. Dysferlin
• A lack of glomerular dysferlin
expression is associated with minimal-
change nephropathy.
• Dysferlin also known as dystrophy-associated
fer-1-like protein is a protein that in humans is
encoded by the DYSF gene.
• Dysferlin is linked with skeletal muscle repair.
25. Dysferlin
• A defect in the DYSF gene, located on
chromosome 2p12-14, results in either of two
types of muscular dystrophy;
Miyoshi myopathy (MM) and
Limb-girdle muscular dystrophy type 2B
(LGMD2B).
26. CD 80 (B7-1)
• CD 80, a protein found in B cells and
responsible for T-cell activation, is
found to be increased in patients with
MCD.
27. Minimal change disease: a CD80
podocytopathy
• Recently, increased expression of CD80 (also
termed B7-1) on podocytes was identified as a
mechanism for proteinuria.
• CD80 is inhibited by binding to CTLA-4, which
is expressed on regulatory T cells.
28. CTLA-4 (Cytotoxic T-Lymphocyte Antigen 4), also
known as CD152 (Cluster of differentiation 152), is a
protein receptor that downregulates the immune
system.
• Interleukin-13 or microbial products via Toll-like
receptors could be factors that induceCD80
expression on podocytes.
• CTLA-4 appears to regulate CD80
expression in podocytes, and to be alteredin
minimal change disease patients.
29. CTLA-4 (Cytotoxic T-Lymphocyte Antigen 4)
• Proteinuria in minimal change disease is
caused by persistent CD80 expression in
podocytes,possibly initiated by stimulation of these
cells by antigens or cytokines.
30. Genetics
• Protein tyrosine phosphatase receptor type O
(PTPRO)- also known as
glomerular epithelial protein 1 (GLEPP1)
has been shown to be mutated in a number of
cases.
32. Synaptopodin & Response to Steroids
• Synaptopodin is a proline-rich protein intimately
associated with actin microfilaments present in the
foot processes of podocytes.
Greater synaptopodin expression in podocytes is
associated with a significantly better response to
steroid therapy. Thus, this marker could be used
in the future to help determine appropriate
therapy.
33. Pathology- Morphology
Light Microscopy:
• For years pathologists found no
changes when viewing specimens
under light microscopy; hence the
name minimal change disease/Nil
lesions/Nil disease.
34. Morphology
• Lipoid Nephrosis:
• Cells of the Proximal Tubule are often filled
with lipids but this is probably secondary
to resorption of lipoproteins which are
normally not filtered by a healthy glomerulus
(This is why this disease was originally called
"Lipoid Nephrosis")
36. Pathology- Morphology
• Electron microscopy:
HALLMARKS
1.Diffuse loss of (diffuse & uniform effacement
of) visceral epithelial cells (podocyte) foot
processes,
2.Vacuolation, and
3. Growth of microvilli on the visceral
epithelial cells.
Occasional focal detachments.
41. Prognosis
• Good.
• >90% respond to corticosteroids
• Proteinuria recurs in > 2/3 of cases
• Some of whom become steroid dependent
• < 5% develop CRF after 25 years.