Nephrotic syndrome is characterized by nephrotic range proteinuria, hypoalbuminemia, hyperlipidemia, and edema. It can be primary, caused by diseases limited to the kidney, or secondary, caused by diseases involving other organ systems. Primary causes include minimal change disease, focal segmental glomerulosclerosis, and membranous nephropathy. Management involves treating any underlying causes, controlling edema and hyperlipidemia, and using corticosteroids or other immunosuppressive drugs to induce remission in frequent relapsers or steroid-dependent patients.
Management Of Nephrotic Syndrome
Objectives
To briefly review the definition & etiology of nephroticsyndrome.
To understand the terminology pertaining to clinical course of nephroticsyndrome.
To understand the management of nephroticsyndrome:Specific management & Supportive care and management of complications
Management of congenital nephrotic syndrome
Management Of Nephrotic Syndrome
Objectives
To briefly review the definition & etiology of nephroticsyndrome.
To understand the terminology pertaining to clinical course of nephroticsyndrome.
To understand the management of nephroticsyndrome:Specific management & Supportive care and management of complications
Management of congenital nephrotic syndrome
This presentation was done by Dr. Julius P. Kessy,MD. An intern Doctor at Dodoma Regional Referral Hospital (DRRH) during pediatrics unit clinical meeting and supervised by Dr. Christina K. Galabawa,MD,Mmed2, Pediatrics and Child Health, University of Dodoma (UDOM) in November, 2017.
Nephrotic syndrome is a kidney disorder that causes your body to pass too much protein in your urine. Nephrotic syndrome is usually caused by damage to the clusters of small blood vessels in your kidneys that filter waste and excess water from your blood.
Let's learn the pharmacology related to nephrotic syndrome - features of nephrotic syndrome with underlying mechanisms, objectives of treatment, and management of the nephrotic syndrome.
Glomerulonephritis is inflammation of the tiny filters in your kidneys (glomeruli). Glomeruli remove excess fluid, electrolytes and waste from your bloodstream and pass them into your urine.
Nephrotic syndrome may be caused by primary (idiopathic) renal disease or by a variety of secondary causes. Patients present with marked edema, proteinuria, hypoalbuminemia, and often hyperlipidemia.
Nephrotic syndrome is a primary glomerular disease characterized by the following:
Marked increase in protein in the urine (proteinuria)
Decrease in albumin in the blood (hypoalbuminemia)
Edema (The swelling (edema), can be most noticeable on the face, around the eyes, around the feet and ankles, and in the belly area (or the abdomen).
High serum cholesterol and low-density lipoproteins (hyperlipidemia)
Nephrotic syndrome is a clinical disorder characterized by marked increase of protein in the urine ( proteinuria ), decrease in albumin in the blood (hypoalbuminemia ),edema, & excess lipids in the blood ( hyperlipidemia )
Pathophysiology
Nephrotic syndrome can occur with almost any intrinsic renal disease or systemic disease that affects the glomerulus.
Although generally considered a disorder of childhood, nephrotic syndrome does occur in adults, including the elderly. Causes include:
Chronic glomerulonephritis
Diabetes mellitus with intercapillary glomerulosclerosis
Amyloidosis of the kidney
Systemic lupus erythematosus
Multiple myeloma and renal vein thrombosis.
NSAIDs
Pre eclampsia
This presentation was done by Dr. Julius P. Kessy,MD. An intern Doctor at Dodoma Regional Referral Hospital (DRRH) during pediatrics unit clinical meeting and supervised by Dr. Christina K. Galabawa,MD,Mmed2, Pediatrics and Child Health, University of Dodoma (UDOM) in November, 2017.
Nephrotic syndrome is a kidney disorder that causes your body to pass too much protein in your urine. Nephrotic syndrome is usually caused by damage to the clusters of small blood vessels in your kidneys that filter waste and excess water from your blood.
Let's learn the pharmacology related to nephrotic syndrome - features of nephrotic syndrome with underlying mechanisms, objectives of treatment, and management of the nephrotic syndrome.
Glomerulonephritis is inflammation of the tiny filters in your kidneys (glomeruli). Glomeruli remove excess fluid, electrolytes and waste from your bloodstream and pass them into your urine.
Nephrotic syndrome may be caused by primary (idiopathic) renal disease or by a variety of secondary causes. Patients present with marked edema, proteinuria, hypoalbuminemia, and often hyperlipidemia.
Nephrotic syndrome is a primary glomerular disease characterized by the following:
Marked increase in protein in the urine (proteinuria)
Decrease in albumin in the blood (hypoalbuminemia)
Edema (The swelling (edema), can be most noticeable on the face, around the eyes, around the feet and ankles, and in the belly area (or the abdomen).
High serum cholesterol and low-density lipoproteins (hyperlipidemia)
Nephrotic syndrome is a clinical disorder characterized by marked increase of protein in the urine ( proteinuria ), decrease in albumin in the blood (hypoalbuminemia ),edema, & excess lipids in the blood ( hyperlipidemia )
Pathophysiology
Nephrotic syndrome can occur with almost any intrinsic renal disease or systemic disease that affects the glomerulus.
Although generally considered a disorder of childhood, nephrotic syndrome does occur in adults, including the elderly. Causes include:
Chronic glomerulonephritis
Diabetes mellitus with intercapillary glomerulosclerosis
Amyloidosis of the kidney
Systemic lupus erythematosus
Multiple myeloma and renal vein thrombosis.
NSAIDs
Pre eclampsia
Seminar of Endocarditis by Sudeep,(Pharm.D.)SUDEEP
Presentation of Endocarditis.
Pharmaco therapeutics of disease endocarditis(Inflammation of endocardium).
Definition,causes,etiology,symptoms and treatment of disease.
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.
Nephrotic syndrome, Characterized by heavy proteinuria>3.5g/m/day in adults,>...FarsanaM
Nephrotic syndrome, in paediatric patients(children), mainly Minimal change nephrotic syndrome (MCNS),Characterized by heavy proteinuria>3.5g/m/day in adults,>1g/m/day in children, hypoalbuminemia <2.5g/dL, oedema, hyperlipidemia 200mg/dL, Pathogenesis of MMCNS injury to the glomerular visceral epithelial cell( Podocyte) foot processes
Rapidly progressive glomerulonephritis in childrenNishatTasnim46
Rapidly progressive or crescentic glomerulonephritis is a medical emergency and diagnostic challenge in paediatric population. There is a significant risk of development of complications such as CKD in the long term. This seminar was prepared to increase knowledge about early diagnosis and management of this condition in a tertiary level hospital.
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.
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
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.
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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.
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
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.
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.
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3. Nephrotic Range Proteinuria 24 hour urine..40mg/m2/h…difficult First morning urine sample…protein and creatinine ratio….more than 2-3:1
4. Classification of nephrotic syndrome ETOLOGICAL CLASSIFICATION Primary NEPHROTIC syndrome. Disease limited to kidney Secondary NEPHROTIC syndrome. Other systems involved HISTOLOGICAL CLASISIFICATION MCD FSGN MN MPGN
5.
6. Primary nephrotic syndrome /idiopathic nephrotic syndrome Steroid resistant INS (SRNS) Steroid sensitive IN (SSNS) response to steroids has a high correlation with histological subtype and prognosis
8. PODOCYTE BIOLOGY Effacement of podocytes is now thought to be the primary pathology. -ve charge of the basement membrane is also important.
9. GENETICS. Nephrin Transmembrane protein encoded by NPHS 1 on chromosome 19.(FINISH type congenital NS. Podicin Encoded by NPHS 2 on chromosome 1. Autosomal recessive. Mutations in α-actinin-4, encoded by the gene ACTN4 on chromosome 19 and TRPC6 on chromosome 11, are associated with autosomal dominant forms of FSGS
11. Pathophysiology cont… Decreased plasma oncotic pressure may play a role in increased hepatic lipoprotein synthesis, as demonstrated by the reduction of hyperlipidemia in patients with INS receiving either albumin or dextran infusions Patients with nephrotic syndrome are at increased risk for thrombosis. Abnormalities described in INS include increased platelet activation and aggregation; elevation in factors V, VII, VIII, and XIII and fibrinogen; decreased antithrombin III, proteins C and S, and factors XI and XII; and increased activities of tissue plasminogen activator and plasminogen activator inhibitor-1. Decreased levels of Ig G and increased losses of factor B.
12.
13. INVESTIGATIONS ESTABLISH nephrotic syndrome Nephrotic range proteinuria Hypoalbuminemia Hyperlipidemia Primary or secondary nephrotic syndromes If Primary, Whether in renal failure?.... Renal functions.
14. Investigations Urea creatinine and electrolytes CBC Testing for hep B and C Complement system ANA,Anti double stranded DNA antibodies. Imaging;U/S abdomen and chest. X ray chest. Genetic testing. Renal biopsy
15. INTERPRETATIONS Anemia , raised urea creatinine ,acidosis,hyperkalemia,hyperphosphatemia,indicate Chronic renal disease. Hyponatremia may be due to hyperlipidemia and due to water retention(pseudohyponatremia. Raised Hb and haemetocrat indicates haemodilution.reduced intravascular volume. Platelet is raised. Check liver enzymes..for Hepatitis B and C.and do screening for viruses.
16. MANAGEMENT OF NEPHROTIC SYNDROME A trial of corticosteroids is the first step in treatment of idiopathic nephrotic syndrome (INS) in which kidney biopsy is not initially indicated. patients aged 1-8 years with normal kidney function Normal kidney functions No macroscopic gross haemeturia No symptoms of systemic disease. Normal complement levels Negative viral screen No family hisory.
17. IMPORTANT DEFINITIONS RESPONSE; protein free urine on 3 consecutive days within 7 days. RELAPSE; protein +ve urine on 3 consecutive days within one week with edema. FREQUENT RELAPSING NS; steroid sensitive nephrotic syndrome with 2 or more relapses in 6 months or more than 3 in one year. STEROID DEPENDANT; responder who relapses while steroid is being tapered or within 14 days of stopping steroid treatment.
18. INITIAL NON RESONDER; no response during initial 8 weeks of therapy. LATE NON RESPONDER; an initial steroid responder who fails to respond to 4 week treatment in relapse.
19. SSNS steroid sensitive nephrotic syndrome Corticosteroids INDUCTION THERAPY Exclude active infections and other contraindications to steroids Oral prednisilone 60mg/m2/day…either single or divided doses for 4 weeks. 6 weeks therapy proves better . MAINTAINANCE THERAPY Oral prednisilone at 40mg/m2/day single morning dose at alternate Days for 4-6 weeks. Longer duration of maintenance therapy results in fewer relapses.
20. Relapse therapy For infrequent relapses steroid therapy may be resumed at 60mg/m2/day until proteinuria resolves.. Then switch to 40mg/m2/day for alternate days for 4 weeks. Other therapy Pneumococcal vaccines to all the patients. Diuretic therapy for symptomatic edema. with furosamide 2mg/kg/day. Anasarca with low intravascular volume ,albumin infusion, slow 1mg/kg/day can be considered.
21. HOME MONITORING Home monitoring of urine protein and fluid status is important. Parents should be trained to monitor first morning urine by dipstick. Record of daily weight,urine protein and steroid dose should be kept in log book. Any increase in urine protein or daily weight should be reported as early as possible.
23. DOSING AND REGIMENS Cyclophosphamide (2–2.5 mg/kg daily) is given orally for 8-12 weeks. Steroids are usually overlapped with initiation of CYP then tapered Patients must have weekly CBC counts to monitor for leukopenia. Patients must also maintain adequate hydration and take CYP in the morning (not at bedtime) to limit the risk of hemorrhagic cystitis
24.
25. Deterrence/Prevention Yearly influenza vaccination is recommended to prevent serious illness in the immunocompromised patient, as well as to prevent this possible trigger of relapse. Pneumococcal vaccination should be administered to all patients with INS to reduce the risk of pneumococcal infection. Vaccination should be repeated every 5 years while the patient continues to have relapses. Routine childhood vaccines with live virus strains are contraindicated in patients taking steroids and until off steroid treatment for a minimum of 1 month. Because of the high risk of varicella infection in the immunocompromised patient, in the nonimmune patient, post exposure prophylaxis with varicella-zoster immune globulin is recommended. Patient with varicella-zoster infection should be treated with acyclovir and carefully monitored Routine, nonlive viral vaccines should be administered according to their recommended schedules