In this presentation I've tried to cover the maximum part related to hematuria in concise way to understand it better. It covers microscopic hematuria, macroscopic hematuria, classification of glomerular and non-glomerular hematuria, hereditary and acquired causes of hematuria with diagrammatic presentation of pathogenesis for all the spectrum.
Blood in urine is known as haematuria. It can be visible or non-visible. There are many causes for this. It is essential to differentiate haematuria from other causes of red colour in urine.
HELLO FRIENDS HERE CAUSES OF HEMATURIA IS HERE MANAGEMENT IN NEXT PRESENTATION ...YOU CAN SEE AND SUBSCRIBE OVER YOU TUBE ...LEARN UROLOGY IS CHANNEL NAME
FOLLOW THE YOU TUBE CHANNEL FOR FUTURE UROLOGY VIDEO
https://www.youtube.com/channel/UCINcUe475Y3c3BvXHvZ8wEw
Blood in urine is known as haematuria. It can be visible or non-visible. There are many causes for this. It is essential to differentiate haematuria from other causes of red colour in urine.
HELLO FRIENDS HERE CAUSES OF HEMATURIA IS HERE MANAGEMENT IN NEXT PRESENTATION ...YOU CAN SEE AND SUBSCRIBE OVER YOU TUBE ...LEARN UROLOGY IS CHANNEL NAME
FOLLOW THE YOU TUBE CHANNEL FOR FUTURE UROLOGY VIDEO
https://www.youtube.com/channel/UCINcUe475Y3c3BvXHvZ8wEw
Hematuria for undergraduates
this is a presentation i prepared for medical students about hematuria, hope u like it
for more urology resources visit:
www.uronotes2012.blogspot.com
Haematuria is RBC in urine. It can be gross haematuria or microscopic haematuria. According to the site affected haematuria can be devided in to glomerular haematuria and non glomerular haematuria. Urinary tract infections, Glomerulonephritis, Systemic lupus erythematosus, Hemorrhagic uremic syndrome, IgA nephropathy, Alport syndrome, Vasculitis, Renal vein thrombosis, Henoch schonlein purpura, Hypercalciuria, Polycystic kidney disease, Bladder carcinoma, Urethral trauma and Inherited diseases like Bleeding disorders, Renal calculi formation, Sickle cell disease can cause haematuria. Investigations help to make a differential diagnosis.
Hematuria for undergraduates
this is a presentation i prepared for medical students about hematuria, hope u like it
for more urology resources visit:
www.uronotes2012.blogspot.com
Haematuria is RBC in urine. It can be gross haematuria or microscopic haematuria. According to the site affected haematuria can be devided in to glomerular haematuria and non glomerular haematuria. Urinary tract infections, Glomerulonephritis, Systemic lupus erythematosus, Hemorrhagic uremic syndrome, IgA nephropathy, Alport syndrome, Vasculitis, Renal vein thrombosis, Henoch schonlein purpura, Hypercalciuria, Polycystic kidney disease, Bladder carcinoma, Urethral trauma and Inherited diseases like Bleeding disorders, Renal calculi formation, Sickle cell disease can cause haematuria. Investigations help to make a differential diagnosis.
Membranous GN
MOST COMMON cause is idiopathic (85%); peak age 30-50; male:female, 2:1
May be secondary to:
Drugs-captopril, penicillamine, gold, mercury, trimethadione, NSAIDS
Infections-malaria (P. malariae), leprosy, schistosomiasis, syphilis, hepatitis B and C, filariasis, hydatid disease and enterococcal endocarditis
Diseases-malignancy (Carcinoma of breast, lung, colon, stomach, and esophagus) melanoma, renal cell CA, SLE, sarcoidosis, diabetes, thyroiditis, sickle cell anemia, Crohn’s disease
Approach to Pancytopenia with cases.pptxYogeetaTanty1
Approach to pancytopenia with case based discussion and brief details regarding each condition. Causes of pancytopenia. Details of congenital causes of aplastic anemia.
This is about glomerulonephritis and all that you need to know. It contains different images illustrating this subject matter, well defined outline, different aspect of glomerulonephritis, which include acute and chronic glomerulonephritis, nephritic and nephrotic syndrome, investigations, how to diagnose glomerulonephritis, treatment and important discussions on Glomerulonephritidis. It is a presentation you need to check out.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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
- 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
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
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
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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.
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
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.
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.
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
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.
2. • Macroscopic (gross) Hematuria
Visible (Red Urine)
• Microscopic Hematuria (AUA)
>3RBC/HPF from two of
three urinary sediments
without a urinary tract
infection, or menstruation on
microscopic evaluation
Definition
4. • any glomerular disease may present with hematuria
• approximately 50% of patients with idiopathic hematuria have a
glomerular disease
• most patients also have other signs such as proteinuria, red cell casts, or
renal insufficiency
• there are three disorders that account for most cases of persistent isolated
hematuria due to glomerular disease: IgA nephropathy, hereditary nephritis
(alport syndrome), and thin basement membrane nephropathy
5. Thin basement membrane disease or
benign familial
hematuria
• Mutations of the type IV collagen genes COL4A3 and COL4A4
• TBMN is often familial, probably with autosomal dominant inheritance
• A family history of hematuria is noted in 30 to 50% of cases
• Persistent or intermittent asymptomatic microscopic hematuria
• The long-term prognosis is excellent in most patients with true thin
basement membrane nephropathy
• We don't biopsy these patients
• Slowly progressive renal insufficiency can occur and is often manifested on
renal biopsy by focal segmental glomerulosclerosis
6. uniform thinning of lamina densa of glomerular basement membrane to 200
nm in > 50% of glomerular capillaries
7. • Inherited progressive form of glomerular disease
• Often associated with sensorineural hearing loss and ocular
abnormalities
• Primary basement membrane disorder arising from mutations in genes
encoding several members of the type IV collagen protein family
• X-linked (80%), Autosomal recessive (15%), Autosomal dominant (5%)
• Initial renal manifestation of Alport syndrome is asymptomatic persistent
microscopic hematuria, which is present in early childhood in affected
patients
• ESRD usually occurs between the ages of 16 and 35 years in patients with X-
linked or autosomal recessive disease and they end up on dialysis
Alport syndrome
10. 4/10 criteria must be met for the diagnosis of Alport syndrome
• Family history of nephritis of unexplained haematuria in a first degree relative of the index case or in a
male relative linked through any numbers of females.
• Persistent haematuria without evidence of another possibly inherited nephropathy such as thin GBM
disease, polycystic kidney disease or IgA nephropathy.
• Bilateral sensorineural hearing loss in the 2000 to 8000 Hz range.
• The hearing loss develops gradually, is not present in early infancy and commonly presents before the age
of 30 years.
• A mutation in COL4A.
• Immunohistochemical evidence of complete or partial lack of the Alport epitope in glomerular, or epidermal
basement membranes, or both.
• Widespread GBM ultrastructural abnormalities, in particular thickening, thinning and splitting.
• Ocular lesions including anterior lenticonus, kerataconus, posterior subcapsular cataract, posterior
polymorphous dystrophy and retinal flecks.
• Macrothrombocytopenia or granulocytic inclusions.
• Diffuse leiomyomatosis of esophagus or female genitalia, or both.
11. Light microscopy shows mesangial cell proliferation and capillary wall thickening,
progressing to glomerular sclerosis and tubulo-interstitial changes
12. This shows glomerular basement membrane changes including splitting of
lamina densa and lamellation
15. • IgA nephropathy is the most common cause primary glomerulonephritis
• 2:1 male to female predominance
• Greatest frequency in Asians and Caucasians
• Relatively rare in blacks
• Negative family history
• See in someone with a recent history of cold or sore throat and then they have
hematuria
• Clinical presentation
• One or recurrent episodes of gross hematuria, usually following an upper respiratory
infection
• Microscopic hematuria and usually mild proteinuria
• Nephrotic syndrome
• Acute rapidly progressive glomerulonephritis
19. Tubulointerstitial changes are mild (periodic acid-Schiff [PAS]) (A) In high-power views, the glomerulus shows a
cellular crescent as well as endocapillary hypercellularity (PAS) (B), diffuse mesangial and endocapillary
hypercellularity (methenamine silver) (C), and subepithelial, 'hump'-like deposits (arrow) (Masson's trichrome) (D).
20.
21.
22. Prognosis
• if you see high proteinuria then it is a bad prognosis. If you see little
proteinuria then there is a good prognosis.
• Patients with IgA nephropathy and little or no proteinuria (<500 mg/day)
have a low risk of progression in the short term.
• Among patients who develop overt proteinuria and/or elevated serum
creatinine concentration, progression to ESRD is approximately 15 to 25
percent at 10 years and 20 to 30 percent at 20 years.
23. Fabry’s disease
• X-linked inherited disorder
• Lysosomal storage disease
• Deficiency of the enzyme alpha galactosidase A
• Dysfunctional metabolism of sphingolipid
• Accumulation of globotriasyceramide in the blood vessels, other tissue and organs.
• Kidney involvement
• Podocytes (abundant)
• Mesangial cells
• Parietal epithelial cells
• Endothelial cells
• Nonspecific late changes reflecting chronic injury
• GBM and TBM changes, mesangial expansion
• Segmental an global glomerular sclerosis (scarring)
• Tubular atrophy and interstitial fibrosis (scarring)
24.
25.
26. disease. (A) Vacuolation of podocytes. (B) Tubular and interstitial deposits. (C)
Deposits in blood vessels. (D) EM: zebra bodies in the cytoplasm of podocytes.