An array of presentation of lymphoma spillover in the peripheral smear and bone marrow. All types of lymphomas are discussed along with a bouquet of HPE pictures
An array of presentation of lymphoma spillover in the peripheral smear and bone marrow. All types of lymphomas are discussed along with a bouquet of HPE pictures
Leukemia and lymphoma PATHOLOGY REVISION NOTES TONY SCARIA
PATHOLOGY REVISION NOTES BASED ON HIGH YIELD TOPICS
AND LECTURE NOTES
LEUKEMIA AND LYMPHOMA
HIGH YIELD TOPICS
MEDICINE HEMATOLOGY BASICS
IMAGE BASED QUESTIONS
PERIPHERAL SMEAR
HYPERPARATHYROIDISM
PRIMARY
BROWN TUMOUR
SALT AND PEPPER APPEARANCE OF SKULL
COD FISH SPINE
,
normal calicum metabolism
,
secondary hyperparathyroidism
,
albert hereditary osteodystrophy
,
pseudopseudohypoparathyroidism
,
hypocalcemia
HIGH YIELD
Systemic diseases associated with renal diseaseTONY SCARIA
diabetic nephropathy
leprosy
hepatitis c
hepatitis b
toxoplasmosis
mechanism of diabetic nephropathy
renal disease
medicine
pathology
last minute revision notes
high yield topic
hyaline arteriosclerosis
armanni ebstein cells
papillary necrosis
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.
Hepatobiliary system radiology revision notesTONY SCARIA
hepatobiliary system
hepatic segments
image based questions
last minute revision
radiology radiodiagnosis
hepatic investigations
based image based questions f
hematology revision notes for neet pg aiims pg preparation based on lecture notes
high yield point based on previous year questions
image based questions for neet pg aiims preparation
arthritis
c anca
p anca
SLE
manifestation
treatment
juvenile dermatomyositis
v sign
shawl sign
arthritis
psoriatic arthritis
rheumatoid
rheumatic
arthritis type
synovial fluid
cells
symptoms pathology
treatment
synoc
derna
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
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
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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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.
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
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
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.
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!
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.
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
34. Proteinuria types
•
Overflow
proteinuria
Tubular proteinuria Glomerular
proteinuria
Functional Orthostatic Persistent non
nephrotic
In multiple myeloma • Anxiety
• Stress
Overcomes ability of
proximal tubule to
reabsorb light chains
• <2g/day
• Mostly beta 2
macroglobulin is
lost
• >2g/day
• Mostly albumin
is lost
• Loss of protein
150-500mg
• Proteinurial
alone in standing
position
• <1g/day
• No proteinuria in
lying down
position early
morning sample
–ve
TONY SCARIA 2010
KMC
41. Causes of NS
Systemic causes Glomerular disease
• Diabetes mellitus (most common cause),
SLE, Amyloidosis
• Drugs: Gold, penicillamine probenecid ,
street heroin, captopril, NSAIDs
• Infections: Bacterial endocarditis ,
hepatitis B , shunt infections, syphilis,
malaria
• Malignancy: Hodgkin’s and other
lymphomas leukemia, carcinoma of
breast and GI tract
• Allergic reactions
• 1. Minimal change disease (90% in
children and 15% in adults)
• 2. Membranous (40% in adults)
• 3. Focal segmental glomerulosclerosis
• 4. Membranoproliferative GN
TONY SCARIA 2010
KMC
44. Mc cause of nephrotic syndrome
In children Minimal change disease
In adults focal segmental glomerulosclerosis (FSGS)
In old age Membranous GN
Over all MC cause FSGS
TONY SCARIA 2010
KMC
45. Minimal change ds
• Lipoid nephrosis
• Most common cause of NS in children (2-7yrs)
• Selective proteinuria of albumin frothy urine
• Edema
• Hypertension not a feature
TONY SCARIA 2010
KMC
49. MINIMAL CHANGE DS
• No abnormality on electron
microscopy
• Elctron microscopy
obliteration & fusion of foot
process
• Immunofluroscopy no
immune deposits
• Serum compliment –> normal
level
TONY SCARIA 2010
KMC
51. • Clinical Features-
• Patient usually presents with insidious onset of generalized edema,
without a decrease in urine output.
• Patient may complain of passing frothy urine due to presence of protein.
• Nephrotic syndrome is associated with = ↑LDL, ↑Tg, ↓HDL
• Patient of nephrotic syndrome can develop spontaneous peripheral arterial or
venous thrombosis
• Increased susceptibility to infection
• MC cause is streptococcus pneumoniae followed by E coli
TONY SCARIA 2010
KMC
52. Minimal change ds not associated with
• HTN
• Microhematuria
• AKI
TONY SCARIA 2010
KMC
53. Proteinuria in GN
• Effacement of foot process (Earlier called fusion of foot process) is
believed to play an important role in causes proteinuria in MCD.
• Proteinuria occur due to.
• 1. Loss of negative charge (Loss of polyanions)
• 2. Disruption of components of slit diaphragm (Demonstrated in congenital
nephrotic syndrome of the Finnish type)
• 3. Loss of actin cytoskeleton
TONY SCARIA 2010
KMC
54. Urine in NS
• Lipoid cast (d/t lipiduria)
• Hyaline cast
• NO RBC
• Mlatese cross appearance
lipiduria
TONY SCARIA 2010
KMC
55. Hypercoagulability in NS
• Spontaneous thrombosis of limb arteries
• Renal vein thrombosis
TONY SCARIA 2010
KMC
56. Renal vein thrombosis in NS
• More common in membranous nephropathy
• Present with abdominal pain & haematuria
• Renal vein thrombosis due to
• 1. Increase Fibrinogen
• 2. Increase Lipoproteins
• 3. Reduced antithrombin III &protein C
TONY SCARIA 2010
KMC
57. Renal vein thrombosis
• Trauma
• Extrinsic compression (lymph nodes, aortic aneurysm, tumor)
• Invasion by renal cell carcinoma
• Dehydration (infants)
• Nephrotic syndrome specially membranous GN (adults)
• Pregnancy or oral contraceptives
TONY SCARIA 2010
KMC
60. Congenital NS
Gene Protein Disease Inheritance
NPHS1 Nephrin in slit
diaphragm
Nephrotic syndrome
of finnish type
(FSGS)
AR inheritance 19p13.1
NPHS2 Podocin in slit
diaphragm
Steroid resistant
NS(FSGS)
AR 1q25
FSGS1 α actinin 4 FSGS Dominant 19p13
TONY SCARIA 2010
KMC
61. Complications of NS
• Infections (pneumococcal peritonitis) MC complication
• Hypercholesterolemia (atherosclerosis, xanthomata)
• 'The lipid profile in Nephrotic syndrome is characterized by elevations in total
plasma cholesterol, VLDL and LDL and often (increases in later stages) triglyceride &
reduced HDL.
• Venous thrombosis and pulmonary embolism (urinary loss of antithrombin
III, low plasma volume, increased Fibrinogen)
• Hypovolemia and renal failure
• Loss of specific binding proteins, e.g. transferrin, thyroid binding globulin.TONY SCARIA 2010
KMC
62. Indications for renal biopy in NS
• To r/o causes other than MCNS
• Age <1yr or > 8 yrs
• Adult is less likely to be MCNS mandatory renal biopsy
• Gross hematuria
• HTn
• Renal insufficiency
• Low C3
• Initial steroid resistance
TONY SCARIA 2010
KMC
63. Rx
• Salt restriction < 2g/day
• Protein 1g/kg/day
• Target BP
TONY SCARIA 2010
KMC
66. Minimal change ds progressing to AKI
• Generally no features of AKI
• But can occur if
• Severe hypoalbuminemia pre renal failure
• RVT
TONY SCARIA 2010
KMC
68. Membranous GN
• It is characterized morphologically by the presence of subepithelial
immunoglobulin-containing deposits along the GBM.
• Early in the disease, the glomeruli may appear normal by light
microscopy, but well-developed cases show diffuse thickening of the
capillary wall
TONY SCARIA 2010
KMC
74. Pathogenesis of membranous GN
Primary membranous GN Secondary membranous GN
autoantibodies that cross-react with antigens
expressed by podocytes
Secondary to other systemic ds
Rat model Human model
Ab against megalin Ag
of rat podocyte
heymann nephritis
Ab against PLA2 receptor of
human podocyte
TONY SCARIA 2010
KMC
77. CF of membranous GN
• Massive proteinuria
• Hematuria & HTn in 15-35 % cases
• Patients present with edema, nephrotic proteinuria and high BP.
• Renal insufficiency and abnormal urine sediment may develop later.
• Renal vein thrombosis is common.
TONY SCARIA 2010
KMC
80. FSGS
• sclerosis affecting some but not all glomeruli (focal involvement) and
involving only segments of each affected glomerulus (segmental
involvement)
TONY SCARIA 2010
KMC
82. Focal & segmental involvement of glomeruli
in FSGS
TONY SCARIA 2010
KMC
83. Pathogenesis of FSGS
• injury to the podocytes initiating event of primary FSGS
• Lymphocyte produced factor increasing permeability
• The deposition of hyaline masses in the glomeruli represents the
entrapment of plasma proteins and lipids in foci of injury where
sclerosis develops.
• IgM and complement proteins commonly seen in the lesion are also
believed to result from nonspecifc entrapment in damaged glomeruli
TONY SCARIA 2010
KMC
84. Causes of FSGS
• Idiopathic (majority)
• In associated with systemic diseases or drugs:
• 1. HIV infection
• 2. Diabetes mellitus
• As consequence of sustained glomerular capillary hypertension
• Congenital oligo nephropathies
• Unilateral renal agenesis
• Reflux nephropathy
• Glomerulonephritis or tubulointerstitial nephritis
• Sickle cell nephropathy
• Heroin use
• Congenital Nephrotic syndrome
• NPH1
• NPH2
• FSGS1 autosomal dominant FSGS
• Mutation in TRPC6
TONY SCARIA 2010
KMC
85. Mutated TRPC6 adult onset type FSGS
(increasing Ca2+ influx)
TONY SCARIA 2010
KMC
86. APOL1 gene mutation in FSGS
• apolipoprotein L1 gene (APOL1) on chromosome 22 appears to be
strongly associated with an increased risk of FSGS and renal failure
TONY SCARIA 2010
KMC
87. Histologic variants of FSGS
Collapsing
variant
• Worse
prognosis
Glomerular tip
variant
• Best
prognosis
Perihilar
variant
Cellular
variant
TONY SCARIA 2010
KMC
89. • Light microscopy
• increased mesangial matrix,
obliterated capillary lumina, and
deposition of hyaline masses
(hyalinosis) and lipid droplets.
• Electron microscopy
• podocytes exhibit effacement of foot
processes, as in minimal change
disease
• IF
• Nonspecific trapping of Ig (especially
IgM) & complement(C3) TONY SCARIA 2010
KMC
90. Collapsing variant of FSGS
• Worst prognosis
• It is characterized by collapse of
the glomerular tuft and podocyte
hyperplasia
• associated with HIV infection,
drug-induced toxicities, and some
microvascular injuries
TONY SCARIA 2010
KMC
91. • CF:
• Proteinuria is present and is usually nonselective.
• Hypertension, reduced GFR(arteriolar obliteration by sclerosis),
abnormal tubular function and abnormal urinary sediments
(leukocyturia, hematuria) are seen.
• Hyperlipidemia is severe in cases with focal sclerosis.
TONY SCARIA 2010
KMC
92. Relfux nephropathy & FSGS
• FSGS may develop following acquired loss of nephrons from reflux
nephropathy
• Association of reflux nephropathy and proteinuria suggest an
irreversible glomerular lesion most commonly FSGS
TONY SCARIA 2010
KMC
97. Type 1 (MC SUBTYPE) Type II Type III
Sub endothelial electron dense deposits lamina densa and the subendothelial
space of the GBM
are transformed into an irregular, ribbon-
like, extremely
electron-dense structure, resulting from
the deposition of
material of unknown composition
DENSE DEPOSIT DISEASE
Double contours of GBM & subendothelial
deposits subepithelial deposits
Subendothelial deposits of occasionally
granular epithelial & mesangial Ig
Intramembranous deposition
Activation of classical & alternate pathway Activation of alternate pathway
• Idiopathic
• Bacterial endocarditis
• SLE
• Hepatitis C
• Mixed cryoglobulinemia
• Hepatitis B
• Cancer: Lung, breast, and ovary
(germinal)
• Idiopathic
• C3 nephritic factor–associated
• Partial lipodystrophy
• Idiopathic
• Complement FACTOR deficiency
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100. Type I MPGN
• discrete subendothelial electron-dense deposits
• C3 is deposited in an irregular granular pattern, and IgG and early
complement components (C1q and C4) often are also present,
indicative of an immune complex pathogenesis
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112. Nephritic syndrome
• a/c glomerulonephritis
• Hypertension,
• Hematuria with red cell cast high coloured urine
• non nephrotic Proteinuria
• Normal albumin level
• Azotemia & Oliguria a/w AKI
• RBC cast are present in the urine.
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113. nephritic syndromw
Mc cause in
Children Post streptococcal GN
Adults IgA nephropathy
Overall IgA nephropathy
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117. • Postinfectious glomerulonephritis
• occur as a sequela of disease caused by bacteria, viruses, fungi, protozoa,
and helminths
• Post streptococcal GN most common cause of GN in childhood
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118. Nephritis develops 1–3 weeks after pharyngeal (more common in
winter) or cutaneous infection with (more common in summer)
‘nephritogenic’ strains of group A beta – hemolytic streptococci
Group A beta haemolytic
streptococci
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125. • Light microscopy
• diffuse increased cellularity of the glomerular tufts that affects nearly all
glomeruli
• Electron microscopy
• deposited immune complexes arrayed as subendothelial, intramembranous, or, most
often, subepithelial “humps” nestled against the GBM
• Immunofluorescence studies reveal scattered granular deposits of IgG
and complement within the capillary walls and some mesangial areas,
corresponding to the deposits visualized by electron microscopy.
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128. IF deposits starry sky appaearance in PSGN
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129. CF of PSGN
• sudden onset of hematuria and edema
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130. Lab findings
• Hypocomplementemia
• elevated titers of
• antistreptolysin 0,
• antihyaluronidase, and
• anti-deoxyribonuclease B antibodies
• Unfavourable prognostic factors
• Prolonged persistent heavy proteinuria
• Abnormal GFR
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131. Rx
• Hypertension must be treated aggressively,
• Furosemide or bumetanide is required for the underlying edema-
inducing disease.
• Antibiotic - penicillin.
• Prophylaxis following poststreptococcal glomerulonephritis is not
indicated because recurrences are exceedingly rare.
• Early treatment of pharyngitis does not prevent development of acute GN.
• Immunosuppressive agents or corticosteroids have no therapeutic
role.
• Recurrence is uncommon with PSGNTONY SCARIA 2010
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132. IgA Nephropathy (Berger’s Disease)
• Most common causes of recurrent microscopic or gross hematuria
• MC of GN world wide
• IgA nephropathy is a type of mesangioproliferative
glomerulonephritis with IgA deposition in the mesangium
• Pathogenesis
• Genetic or acquired defects in immune regulation
• Increased IgA1 secretion (only IgA1 is nephritogenic)
• Decreased clearance of IgA
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135. • Light microscopy
• Mesangial proliferation
• Cresents may be present
• Electron microscopy
• Mesangial deposits of IgA IgG or IgM with C3
• Compliment level remain same
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138. IgA nephropathy PSGN
Onset of hematuria after URTI 1-4 days 1-4 weeks
Serum C3 level Normal Transiently decreases for 6-8 weeks
Recurrence Common Rare
Antibody titre Not elevated Elevated ASO titre
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139. Other causes of mesangioproliferative GN
Mesnagioproliferative GN
• IgA nephropathy
• HSP
Proliferation of mesangial cells and
deposition of IgA in matrix
• Hematuria
• Proteinuria
• Hypertension
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141. RPGN
• RPGN is defined by 2 criteria
• 1. Presence of epithelial crescents in more than 70% of glomeruli
• 2. Occurrence of rapidly progressive renal failure, End stage disease occurs
within month
• Presents with nephritic syndrome rapidly progresses to loss of
renal function
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147. Type I RPGN Type II RPGN Type III RPGN
Anti GBM mediated
Ab against α3 chain of collagen IV
Immune complex mediated Pauci immune
ANCA associated
Most common
IF linear deposits along
basement membrane
IF granular deposits IF no deposits
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149. Type I RPGN Type II RPGN Type III RPGN
• Idiopathic
• Good pastures syndrome
• Idiopathic
• SLE
• Ig A nephropathy
• MPGN
• Cryoglobulinemia
• Post infectious GN
• Idiopathic
• Granulomatosis with polyangitis
• Microscopic polyangitis
• Best prognosis
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150. Prognosis of RPGN
• The prognosis of RPGN depends upon Number of crescents.
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151. • Diagnosis
• Renal biopsy
• Rx
• Plasmapheresis & immunosuppression
• In immune complex glomerulonephritis, treatment depends on the
individual causative disorder.
• In pauci-immune deposit disease, treatment involves pulse
methylprednisolone and cyclophosphamide.
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153. Good pasture syndrome
• characterized by formation of Anti GBM antibodies that attack both
pulmonary capillaries and the Glomerulus
• Type II hypersensitivity
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154. Triad of goodpasture syndrome
• Anti GBM ab
• Directed against Non collagenous domain of type α3 collagen
• Glomerulonephritis (usually crescentic)
• Pulmonary hemorrhage (Hemoptysis may precede nephritis).
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157. Ab in good pasture syndrome
• Circulating Anti GBM antibodies (lgG): Positive
• ANCA antibodies: Typically Negative (ANCA negative vasculitis)
• ANA antibodies: usually normal
• C3 levels: Usually normal
• Antibodies against Non collagenous Domain (NCL) of a3 chain of
collagen type IV
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158. CF in good pasture syndrome
• 1. Hemoptysis (Frank)
• 2. Dyspnea
• 3. Hematuria
• 4. Proteinuria
• 5. Edema
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159. Pathology in good pasture
syndrome
• Diffuse crescentic Glomerulonephritis
• Linear IgG staining along basement
membrane on immunofluorescence
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175. HSP
• MC vasculitis of childhood
• Characterised by leukocytoclastic vasculitis & IgA deposition in small
vessels of skin joints GIT & kidney
• Renal involvement hematuria and proteinuria.
• Serum IgA is normal or raised, platelet count is normal.
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176. LAB DIAGNOSIS OF HSP
• Antinuclear antibody (ANA) Negative
• Antineutrophil cytoplasmic Negative
• Antibodies (ANCA) Negative
• Complement (C3, C4) Normal
• Cryoglobulins Negative
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179. American college of rheumatology Pediatric rheumatology European society criteria
2 of the following
Palpable purpura
Age at onset <20 yr
Bowel angina (post prandial abdominal pain/
bloody diarrhea)
Biopsy demonstrating intramuscular
granulocytes in arterioles or venules
Palpable purpura (in absence of coagulopathy or
thrombocytopenia
Abdominal pain
Arthritis or arthralgia
Biopsy IgA deposition
Renal involvement
• Proteinuria
• Hematuria
• Red cell cast
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186. c/c glomerulonephritis
• poststreptococcal (1% to 2%); least common chance of progression
• rapidly progressive (crescentic) (90%) most common chance of
progression
• membranous (30% to 50%),
• focal segmental glomerulosclerosis (50% to 80%),
• membranoproliferative GN (50%),
• IgA nephropathy (IgAN, 30% to 50%).
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188. c/c glomerulonephritis
• arterial and arteriolar sclerosis
• Marked atrophy of associated
tubules, irregular interstitial
fibrosis, and mononuclear
leukocytic infiltration of the
interstitium
• obliteration of glomeruli,
transforming them into acellular
eosinophilic masses,
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190. Diabetic nephropathy
• Most important predictor of diabetic nephropathy is duration of
disease
• 20 yrs prediction of nephropathy
• Type 1 30 -40 %
• Type 2 15-20 %
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191. Mechanism of diabetic nephropathy
• Nonenzymatic glycosylation of proteins of basement membrane
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192. • Earliest lab finding in diabetic nephropathy increase in GFR
• early stages of diabetic nephropathy are characterized by an
increased GFR, increased glomerular capillary pressure, glomerular
hypertrophy, and an increased glomerular filtration area
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193. Lesions seen in diabetic nephropathy
glomerular lesions renal vascular lesions, principally
arteriolosclerosis
pyelonephritis, including
necrotizing papillitis
• capillary basement membrane
thickening (earliest lesion)
• diffuse mesangial
sclerosis(most common
histologic finding)
• nodular glomerulosclerosis
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194. Glomerular lesions
Capillary basement membrane
thickening
Diffuse glomerulosclerosis Nodular glomerulosclerosis
• Earliest lesion • diffuse increase in mesangial
matrix along with mesangial cell
proliferation and
• Glomerular lesion made
distinctive by ball-like deposits
of a laminated matrix situated in
the periphery of the glomerulus
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206. • Ball-on-tee appearance: Contrast material filling central excavations in the
papilla of the interpolar region gives ball-on-tee appearance.
• Lobster claw sign: Excavation extending from the caliceal fornices produces
the lobster claw deformity.
• Signet ring sign: The necrotic papillary tip may remain within the excavated
calyx, producing the signet ring sign when the calyx is filled with contrast
material.
• Club shaped saccular calyx: Due to sloughed papillaTONY SCARIA 2010
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208. Hepatitis C • Cryoglobulinemic glomerulonephritis
• Membranous glomerulonephritis (MGN)
• Membrano prolferative glomerulo
nephritis(MPGN)
Hepatitis B • In children MGN
• In adults MPGN
• Over all MGN
Toxoplasmosis • MPGN
Syphilis
Schistosomiasis
• MGN
Leprosy • Secondary amyloidosis
• Mesangiocapilalry GN
• MPGN1
• Membranous GN
Malaria • Plasmodium malaria NS
• Plasmodium falciparum renal failure
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209. Essential mixed cryoglobulinemia
• Cold precipitable monoclonal or polyclonal immunoglobulins
• It causes cutaneous vasculitis synovitis palpable purpura
• It causes proliferative GN most commonly MPGN type 1
• a/w hepatitis C
• Hypocomplimentinemia
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210. Fibronectin nephropathy
• Autosomal dominant
• d/t accumaltion of plasma fibronectin
• Presents with Massive proteinuria
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