This document summarizes 8 renal biopsy cases from 2001-2005. Case 1 involves a patient with proteinuria and was diagnosed with immunotactoid glomerulonephritis. Case 2 involves a lupus nephritis patient with acute renal failure who was diagnosed with diffuse proliferative lupus nephritis. Case 3 involves a 3-year old boy with hypertension, hematuria and proteinuria who was diagnosed with C1q glomerulopathy.
Sickle cell anemia is a genetic diseases where red blood cells can take shape of a crescent or a sickle . And this allows them to be more easily destroyed – causing anemia and other complexities
Chronic myelogenous leukemia (CML) - pluripotential stem cell disease
A malignancy the treatment of which has been revolutionised over the last decade.
Here is a comprehensive discussion on the disease
Sickle cell anemia is a genetic diseases where red blood cells can take shape of a crescent or a sickle . And this allows them to be more easily destroyed – causing anemia and other complexities
Chronic myelogenous leukemia (CML) - pluripotential stem cell disease
A malignancy the treatment of which has been revolutionised over the last decade.
Here is a comprehensive discussion on the disease
lupus nephritis is a autoimmune disease, commonly seen in adult and child and the medical or nursing care is also very important for this type of disease condition.
lupus nephritis is a autoimmune disease, commonly seen in adult and child and the medical or nursing care is also very important for this type of disease condition.
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.
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.
This presentation i have made to understand the approach to a kidney biopsy in depth. kidney biopsy is not done in all centers and that's why its difficult to understand it. i have put some cases also to understand it better.
Slide deck for annual meeting of Transplant Regenerative medicine Community of Practice of American Society of Transplantation at noon in Room 204 in John B. Hynes Convention Center. Everyone welcome! Many exciting initiatives to discuss!
Kim Solez Xenotransplantation- The Rest of the Story April 8 2022 6.pptxKim Solez ,
Nephrology Grand Rounds Presentation at the University of Alberta discussing the big picture issues surrounding xenotransplantation and its relation to stem cell generated organs and bioengineered organs in the future
Kim Solez Hooking-Up Physical Forces Optimism and Dark Energy Presentation Se...Kim Solez ,
Kim Solez Banff New Media Institute Presentation, "Smart, Sexy, Healthy" ThinkTank, Sept 6 2001
Hooking-Up, Physical Forces, Optimism and Dark Energy: Imagery, Hope, and Health.
Kim Solez 384 years of banff spirit new june 26 2019Kim Solez ,
Kim Solez 384 years of Banff spirit new June 26 2019 The most remarkable slide is number 137. "By Spring of 2019 every erroneous statement we complained about had been reversed. We celebrated by creating a new video trailer on our YouTube channel on June 25 2019." How about that!
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
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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
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!
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.
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.
- 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
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
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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.
25. Diagnosis:
Renal Biopsy: Kappa light chain
disease with extensive glomerular
deposition of fibrillary microtubular
structures approximately 17 nm in
diameter.
Immunotactoid glomerulonephritis.
26. Case 2
20 yr old female, known lupus nephritis,
class 4, previously treated with IV
cyclophosphamide for 10 months,
admitted with acute renal failure,
evidence of TMA, leukopenia,
oliguria/anuria and fluid overload.
Treated with IV MP x 3d, plasmapheresis
and then started on hemodialysis. Repeat
biopsy done. T.Kovithavongs
27. Lupus – on dialysis. ? Stage. ? Chronic
Or active.
28.
29.
30.
31.
32.
33. IF
• IgG-Moderate to strong coarsely granular capillary loop and mesangial
staining.strong granular peritubular staining.
• IgA- Moderate coarsely granular capillary loop and mesangial staining.
• IgM-Mild to moderate coarsely granular capillary loop and mesangial
staining, mild to moderate granular peritubular staining.
• C3- Mild to moderate coarsely granular capillary loop and mesangial
staining.
• C1q-Moderate to strong coarsely granular capillary loop and mesangial
staining, strong granular peritubular staining.
• Kappa- Moderate to strong coarsely granular capillary loop and mesangial
staining, strong staining of granular capillary wall coagula and moderate
granular peritubular staining.
• Lambda- Stong staning of granular capillary wall coagula and moderate
granular peritubular staining.
• Fibrin- Strong staining of glomerular crescent moderate interstitial staining.
• Albumin-Mild hyaline droplet change in tubular cytoplasm.
55. Diagnosis:
Renal Biopsy:Diffuse proliferative
lupus nephritis of moderate activity and
mild to moderate chronicity with many
hyaline thrombi and “fingerprints” by
EM in an active acute interstitial
nephritis involving polymorph infiltrates
with peritubular deposits seen by
electron microscopy.
Occasional glomerular capillary and
arteriolar fibrin thrombi.
56. Case 3
3-year-old boy with hypertension.
Hematuria and proteinuria
Serology all negative
Family history of IgA nephropathy
57.
58.
59.
60.
61.
62.
63. IF
• IgG – moderate mesangial staining.
• IgA – negative.
• IgM – mild to moderate mesangial staining.
• C3 – mild vascular staining.
• C1q – mild to moderate mesangial staining.
• Kappa – mild to moderate mesangial staining.
• Lambda – mild mesangial staining.
• Fibrinogen – negative.
• Albumin – negative.
73. DIAGNOSIS
• Probable C1q glomerulopathy with
mesangial cell proliferation and occasional
crescent formation.
74.
75. Second biopsy Case 3
6 yr old boy with C1q nephropathy diagnosed
by biopsy Dec 2001. Has been on cyclosporine
For ~2 yrs. Initial presentation – HTN, hematuria,
↑creat. For F/U biopsy.
76.
77.
78.
79.
80.
81.
82. IF
• IgG –Trivial to mild mesangial staining.
• IgA –Negative.
• IgM –Mild mesangial staining.
• C3 –Trivial to mild mesangial staining. Mild to
moderate vascular staining.
• C1q –Mild to moderate mesangial staining.
• Kappa –Mild to moderate mesangial staining.
• Lambda−Mild mesangial staining.
• Fibrinogen –Mild interstitial staining.
• Albumin – Negative.
99. Diagnosis:
Renal Biopsy:C1q nephropathy, with
Mesangioproliferative and segmental
Sclerosing lesions.
(A)Chronic changes with estimated
20 – 30% glomerular loss and parenchymal
Scarring.
(B)Associated tubulointerstitial nephritis.
(C)Mild microvascular changes consistent
With cyclosporine nephrotoxicity.
100.
101. Case 4
L native kidney. ARF creatinine = 280,
proteinuria +++,
Hb +++. Fine casts +++. ESR ↑, ANA +, RF
+, C3,
C4 Normal. No previous renal history.
102.
103.
104.
105.
106.
107.
108.
109.
110.
111. IF
• IgG-Negative.
• IgA-Mild to moderate mesangial staining.
• IgM- Moderate vascular staining.
• C3-Moderate vascular staining – trivial to mild
punctate mesangial staining.
• C1q- Negative.
• Kappa- Negative.
• Lambda-Mild to moderate mesangial staining
• Fibrin-Mild to moderate interstitial staining.
• Albumin- Negative.
123. Diagnosis:
Renal Biopsy:Diffuse proliferative
glomerulonephritis with features of
membranoproliferative
glomerulonephritis but with positive
staining for IgA in the mesangium.
Possible IgA nephropathy in the
diffuse proliferative form or
coincidence of two different
glomerular processes.
124. This 36 yo female, evaluated for persistent
microhematuria in the absence of
proteinuria, is a potential kidney donor to
her father. The recipient has ESRD on the
basis of diabetic nephropathy and pANCA
pauci-immune GN. Her mother had ESRD of
unknown cause and is now deceased. There
is no other family history of renal disease
among 5 siblings and her 3 children.
Serological testing was negative.
Case 5
138. 25 year old male, sent to Edmonton from Red
Deer with a serum
creatinine of ~400 and MRA suggestive of
RAS.
Angio was negative so a renal biopsy was
ordered. He has no significant past medical
history prior to being seen in Red Deer. While
admitted there, he was treated for malignant
HTN and his lab work up was unremarkable.
Case 6
139. Case 6
24 year old male with malignant hypertension
And renal failure (Cr 400) NYD.
158. Diagnosis:
Renal Biopsy: IgA nephropathy
with superimposed malignant
phase hypertension with
thrombotic microangiopathy and
extensive parenchymal atrophy
and scarring with widespread
glomerulosclerosis.
159. U03-13285
#015014502108
Ms RS, 41 yo female, lupus Dx 2000..alopecia, leukopenia/anemia,
arthralgias, vasculitis
CyP IV x 5 months then po x 1 months prior to referral (May 2003) because of
necrotizing vasculitis … stopped because of neutropenia
•Exam reveals
•BP 110/76
•patchy vitiligo, alopecia
•no active joints
•PMHx
–lupus as above
•Meds:
–prednisone
–Plaquenil,
•Labs initially:
•SCr 75, CrCl ~ 90
ml/min
•urine 2+ protein/ 2+
blood
•P:C ratio 135
mg/mmol
•24 hr protein 1.9 g
•Hgb 90, WBC 2.2
•C3/C4 low, anti
dsDNA high
176. Diagnosis:
Renal Biopsy:
Mixed membranous and proliferative
glomerulonephritis with features
suggesting SLE.
Low activity and low chronicity. No
glomeruli in material for EM.
177. Second biopsy
Native left kidney. Known SLE
previous renal bx 2003. Now ↑↑ SCr.
↑ Ds DNA Ab.
?Active nephritis.
208. Diagnosis:
Renal Biopsy: Diffuse proliferative
lupus nephritis with crescent
formation and extensive glomerular
sclerosis.
Moderate activity and moderate
chronicity.
209. Case 7
Ms RS, 41 yo female, lupus Dx 2000..alopecia, leukopenia/anemia,
arthralgias, vasculitis
CyP IV x 5 months then po x 1 months prior to referral because of necrotizing
vasculitis … stopped because of neutropenia
•Exam reveals
•BP 110/76
•patchy vitiligo, alopecia
•no active joints
•PMHx
–lupus as above
•Meds:
–prednisone
–Plaquenil,
•Labs initially:
•SCr 75, CrCl ~ 90
ml/min
•urine 2+ protein/ 2+
blood
•P:C ratio 135
mg/mmol
•24 hr protein 1.9 g
•Hgb 90, WBC 2.2
•C3/C4 low, anti
dsDNA high
226. Diagnosis:
Renal Biopsy:
Mixed membranous and proliferative
glomerulonephritis with features
suggesting SLE.
Low activity and low chronicity. No
glomeruli in material for EM.
227. Case 8 second biopsy
Native left kidney. Known SLE
previous renal bx 2003. Now ↑↑ SCr.
↑ Ds DNA Ab.
?Active nephritis.
258. Diagnosis:
Renal Biopsy: Diffuse proliferative
lupus nephritis with crescent
formation and extensive glomerular
sclerosis.
Moderate activity and moderate
chronicity.
259. ID: 77 year old female
RFR: nephrotic syndrome
HPI: Patient has a 7 month history of peripheral edema, mostly in lower
extremities and hands. Noted to have rapid onset of ~ 1 week. No further
urinary symptoms or hematuria.
No constitutional symptoms or vasculitis symptoms. One prior blood
transfusion 20 years ago; no history of hepatitis. No history of diabetes.
Hypertension diagnosed 2 months prior to referral. On Diclofenac
irregularly: 3-4 pills per month although higher usage in remote past.
Otherwise healthy. Other meds: Ramipril, HCTZ, Lipitor, Lakota,
multivitamin, Siberian ginseng, cayenne pepper.
Exam: Looked well. bp: 135/65. bilateral edema in lower extremities to
knees and edema of hands. otherwise unremarkable.
Labs: Cr 79, urea 5.6 albumin 22 total protein 49 urinalysis: 3+ protein,
3+ Hb Pr:Cr ratio 915 mg/mol
SPEP, UPEP: no free light chains; C3 C4 normal; ANCA, Hep B, Hep C
neg.