Retinoblastoma is a rare form of eye cancer that affects young children. It occurs when nerve cells in the retina develop genetic mutations causing uncontrolled growth. In about 40% of cases it is inherited from a parent with a faulty gene. Symptoms include a white pupil, eye misalignment, poor vision, and eye swelling/redness. Treatment aims to preserve the child's life, then vision, and minimize side effects. Options include thermotherapy, laser photocoagulation, and cryotherapy. Children also face risks of cancer recurrence or developing other cancers.
Retinoblastoma Eye (retina cancer) Surgery in India – Full informationnidhi21
Retinoblastoma (Rb) is a cancer of the retina. Retinoblastoma is the most common primary ocular malignancy of childhood. Although this disorder can occur at any age, it usually develops in young children. Most cases of retinoblastoma occur in only one eye, but both eyes can be affected. Untreated, retinoblastoma is almost always fatal, hence the importance of early diagnosis and treatment.
This is a beginner's guide to retinoblastoma. I have briefly covered all the aspects of this most common intraocular tumor of childhood. Hope it will help the undergraduate medical students. Please check out our blog, http://pgblaster.wordpress.com for more presentations and useful stuffs like this one.
Retinoblastoma Eye (retina cancer) Surgery in India – Full informationnidhi21
Retinoblastoma (Rb) is a cancer of the retina. Retinoblastoma is the most common primary ocular malignancy of childhood. Although this disorder can occur at any age, it usually develops in young children. Most cases of retinoblastoma occur in only one eye, but both eyes can be affected. Untreated, retinoblastoma is almost always fatal, hence the importance of early diagnosis and treatment.
This is a beginner's guide to retinoblastoma. I have briefly covered all the aspects of this most common intraocular tumor of childhood. Hope it will help the undergraduate medical students. Please check out our blog, http://pgblaster.wordpress.com for more presentations and useful stuffs like this one.
Retinoblastoma is caused by mutations (changes) in certain genes. Over the past few decades, scientists have learned how certain changes in a person’s DNA can cause cells of the retina to become cancerous. The DNA in each of our cells makes up our genes, which are the instructions for how our cells function. We usually look like our parents because they are the source of our DNA. But DNA affects much more than how we look. Some genes control when our cells grow, divide into new cells, and die at the right time. Certain genes that help cells grow, divide, or stay alive are called oncogenes. Others that slow down cell division or cause cells to die at the right time are called tumor suppressor genes. Cancers can be caused by DNA changes that turn on oncogenes or turn off tumor suppressor genes. The most important gene in retinoblastoma is the RB1 tumor suppressor gene. This gene makes a protein (pRb) that helps stop cells from growing too quickly. Each cell normally has 2 RB1 genes. As long as a retinal cell has at least one RB1 gene that works as it should, it will not form a retinoblastoma. But when both of the RB1 genes are mutated or missing, a cell can grow unchecked. This can lead to further gene changes, which in turn may cause cells to become cancerous.
This presentation is about a group of eye disorder, Retinitis Pigmentosa. RP is a non-treatable genetic disorder which cause due to degradation of photoreceptor cells in retina. Unfortunately we do not have a proper treatment for RP, but in this presentation I suggest some of options that can help a individual having RP.
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.
Retinoblastoma is caused by mutations (changes) in certain genes. Over the past few decades, scientists have learned how certain changes in a person’s DNA can cause cells of the retina to become cancerous. The DNA in each of our cells makes up our genes, which are the instructions for how our cells function. We usually look like our parents because they are the source of our DNA. But DNA affects much more than how we look. Some genes control when our cells grow, divide into new cells, and die at the right time. Certain genes that help cells grow, divide, or stay alive are called oncogenes. Others that slow down cell division or cause cells to die at the right time are called tumor suppressor genes. Cancers can be caused by DNA changes that turn on oncogenes or turn off tumor suppressor genes. The most important gene in retinoblastoma is the RB1 tumor suppressor gene. This gene makes a protein (pRb) that helps stop cells from growing too quickly. Each cell normally has 2 RB1 genes. As long as a retinal cell has at least one RB1 gene that works as it should, it will not form a retinoblastoma. But when both of the RB1 genes are mutated or missing, a cell can grow unchecked. This can lead to further gene changes, which in turn may cause cells to become cancerous.
This presentation is about a group of eye disorder, Retinitis Pigmentosa. RP is a non-treatable genetic disorder which cause due to degradation of photoreceptor cells in retina. Unfortunately we do not have a proper treatment for RP, but in this presentation I suggest some of options that can help a individual having RP.
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.
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
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.
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
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.
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
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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
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
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
1. RETIONOBLASTOMA
• Retinoblastoma is an eye cancer that begins in the retina — the
sensitive lining on the inside of your eye. Retinoblastoma most
commonly affects young children, but can rarely occur in adults.
• A rare form of eye cancer, retinoblastoma is the most common form
of cancer affecting the eye in children. Retinoblastoma may occur in
one or both eyes.
2. Causes
• Retinoblastoma occurs when nerve cells in the retina develop genetic
mutations. These mutations cause the cells to continue growing and
multiplying when healthy cells would die. This accumulating mass of
cells forms a tumor. Alterations in RB1 or MYCN can give rise to
retinoblastoma.
• Retinoblastoma cells can invade further into the eye and nearby
structures. Retinoblastoma can also spread (metastasize) to other
areas of the body, including the brain and spine.
• For most instances of retinoblastoma, it's not clear what causes the
genetic mutation that leads to cancer. However, it's possible for
children to inherit a genetic mutation from their parents.
3. During the early stages of a baby's development, retinal eye cells grow very quickly and then stop
growing.
But in rare cases, 1 or more cells continue to grow and form a cancer called retinoblastoma.
In about 4 out of 10 (40%) cases, retinoblastoma is caused by a faulty gene, which often affects both
eyes (bilateral).
The faulty gene may be inherited from a parent, or a change to the gene (mutation) may occur at an
early stage of the child's development in the womb.
It's not known what causes the remaining 6 out of 10 (60%) retinoblastoma cases. In these cases,
there's no faulty gene and only 1 eye is affected (unilateral).
4.
5. Symptoms
• Because retinoblastoma mostly affects infants and small children,
symptoms aren't common. Signs you may notice include:
• A white color in the center circle of the eye (pupil) when light is shone
in the eye, such as when someone takes a flash photograph of the
child
• Eyes that appear to be looking in different directions
• Poor vision
• Eye redness
• Eye swelling
6. Retinoblastoma that is inherited
• Gene mutations that increase the risk of retinoblastoma and other
cancers can be passed from parents to children.
• Hereditary retinoblastoma is passed from parents to children in an
autosomal dominant pattern, which means only one parent needs a
single copy of the mutated gene to pass the increased risk of
retinoblastoma on to the children. If one parent carries a mutated
gene, each child has a 50% chance of inheriting that gene.
7.
8.
9. Complications
• Children treated for retinoblastoma have a risk of cancer returning in
and around the treated eye. For this reason, your child's doctor will
schedule follow-up exams to check for recurrent retinoblastoma.
• Additionally, children with the inherited form of retinoblastoma have
an increased risk of developing other types of cancers in any part of
the body in the years after treatment, especially pine blastoma, a
type of brain tumor. For this reason, children with inherited
retinoblastoma may have regular exams to screen for other cancers.
10.
11. TREATMENT
• The priority of retinoblastoma treatment is to preserve the life of the child, then
to preserve vision, and then to minimize complications or side effects of
treatment. The exact course of treatment depends on the individual case and is
decided by the ophthalmologist in discussion with the paediatric oncologist.
• The various treatment modalities for retinoblastoma includes
• Thermotherapy involves the application of heat directly to the tumor,
usually in the form of infrared radiation. It is also used for small tumors.
• Laser photocoagulation is recommended only for small posterior tumors.
An argon or diode laser or a xenon arc is used to coagulate all the blood
supply to the tumor.
• Cryotherapy induces damage to the vascular endothelium with secondary
thrombosis and infarction of the tumor tissue by rapidly freezing it. It may
be used as primary therapy for small peripheral tumors or for small
recurrent tumors previously treated with other methods.
12.
13. Retinitis pigmentosa
• Retinitis pigmentosa (RP) is a group of rare eye diseases that affect the
retina (the light-sensitive layer of tissue in the back of the eye). RP makes
cells in the retina break down slowly over time, causing vision loss.
• Also known as hereditary retinal dystrophy
• RP is a genetic disease that people are born with. Symptoms usually start in
childhood, and most people eventually lose most of their sight.
• There’s no cure for RP. But vision aids and rehabilitation (training) programs
can help people with RP make the most of their vision.
14. What causes RP?
• Most of the time, RP is caused by changes in genes that control cells in the retina. These
changed genes are passed down from parents to children.
• RP is linked to many different genes and can be inherited in different ways .Its
transmission is Autosomal recessive in most cases. Other modes of transmission include
autosomal dominant and X-linked
• Retinal cells may contain a variety of mutations and this depends o the underlying
genetic cause
• Mutations can trigger apoptosis (programmed cell death) of retinal photoreceptors.
• Apoptosis of some cells can trigger apoptosis of surrounding cells
• Retinal pigment epithelial cells can detach and deposit into perivascular areas, leaving
bony spicule –shaped melanin deposits..
• Sometimes RP happens as part of other genetic conditions, like Usher syndrome. Usher
syndrome causes both vision and hearing loss.
15.
16. symptoms of RP
• The most common early symptom of RP is loss of night vision —
usually starting in childhood. Parents may notice that children with RP
have trouble moving around in the dark or adjusting to dim light.
• RP also causes loss of side (peripheral) vision — so you have trouble
seeing things out of the corners of your eyes. Over time, your field of
vision narrows until you only have some central vision (also called
tunnel vision).
• Some people with RP lose their vision more quickly than others.
Eventually, most people with RP lose their side vision and their central
vision.
17. Other symptoms of RP
include:
•Sensitivity to bright light
•Loss of color vision
18.
19. How will my eye doctor check for RP?
• Eye doctors can check for RP as part of a comprehensive dilated eye exam. The exam is
simple and painless — the doctor will give you some eye drops to dilate (widen) your
pupil and then check your eyes for RP and other eye problems. The exam includes a
visual field test to check peripheral (side) vision.
• Other tests for RP include:
• Electroretinography (ERG). ERG lets the eye doctor check how well your retina responds
to light.
• Optical coherence tomography (OCT). This test uses light waves to take a detailed picture
of your retina.
• Fundus autofluorescence (FAF) imaging. In this test, the eye doctor uses blue light to take
a picture of the retina.
• Genetic testing. Your doctor may suggest a genetic test to learn more about the type of
RP they have. This can tell you how your RP symptoms may change over time.
20. treatment for RP
• here’s no cure for RP, but low vision aids and rehabilitation (training)
programs can help people with RP make the most of their vision.