This document discusses diabetic retinopathy, which refers to retinal changes seen in patients with diabetes mellitus. It first describes the normal retinal structure and then defines diabetic retinopathy and its causes such as duration of diabetes and poor metabolic control. It classifies diabetic retinopathy into non-proliferative and proliferative stages and discusses their clinical features and management approaches including screening, medical treatments like controlling risk factors and intravitreal steroids, photocoagulation procedures, and surgical treatment for advanced cases.
Diabetic retinopathy is a complication of diabetes, caused by high blood sugar levels damaging the back of the eye (retina). It can cause blindness if left undiagnosed and untreated. However, it usually takes several years for diabetic retinopathy to reach a stage where it could threaten your sight.
The retina is the light-sensitive layer of cells at the back of the eye that converts light into electrical signals. The signals are sent to the brain which turns them into the images you see.
The retina needs a constant supply of blood, which it receives through a network of tiny blood vessels. Over time, a persistently high blood sugar level can damage these blood vessels in 3 main stages:
background retinopathy – tiny bulges develop in the blood vessels, which may bleed slightly but don't usually affect your vision
pre-proliferative retinopathy – more severe and widespread changes affect the blood vessels, including more significant bleeding into the eye
proliferative retinopathy – scar tissue and new blood vessels, which are weak and bleed easily, develop on the retina, this can result in some loss of vision
Superficial punctate keratitis by optometry fans site, definition of SPK, causes of superficial punctate keratitis, symptoms of superficial punctate keratitis, treatment of superficial punctate keratitis, management and treatment of SPK
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
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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
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2 Case Reports of Gastric Ultrasound
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
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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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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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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
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
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.
2. Normal structure
• Retina-
• The innermost tunic of the eyeball, is a
thin, delicate and transparent membrane. It
is the most highly-developed tissue of the
eye. It appears purplish-red due to the
visual purple of the rods and underlying
vascular choroid.
7. DIABETIC RETINOPATHY
• Retinal changes seen in patients with
diabetes mellitus. With increase in
the life expectancy of diabetics, the
incidence of diabetic retinopathy
(DR) has increased.
8. Etiopathogenesis
• 1. Duration of diabetes is the most important determining
factor. Roughly 50 percent of patients develop DR after 10
years, 70 percent after 20 years and 90 percent after 30 years
of onset of the disease.
• 2. Sex. Incidence is more in females than males (4:3).
• 3. Poor metabolic control is less important than duration, but
is nevertheless relevant to the development and progression
of DR.
• 4. Heredity. It is transmitted as a recessive trait without sex
linkage.
• 5. Pregnancy may accelerate the changes of diabetic
retinopathy.
• 6. Hypertension, when associated, may also accentuate the
changes of diabetic retinopathy.
• 7. Other risk factors include smoking, obesity .
10. Classification
I. Non-proliferative diabetic retinopathy (NPDR)
Mild NPDR
Moderate NPDR
Severe NPDR
Very severe NPDR
II. Proliferative diabetic retinopathy (PDR)
III. Diabetic maculopathy
IV. Advanced diabetic eye disease (ADED)
11. Clinical feature
• Microaneurysms in the macular area
• Retinal haemorrhages both deep and superficial
haemorrhages .
• Hard exudates-yellowish-white waxy-looking patches are
arranged in clumps or in circinate pattern. These are
commonly seen in the macular area.
• Retinal oedema characterized by retinal thickening.
• Cotton-wool spots (if > 8, there is high risk of developing
PDR).
• Venous abnormalities, beading, looping and dilatation.
Intraretinal microvascular abnormalities (IRMA).
• Dark-blot haemorrhages representing haemorrhagic
retinal infarcts.
12. 1. Mild NPDR
• At least one microaneurysm or intraretinal
hemorrhage.
• Hard/soft exudates may or may not be
present.
16. 3. Severe NPDR.
• Four quadrants of severe microaneurysms/
intraretinal hemorrhages.
• Two quadrants of venous beading.
• One quadrant of IRMA changes
18. 4. Very severe NPDR
• Four quadrants of severe microaneurysms/
intraretinal hemorrhages.
• Two quadrants of venous beading.
• One quadrant of IRMA changes.
20. II. Proliferative diabetic retinopathy
(PDR)
• Proliferative diabetic retinopathy develops in
more than 50 percent of cases after about 25
years of the onset of disease.
•
• The hallmark of PDR is the occurrence of
neovascularisation over the changes of very
severe non-proliferative diabetic retinopathy.
•
• Vitreous detachment and vitreous haemorrhage
may occur in this stage
21. III. Diabetic maculopathy
• Changes in macular region need special
mention, due to their effect on vision.
• The diabetic macular edema occurs due to
increased permeability of the retinal
capillaries.
• It is termed as clinically significant macular
edema.
• Thickening of the retina at or within 500
micron of the centre of the fovea.
22. IV. Advanced diabetic eye disease
• It is the end result of uncontrolled
proliferative diabetic retinopathy.
•
• Persistent vitreous haemorrhage,
• Tractional retinal detachment and
• Neovascular glaucoma.
23. Investigations
• Urine examination,
• Blood sugar estimation.
• Fundus fluorescein angiography should be
carried out to elucidate areas of
neovascularisation, leakage and capillary
nonperfusion
24. Management
• I. Screening for diabetic retinopathy.
• Every year, till there is no diabetic retinopathy
or there is mild NPDR.
• Every 6 months, in moderate NPDR.
• Every 3 months, in severe NPDR.
• Every 2 months, in PDR with no high risk
characteristic
25. Medical treatment
1. Control of systemic risk factors
2. Role of pharmacological
modulation.
3. Role of intravitreal steroids
26. III. Photocoagulation.
• i. Macular photocoagulation.
Focal treatment
Grid treatment.
• ii. Panretinal photocoagulation
30. IV. Surgical treatment.
• It is required in advanced cases of PDR. Pars
plana vitrectomy is indicated for dense
persistent vitreous haemorrhage, tractional
retinal detachment, and epiretinal
membranes. Associated retinal detachment
also needs surgical repair.
