This document summarizes vernal keratoconjunctivitis (VKC), a recurrent seasonal allergic eye condition that mostly affects children. It affects the conjunctiva and cornea and is caused by a type 1 and 4 hypersensitivity reaction to allergens. Symptoms include intense itching, redness, tearing and photophobia. Treatment involves avoiding allergens, lubrication, mast cell stabilizers, antihistamines, topical steroids, and in severe cases oral steroids, NSAIDs or cyclosporine may be used. Complications include shield ulcers of the cornea which may require surgical treatment.
Summary of updated information about the disease of Atopic dermatitis, aetiology, immunopathogenesis, main clinical features and dianostic criteria, concepts of managemnt of Atopic dermatitis including newest treatment trends.
Atopic dermatitis (AD), also known as atopic eczema, is a long-term type of inflammation of the skin (dermatitis). It results in itchy, red, swollen, and cracked skin. Clear fluid may come from the affected areas, which often thickens over time. While the condition may occur at any age
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
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
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
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
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
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
2. Recurrent,bilateral,seasonal external ocular allergy
primarily affects children and young adults
Predisposing factors ::
AGE- 80% <14 yrs
SEX- Males>Females
SEASON-exacerbates during spring
FAMILY H/O allergic disease
PERSONAL H/O atopic diseases like asthma,hay fever
DRY and HOT environments
3. IMMUNE PATHOLOGY
• type 1 AND type 4 hypersensitivity plays an important role
ALLERGENS
OCULAR SURFACE
BIND TO MAST CELL IgE
ACTIVATION OF MAST CELL
CALCIUM ENTERS THE CELL
DEGRANULATION OF MAST CELL
RELEASE OF MEDIATORS
4.
5. • Early phase mediators like histamine,protease cause itching
redness swelling degradation of neighbouring cells and
inflammatory cell accumulation
• Other mediators like PG’S,LT’S,PAF,CYTOKINES,CHEMOKINES
also mediate redness,swelling,infiltration of eosinophils and
neutrophils
• EOSINOPHILS release MBP and ECP are epitheliotoxic and
involved in corneal damage
• Tear levels of ECP are considered as local markers of
eosinophil activation and correlated with clinical signs and
symptoms
7. SIGNS
– Papillary reaction.
– Conj redness and edema
– GPC.
– Limbal gelatinous infiltrate.
– Trantas dots.
– Mucus discharge.
– Pseudoptosis.
– Tarsal conjunctival fibrosis.
THREE clinical forms
1.Palpebral type
2.Limbal type
3.Mixed type
8. Progression of vernal conjunctivitis
Diffuse papillary hypertrophy, most marked on superior tarsus
Formation of cobblestone papillae Rupture of septae - giant papillae
12. Diagnostic approaches:
Clinically.
Specific IgE maybe assayed in serum and tears.
CBC for eosinophilia.
Tear levels of tryptase
Conj scraping and tear cytology:
Eosinophils.
Basophils.
Neutrophils.
13. Histopathology:
Proliferative and degenerative changes in the epithelium:
Occur early with marked acanthosis, and intraepithelial pseudocysts.
Prominent cellular infiltration in the substantia propria:
Eosinophils, neutrophils, basophils, lymphocytes, and plasma cells.
Resident plasma cells and fibroblasts are also increased.
Typically mast cells contain enzymes tryptase and chymase
Hyperplasia of the connective tissues:
Mainly type III collagen, they run parallel to the surface forming the
fibrous structure for giant papillae.
14.
15. TREATMENT
NON PHARMACOLOGICAL INTERVENTION
Avoidance of allergens remains the first step
Cold compression provide symptomatic relief
especially itching
Lubrication with preservative free drops may wash
out allergans from conjunctival sac
Change of climate
16. PHARMACOLOGICAL INTERVENTION
FOR MILD CASES
1.Cool compress
2.Ocular lubricants
3.Decongestant
antihistaminics
4.Mast cell stabilisers
5.Environment control
FOR MODERATE TO SEVERE
CASES
1.topical/oral antihistaminics
2.Mast cell stabilisers
3.NSAIDS
4.Topical steroids
5.Acetyl cysteine to eliminate
mucous
18. STEROIDS
TOPICAL STEROIDS
For moderate to severe forms
Careful monitoring to detect steroid induced glaucoma and steriod
responder
MOA-inhibitis phospholipase which convert phospholipids to arachodonic
acid
EXAMPLES-
1.Prednisolone 0.01 to 1% hourly to BID
2.loteprednol 0.2 to 0.5% QID
3.flouromethalone BID TO QID
S/E may cause IOP raise and cataract formation
PULSE THERAPY
19. MAST CELL STABILISERS
Plays an important role
Most effective when began before the onset of symptoms,may need 14
days for clinical effects to occur
Until then topical antihistaminics and steroids can be used
Examples
1.cromolyn sodium QID
2.lodaxamide 0.1% QID
MOA Block influx along mast cell mem,inhibits degradation
S/E Burning/sting
LODAXAMIDE IS 2500 TIMES MORE POTENT
21. NSAIDS
TOPICAL
MOAinhibits cox pathway
Examples
--ketorolac 0.5%
--indomethacin 1%
--flubiprofen 0.03%
S/E burn/sting
ORAL
650 mg tid can be tried in severe to intractable cases along with mast cell
stabilisers
22. CYCLOSPORINE 2% QID
Severe to intractable VKC
MOAImmunosuppressive,T CELL inhibition
reduce collagen producn and coz apoptosis of fibroblasts
S/E burning sensation
Subjective and objectve improvement occurs in 3 days and complete
improvement will occur in 6 weeks
23. SURGICAL
SHIELD ULCER
--vision threatining complication of vkc
--treat with topical antibiotic and steriod eye ointment
--occlusive therapy
--if plaque forms in ulcer bed sup keratectomy may be beneficial for
epithelium healing
--non resolving shield ulcer may requrie keratectomy with amniotic
membrane grafting
GAINT PAPILLAE
--surgical excision
--cryotherapy for upper tarsus
--supratarsal steroid injection
--topical tacrolimus for refractile cases