Allergen immunotherapy (AIT) involves controlled exposure to allergens to reduce symptoms of allergic diseases like rhinitis, asthma, and conjunctivitis. It was first attempted in the early 1900s by immunizing people with plant extracts. While initial attempts caused adverse reactions, later studies found controlling the dose prevented this. Today, AIT is accepted for treating respiratory allergies and insect sting reactions but not food allergies or other conditions.
Steroids and their use in ENT
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BY:
DR RAI M. AMMAR MADNI
Steroids and their use in ENT
Get in touch with us at:
www.facebook.com/drraiammar
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For Any Book or Notes Visit Our Website:
www.allmedicaldata.wordpress.com
www.drraiammar.blogspot.com
YouTube Channel :
https://www.youtube.com/channel/UCu-oR9V3OdFNTJW5yqXWXxA
BY:
DR RAI M. AMMAR MADNI
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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.
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.
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.
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.
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
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
Presentation allergic rhinitis madan
1. Dr Madan
Jr ENT
ALLERGIC RHINITIS & VMR
AETIOLOGY, PATHOGENESIS,
CLINICAL FEATURE
TREATMENT AND ROLE OF
IMMUNOTHERAPY
2. • ―IgE mediated hypersensitivity disease of mucous
membranes of nasal airways characterized by
sneezing, watery nasal discharge , itching and nasal
obstruction‖
Durham et al.,1999
• Clinically defined : two or more nasal symptom:
running
blocking
itching
and sneezing
Definition
3. • Important health problem : social life, school performance,and work
productivity.
• Global health problem
• Prevalence : 10-20%
• Higher in pediatric age group - 42% - Wright et al .,1994
• AR -> 50% of all allergy cases seen in India
• Affecting every 6th person
• Peak age - 13 to 14.
Approx. 80% - develop symptoms < 20 - Skoner et al., 2001
AR : Epidemiology
4.
5. • Decrease in infectious diseases is causally linked
to the increase in the incidence of allergic and
autoimmune diseases .
Hygiene Hypothesis
7. Atopy :
• Tendency to develop specific IgE in response to normally
innocuous environmental allergens
• Eg. allergic rhinoconjunctivitis, asthma, atopic dermatitis
& food allergies
• Multiple genetic loci on chromosomes 5q, 11q, 12q,
• Family history - major risk factor
• 13% -/- parent
• 29% +/- parent/sibling
• 47% +/+ parents
Atopy, Risk Factors, and Comorbid Disorders
8. Higher socioeconomic status
Polluted environments
Late entry into daycare
Kramer et al ., 1999
Heavy maternal smoking
during first year of life
Risk factors
13. Eosinophil
• Developed in bone marrow - IL3,IL5, GM-CSF
• Half life of 8-18 hrs – blood
Half life of several days - peripheral tissue
• Eosinophil migration ( into peripheral tissue)
• Toxic inflammatory mediators in eosinophil:
Major basic protein, eosinophil peroxidase, eosinophil
cationic protein
• Synthesize and release lipid mediators:
leukotriene C4
Pathophysiology
14. Irritation of free
nerve endings---- Itching and sneezing
Increased
mucus production ------ Rhinorrhoea
Vasodilation -------- Congestion
Increased
vascular permeability---- Oedema
How are the symptoms caused?
Pathophysiology
28. •Rapid, efficient & cost effective
•Antigens - representative of that patient may
encounter & geographically based.
Negative result usually requires no additional testing
Positive result requires further testing of other
antigens in the group or family.
Contain multiple antigens, (pollen, mold, weeds, dust
mite, animal dander)
Skin prick
29. Superficial skin reaction, does not penetrate dermis
Highly specific, sensitive, convenient and safe
Requires positive (histamine) and negative (saline) control
Method
Drop of standardized allergen extract-volar aspect of forearm-pricked into skin-
lancet
Positive control (histamine) ,-ve control (saline or diluent) –innoculated
Separate lancet -each test
Read -mean wheal diameter -15 mins
Reactions ->2 mm - <5 yrs
>3 mm- >5 yrs
+ve results - 2mm greater than –ve results
Skin prick
30. 0.01-0.05 mL - antigen
wheal and flare measured after 10-20 min
can be used to detect most low-degree atopies
does not permit accurate quantitation of sensitivity
Causes relatively minimal patient discomfort
Disadvantages
• higher risk of anaphylaxis
• longer time
• Possible false positive
Intradermal test
31. Modified method of IDT
Serially diluted antigen extracts used
-determine minimal amt of antigen -comparing size of
wheal
Principle -lowest concentration of antigen -produces -
wheal
1. first wheal more than 2 mm larger than negative control
wheal
2. followed by second wheal that is at least 2 mm larger than
preceding one.
Endpoint signifies -safe starting point for immunotherapy
Skin Endpoint Titration(SET)
32. Indications
Impracticality of skin testing
• Skin disorder, drug inhibition, uncooperatvie patients
Clarification of skin test results
• Bizarre or borderline reactions
Prevention of systemic reactions
• Prior history of anaphylactic reaction, severe asthma,
stinging hypersensitivity
In Vitro Testing
33. RAST (radioallergosorbent assay)
Allergen-specific IgE antibody testing
useful –
if percutaneous testing not practical
patients on-
- beta-blockers
- antihistamines (skin testing is unreliable)
- dermatographism, children cannot tolerate skin
testing
highly specific but not sensitive
(Agency for Healthcare Research and
Quality,2005 )
In vitro testing
34. • Useful - identifying common allergens (e.g., pet dander, dust
mites, pollen, common molds)
• less useful - identifying food, venom, or drug allergies.
• Allergen coupled to - paper disc and incubated with patients
serum
• Disc washed and radioactive anti-IgE added
• Gamma counters quantitates radioactivity
Radioimmunosorbant Assay
(RAST)
35. Involves an additional washing procedure in order to reduce
non-immunologically bound radioactivity
Increased sensitivity to RAST
MRT system divided into 5 classes from 1-5, each
representing approximately fivefold increase in amount of
serum specific IgE antibody present in sample.
Class Counts 0.1ml
Class 1 751-1600 1:500
Class 2 1601-3600 1:2500
Class 3 3601-8000 1:12500
Class 4 8001-18000 1: 62500
Class 5 18001-40000 1: 312,500
Modified RAST
(MRT)
36. Allergen introduced- nose
Reaction - measured
Rarely necessary
Performed when
- +ve history & –ive SPT
- prior to immunotherapy
Allergen –suitable form ( not containing
phenol or other irritants)
Nasal allergen challenge
39. • Exclusive breast feeding-3 month
• Total avoidance of environmental tobacco
smoke,passive smoking for children and prgnant
women
• In infant and pre school children,multifaceted
intervention to reduce early life exposure to
house dust mites
• For indivisuals exposed to occupational
agents,specific prevention measures eliminate or
reducing occupational exposure.
Recommendation for prevention of
allergy :: ARIA
40. • In patients with AR and /or asthma
sensitive to house dust mite allergens, do
not use single chemical or physical
preventive methods aimed at reducing
exposure to house dust mites or their
combination.
• In patients with allergy to indoor molds
animal dander ,avoid exposure to these
allergens at home.
• In pts with occupational asthma ,
immediate and total cessation of
exposure to occupational allergen
Recommendation for prevention of
allergy :: ARIA
41.
42. • Inhibit both early and late phases
• Counter effects of other mediators
• Fast-acting, to control the early phase
• Dosing-od or bd for compliance
• No side effects
• Manage all symptoms
• Intranasal administration
Jaci et al.,1999
The “Ideal” Drug For Allergic Rhinitis Should
HaveThe Following Features:
43. Single most effective agents
Improve all nasal symptoms-nasal
congestion, rhinorrhea, itching &
sneezing
Currently available INS -
beclomethasone dipropionate,
budesonide
fluticasone
flunisonide
mometasone
triamcinolone acetonide.
Intranasal corticosteroids
44. Local : nasal burning , stinging, dryness, and
epistaxis.
( 5% to 10% )
Local candidiasis, sometimes seen with inhaled
corticosteroids rarely seen with nasal
corticosteroids.
Systemic side effects :
minimal or no suppression hypothalamic-pituitary-adrenal axis
(Wilson et al.,1998)
Osteocalcin – (marker of bone turnover ) - unaffected
no increased likelihood of bone fracture - regardless of
dose. (Suissa et al.,2004)
Side effects of INS
45. Medication Adult dosage Child dosage Minimum age
FDA pregnancy/nursing
risk category
Beclomethasone
(Beclovent)
One or two sprays per
nostril twice daily
One or two sprays per
nostril twice daily
Six years C
Budesonide (Rhinocort) One to four sprays per
nostril daily
One or two sprays per
nostril daily
Six years C
Ciclesonide (Omnaris) Two sprays per nostril
daily
NA 12 years C
Flunisolide (formerly
Nasarel)
Two sprays per nostril
twice or three times
daily
Two sprays per nostril
twice daily
Six years C
Fluticasone furoate
(Veramyst)
Two sprays per nostril
daily
One spray per nostril
daily
Two years C
Fluticasone propionate
(Flonase)
Two sprays per nostril
daily
One or two sprays per
nostril daily
Four years C
Mometasone (Nasonex) Two sprays per nostril
daily
One spray per nostril
daily
Two years C
Triamcinolone (Nasacort) One or two sprays per
nostril daily
One or two sprays per
nostril daily
Six years C
46. • Acts - stabilizing H1-
receptor - smooth muscle
cells, nerve endings,
and glandular cells -
reduction in all
symptoms
• Only modest effect -
nasal congestion
H1-antihistamines
47. Medication Minimum age Adult dosage
Second generation
Acrivastine/pseudoephedrine* 12 years 8 mg four times daily
Azelastine (Astelin) Five years Two sprays per nostril twice daily
Cetirizine* (Zyrtec) Six months 5 to 10 mg daily
Desloratadine* (Clarinex) Six months 5 mg daily
Fexofenadine* (Allegra) Two years 180 mg daily or 60 mg twice daily
Levocetirizine (Xyzal) Six years 5 mg daily
Loratadine* (Claritin) Two years 10 mg daily
Olopatadine (Patanol) 12 years Two sprays per nostril twice daily
First generation
Brompheniramine Two years 12 to 24 mg twice daily
Chlorpheniramine* Two years 4 mg four times daily
Clemastine* (Tavist) Six years 1.34 mg twice or three times daily
Cyproheptadine Two years 4 mg three times daily
Diphenhydramine (Benadryl) Two years 25 to 50 mg four times daily
Hydroxyzine (Vistaril) All ages 25 mg four times daily
Promethazine (Phenergan) Two years 25 mg four times daily
Triprolidine (Tripohist) Six years 2.5 mg four times daily
Oral and Intranasal Antihistamines
49. action via a1 and a2 adrenoreceptors
reduction in blood flow - nasal vasculature - increased nasal patency
5 to 10 mins topically
30 mins - orally.
Nasal decongestion - last
8 hours - topical use
24 hours - extended-release oral decongestants
nasal congestion only affected
(Cohan RH et al.,1972)
monotherapy with vasoconstrictors - limited role
oral decongestants + antihistamine- all cardinal symptoms of AR -
targeted.
Decongestants
50. Cysteinyl-leukotrienes (cys-LT)
High concentrations LTC4 - in nasal secretions atopic
individuals after allergen challenge ( Wang D et al.,1995)
LTD4 -increase in nasal mucosal blood flow & nasal airway
resistance
(Bisgaard Het al.,1986)
Blockage of the LT
- 5-lipoxygenase (5-LO) inhibitors
-receptor blockade -cys-LT1 receptor
Zileuton -blocks the 5-LO pathway..
Antileukotrienes
51. Receptor antagonists-
Montelukast & zafirlukast.
Zafirlukast performed no better than placebo
- seasonal AR
( Pullerits T et al.,1999)
Other study - reduction in upper respiratory
responses to cat exposure
(Phipatanakul W et al.,2000)
Montelukast - clinical efficacy seasonal AR
(Chervinsky P et al.,2004)
Antileukotrienes
52. • Montelukast + loratadine -superior reducing day time nasal
symptoms in seasonal AR (Meltzer EO et al.,2000)
• Montelukast could be useful as monotherapy and in
combination with other classes of drugs
Int. Rev. Allergol. Clin. Immunol., 2011
• leukotriene antagonists do not appear more effective than
nonsedating antihistamines.
• less effective than INS
Ratner PH et al.,2003
Useful- concomitant mild persistent asthma and intermittent AR.
Antileukotrienes
53. Actions of Various Nasal Preparations in the
Treatment of Rhinitis
Nasal
Preparation
Sneezing Itching Rhinorrhoea Congestion
Antihistamines +++++ ++++ +++ 0
Anticholinergics 0 0 +++++ 0
Corticosteroids +++++ +++++ +++ +++
Decongestants 0 0 + +++++
Mast cell
stabiliser
+++++ +++ + 0
Antileukotrienes +++ ++ 0 ++++
54. Medical procedure that uses controlled exposure
to known allergens to reduce the severity of
allergic disease
Disease accepted to be treated by immunotherapy:
• Allergic rhinitis
• allergic asthma
• allergic conjunctivitis
• insect sting hypersensitivity
Disease not accepted to be treated by
immunotherapy:
• Food allergy
• urticaria
• atopic dermatitis
Immunotherapy
55. Curtis (1900): immunize people with aqueous extract of
whole weeds
Dunbar(1903): immunize subjects who had grass-sensitive
hay fever with animal derived (horse and goose) grass pollen
antisera to subject’s nasal mucosa
Besredka and Steinhardt(1907): anaphylactic reaction
encountered during immunotherapy is due to immunizing too
rapidly or with too large dose of allergen
Noon and Cantab: introduced weight units for pollen doses
and quantization of individual sensitivity by in vivo testing.
Freeman and Koessler(1914): immunotherapy produced long
lasting results
Cooke(1915): Treatment by pollen immunization of 114
patients with hay fever and asthma.
Immunotherapy :History
56. Inclusion criteria:
IgE mediated disease
Inability to avoid allergen
Inadequecy of drug treatment
Lilited spectrum of allergen
Pts –risk & limitaion of tretment
Contraindications:
age < 5 yrs
use of beta-blockers
autoimmune dz.
pregnancy
uncontrolled asthma FEV1 < 70%
Immunotherapy
57. Gradual increase of allergen-specific IgG antibodies --
especially IgG4 subclasses (blocking antibody)
• intercept and neutralize allergen before it bound to cell-surface IgE
• form IgG-antigen-IgE complex and bind to the IgG receptor resulting
co-aggregation with the IgE receptor and inhibition of IgE receptor
triggering
decreased allergen-specific IgE antibodies
increase IgA and IgM antigen-specific B lymphocytes
• May limit antigen penetration into the body from mucosa
Deviation fromTh2 toTh1 cell
Immunotherapy
Mechanism:
58. • Durhan et al.:
• Randomized, placebo-controlled, double-
blind study
• Patients (32) with allergy to timothy grass-
pollen extract received 3 years of
immunotherapy treatment
• Patients then randomized to continue with
the immunotherapy or to receive placebo
• 15 matched patients never received
immunotherapy as control group
• Presence of symptoms and need for rescue
medication were measured after 3 years
Long term efficacy of
immunotherapy
59. • No significant difference in symptom scores and
use of rescue medication between two
immunotherapy groups, and were lower than
control group
• No difference in the late skin responses (size of
swelling, number of infiltrating T cells, cells
containing IL-4 mRNA) between two
immunotherapy groups, and significantly lower
than control group
• Immunotherapy for grass-pollen allergy for three
to four years induces prolonged clinical remission
accompanied by a persistent alteration in
immunologic reactivity
Long term efficacy of
immunotherapy
60. may prevent progression of rhinitis to asthma in
children
• Preventive AllergyTreatment Study:
• 205 children from 6 pediatric allergy centers in northern Europe
aged 6-14 years with grass or birch pollen allergy
• randomly assigned either to receive specific immunotherapy for 3
years or to a control group
• The children who were treated with immunotherapy had
significantly fewer asthma symptoms after 3 years as evaluated by
clinical diagnosis
may prevent onset of new sensitization in allergic
patients
Advantage of immunotherapy
61. • Proven allergy with skin test or RAST
• With allergic symptoms that are significant to
the patient
• Attempts to avoid allergens fail or impractical
• Treatment with medicine is not fully
successful or when medication is not well
tolerated.
• Young patients without chronic irreversible
changes in the upper airways
• Patient needs to be motivated and compliant
with treatment
Patient selection
62. Subcutaneous immunotherapy - only approved route of
administration in USA
Subcutaneous immunotherapy - involves a weekly
subcutaneous injection of an extract of the allergen, in
solution, in increasing doses until a standard maintenance
dose is reached.
This dose is then injected subcutaneously on a regular basis
(at intervals of approximately 20 days) for not less than 3
years for perennial allergens.
Short term immunotherapy does not affect the cytokine
profile and do not have long-term efficacy after
discontinuation
start at an earlier age, so that adverse changes to the
immune system can be prevented before they become
irreversible
Immunotherapy
63. Considerations in writing an allergy extract (vaccine) prescription are:
• decision as to which allergen extracts to include
• maintenance doses which have been proven to be clinically effective
• potency of the allergen extracts available
• patterns of cross-reactivity and
• deleterious effects of some allergen extracts on others with which they may be mixed.
Writing an allergen extract
(vaccine) prescription
64. Clinical experience indicates that the 1:1000 v/v
dilution of the maintenance vial is generally a safe
starting concentration
Skin endpoint titration can also be used to
determine starting dose, based on dilution which
elicited positive reaction
Patients may also be prick skin tested with each
dilution of extract mix and immunotherapy
commenced with the most dilute concentration
that yields a positive prick skin test.
Starting Concentration
65. Wilson et al.:
• systemic review of literature in Cochrane library
• 22 clinical studies, a total of 979 patients
• double-blinded, placebo-controlled, parallel-group studies
• highly significant reduction in symptoms as well as definite
decrease in medicine intake for symptoms
• whether sublingual therapy equals the efficacy of
subcutaneous immunotherapy is not clear
Sublingual immunotherapy
widely used and investigated in Europe since late 1980’s
keep the extract under the tongue for a couple of minutes and then swallow
it
dose of allergen is greater than subcutaneous immunotherapy (about 3-300
times higher)
Efficacy of sublingual immunotherapy
67. Double blind placebo-controlled study of ragweed
immunotherapy
Observed that SCIT alone induced allergen-
specific IgG4 that partially blocked binding of
allergen-IgE complexes to cells
This binding was completely blocked with the
addition of omalizumab
Immunotherapy with Omalizumab
Klunker S, Saggar LR, et al. Combination treatment with omalizumab
and rush immunotherapy for ragweed induced allergic rhinitis: inhibition
of IgE facilitated allegen binding. J AllergyClin Immunol 2007; 120:688-695.
68. Constant symptoms of profuse , clear rhinorrhea ,
nasal congestion without correlation to specific
antigen exposure or signs of atopy.
• ALSO CALLED noninfectious nonallergic rhinitis or idiopathic rhinitis , is a
chronic nasal dysfunction characterized by nasal hyperreactivity, i.e., nasal
blockage, rhinorrhea, and sneezing in response to nonallergic stimuli such as
•emotional factors
• exposure to cold air
• sudden temperature change
•humidity
• tobacco smoke
• or irritating body sprays and cosmetics
•Segal et al., in a recent report, studied previous nasal trauma as a
causative factor.
VASOMOTOR RHINITIS
69. Several mechanisms have been postulated to explain
the pathophysiology of idiopathic rhinitis
(i) increased permeability of the nasal epithelium
(ii) non-IgE-mediated inflammatory responses;
(iii) neurogenic responses are the most plausible
The classical theory is that vasomotor rhinitis is
caused by autonomic imbalance:
• Underactivity of the sympathetic nervous system
Overactivity of the parasympathetic nervous system
(singer et al).
Mechanisms of vasomotor rhinitis
70. Other theories
increase in vasoactive peptides released from mast cells.
• histamine,
• leukotrienes,
• prostaglandins,
• vasoactive intestinal polypeptide,
• kinins
but release of these peptides is non-IgE mediated, as it
is in allergic rhinitis
Mechanisms of vasomotor rhinitis
71. variable presentation.
Most patients - older
sometimes -seasonal pattern.
Patients present with
rhinorrhea (thick or scanty)
frontal headaches
congested turbinates
but usually no pruritis.
Rates of anxiety and depression are higher in women
with vasomotor rhinitis than in healthy women without
rhinitis
(Addolorato G et al)
Clinical presentation :
72. Vasomotor rhinitis - a diagnosis of exclusion i.e., absence of
• Infection
• Exposure to drugs,
• Significant anatomical disorder of the nose
• Hormonal change
• Negative response to skin prick test,
• Normal serum specific Ig
Lal D and Corey JP. Vasomotor rhinitis update.
The rhinomanometric exercise test
Acta Otorhinolaryngology
Diagnostic approach
73. If the irritant is known, the best treatment is prevention,
Pharmacological: Surgical
Antihistamines Triamcinoline injection
Ant-cholinergic agents Electrical cautrey
Topical steroids Cryosurgery
Decongestants Laser
Vidian neurectomy
Treatment
74. • Topical anticholinergics should be used for rhinorrhea caused
by vasomotor rhinitis.
• Azelastine (Astelin) may be used for vasomotor rhinitis
associated with rhinorrhea, sneezing, postnasal drip, and nasal
congestion.
• Topical corticosteroids may be used for vasomotor rhinitis
associated with nasal obstruction and congestion.
• Cromolyn sodium (Intal) may be used for vasomotor rhinitis
associated with sneezing and congestion in patients older than
two years.
A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented
evidence, usual practice, expert opinion, or case series
American Family Physician
75.
76. The effect of intranasal injection of botulinum toxin A on the
symptoms of vasomotor rhinitis
Intranasal injection of BTX-A is a highly effective, safe, and
simple treatment modality with a long-lasting effect for patients
with VMR. Botulinum toxin A may be a good alternative especially
for the treatment of resistant VMR cases.
Cengiz O zcan, et al
77. Vidius (1509) 1st –identified
Sectioning of GSPN as a treatment for VMR -1st proposed by
Zeilgelmann .
VIDIAN NERVE
78. CRYOSURGERY ON POSTGANGLIONIC FIBERS
(POSTERIOR NASAL BRANCHES) OF THE PTERYGOPALATINE
GANGLION FOR VASOMOTOR RHINITIS
Operative technique
79. • Incision –hard palate
• Mucoperiosteal dissected till
palatal aponeurosis is visible
• Soft palate incised from post
end of hard palate-nasopharynx
• L Shaped incision long limb-just above
the tubal elevation, short limb- b/w post. &
lat. Wall of nasopharynx
• Mucosal elevation-exposed med pterygoid
plate-drilled-canal opened-nerve cut &
cauterized
Transpalatal approach
80. • Using operative microscope
• Incision-sup surface of inf turbinate-post end
of middle turbinate
• Mucoperiosteum elevated
• Ethmoidal creast identified
• Exposing sphenopalatine
foramen-ptergoid canal identified
• Nerve cauterized.
Transnasal approach
81. Step1 –lateralization of middle
turbinate
Step2-perforation of ant wall of
sphenoid sinus(using elevator)- opening
over the ant. Face of sphenoidal sinus
is widened till vidian canal is
identified.
Step3-wall of vidian canal is
perforated –nerve is severed.
Endoscopic intrasphenoidal
82. • Incision –curved incision given in middle
meatus(post end of sup margin of inf
turbinate to horizontal part of ground
lamella)
• Mucoperiosteal elevated
• The sphenopalatine foramen and sup
portion of perpendicular plate of palatine
bone - exposed
• Post. Sup. And post. Inf. Nasal nerve
identified and sectioned.
Endoscopic post. Nasal neurectomy
83. • Palpate the lateral nasal wall behind the uncinate
and above the insertion of the inf turbinate
• Identify the soft membranous part of post
frontanelle
• Identified palatine bone
• C shaped incision
• Mucoperiosteal flap raised
• Dissection is continued till the ant. Face of sphenoid
sinus
• Post. Rim of sphenopalatine foramen widened
• Vidian canal identified—nerve exposed--cut
Endoscopic vidian neurectomy