Nasal discharge, also known as rhinorrhea, is a common symptom that can be caused by a variety of conditions related to the ear, nose, and throat (ENT). It is the result of excess mucus production in the nasal cavity, which can be caused by inflammation or infection of the nasal passages.
Common causes of nasal discharge include allergies, colds, sinus infections, and nasal polyps. Allergies can cause the nasal passages to become inflamed and produce excess mucus, leading to a runny nose. Colds and sinus infections can also cause inflammation and infection, leading to nasal discharge.
Nasal polyps are growths in the nasal cavity that can obstruct airflow and cause chronic inflammation and excess mucus production. Other less common causes of nasal discharge include foreign bodies in the nasal cavity, tumors, and hormonal changes during pregnancy.
Treatment for nasal discharge depends on the underlying cause. For allergies, antihistamines and nasal corticosteroids may be recommended. For colds and sinus infections, decongestants, saline nasal sprays, and antibiotics may be used. Nasal polyps may require surgical removal.
In addition to nasal discharge, other symptoms that may be present with ENT-related conditions include nasal congestion, headache, facial pain or pressure, cough, and sore throat. If nasal discharge is persistent, accompanied by other symptoms, or affects quality of life, it is important to seek medical evaluation by an ENT specialist.
Nasal discharge, also known as rhinorrhea, is a common symptom that can be caused by a variety of conditions related to the ear, nose, and throat (ENT). It is the result of excess mucus production in the nasal cavity, which can be caused by inflammation or infection of the nasal passages.
Common causes of nasal discharge include allergies, colds, sinus infections, and nasal polyps. Allergies can cause the nasal passages to become inflamed and produce excess mucus, leading to a runny nose. Colds and sinus infections can also cause inflammation and infection, leading to nasal discharge.
Nasal polyps are growths in the nasal cavity that can obstruct airflow and cause chronic inflammation and excess mucus production. Other less common causes of nasal discharge include foreign bodies in the nasal cavity, tumors, and hormonal changes during pregnancy.
Treatment for nasal discharge depends on the underlying cause. For allergies, antihistamines and nasal corticosteroids may be recommended. For colds and sinus infections, decongestants, saline nasal sprays, and antibiotics may be used. Nasal polyps may require surgical removal.
In addition to nasal discharge, other symptoms that may be present with ENT-related conditions include nasal congestion, headache, facial pain or pressure, cough, and sore throat. If nasal discharge is persistent, accompanied by other symptoms, or affects quality of life, it is important to seek medical evaluation by an ENT specialist.
Inflammation of the mucosa of sinuses associated with inflammation of the nasal mucosa is called rhinosinusitis (RS).
CLASSIFICATION:
• Acute RS: Symptoms lasting for less than 4 weeks with complete resolution.
• Subacute RS: Duration 4-12 weeks.
• Chronic RS: Duration ~ 12 weeks.
• Recurrent RS: Four or more episodes of RS per year; each lasting for 7-10 days or more with complete resolution in between the episodes.
• Nasal obstruction.
• Nasal discharge/congestion, anterior, or posterior in the form of postnasal drip.
• Facial pain or pressure.
• Alteration in the sense of smell, hyposmia or anosmia.
• Other symptoms include cough, fever, halitosis, fatigue, dental pain, pharyngitis, headache or ear fullness.
Rhinitis commonly known as a stuffy
nose,
is the medical term describing
irritation and inflammation of some internal areas of the nose .
It is the inflammation of the nasal mucosa.
Acute Rhinitis is also known as the common cold.
It may be bacterial or viral.
It may be classified as acute & allergic .
It usually lasts 5 to 7 days.
It may be bacterial or viral or irritants.
Which is caused by Rhinoviruses and Coronaviruses , or bacterial sinusitis .
Inflammation of the mucosa of sinuses associated with inflammation of the nasal mucosa is called rhinosinusitis (RS).
CLASSIFICATION:
• Acute RS: Symptoms lasting for less than 4 weeks with complete resolution.
• Subacute RS: Duration 4-12 weeks.
• Chronic RS: Duration ~ 12 weeks.
• Recurrent RS: Four or more episodes of RS per year; each lasting for 7-10 days or more with complete resolution in between the episodes.
• Nasal obstruction.
• Nasal discharge/congestion, anterior, or posterior in the form of postnasal drip.
• Facial pain or pressure.
• Alteration in the sense of smell, hyposmia or anosmia.
• Other symptoms include cough, fever, halitosis, fatigue, dental pain, pharyngitis, headache or ear fullness.
Rhinitis commonly known as a stuffy
nose,
is the medical term describing
irritation and inflammation of some internal areas of the nose .
It is the inflammation of the nasal mucosa.
Acute Rhinitis is also known as the common cold.
It may be bacterial or viral.
It may be classified as acute & allergic .
It usually lasts 5 to 7 days.
It may be bacterial or viral or irritants.
Which is caused by Rhinoviruses and Coronaviruses , or bacterial sinusitis .
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
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
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
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
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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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
3. 1) Common cold (Coryza)
Aetiology : Several viruses (adeno virus,
picorna virus and its sub-groups sucha s
rhinovirus, coxsackie, and ECHO)
Clinical features : Nasal stuffness,
rhnorrhoea, sneezing, low grade fever,
secondary bacterial invasion may occur.
Treatment : Bed rest, Plenty of fluids,
Anthihistaminics, Nasal decongestants,
Analgesics, Antibiotics, when secondary
infection supervenes.
4. Complications :
Sinusitis, pharyngitis, tonsillitis,
bronchitis, pneumonia and otitis
media.
Influenzal rhinitis - Influenza
viruses A, B or C.
c/f are similar to common cold
Rhinitis associated with
exanthemas. Measles, rubella,
chickenpox.
precede exanthemas by 2-3 days
5. Diphtheritic rhinitis :
• Primary
• Secondary to faucial diphtheria
• May occur in acute or chronic form
• Greyish membrane is seen covering the inferior
turbinate and the floor of nose; membrane is tenacious
and its removal causes bleeding
Treatment : Isolation of the patient, systemic
penicillin and diphtheria antitoxin.
6. Chronic non-specific inflammations of
nose include :
1. Chronic simple rhinitis
2. Hypertrophic rhinitis
3. Atrophic rhinitis
4. Rhinitis sicca
5. Rhinitis caseosa.
7. Aetiology : Predisposing factors
a. Persistence of nasal infection due to sinusitis,
tonsillitis, and adenoids.
b. Chronic irritation from dust, smoke, cigarette
smoking, snuff.
c. Nasal obstruction.
d. Vasomotor rhinitis
e. Endocrinal or metabolic factors, e.g.
hypothyroidism.
a. Pathology : Hyperaemia and oedema of
mucous membrane, Hypertrophy of
seromucinous glands, increase in goblet
cells.
8. Clinical features :
a. Nasal obstruction
b. Nasal discharge. It may be mucoid or
mucopurulent. Postnasal drip.
c. Headache
d. Swollen turbinates – They pit on pressure,
shrink with application of vasoconstrictor
drops (this differentiates the condition from
hypertrophic rhinitis).
e. Post-nasal discharge. Mucoid or
mucopurulent discharge.
9. Treatment :
a. Treat the predisposing factor.
b. Nasal irrigations with alkaline solution.
c. Nasal decongestants.
d. Antibiotics help to clear nasal infection.
10. Characterized by thickening of mucosa,
submucosa, seromucinous glands,
periosteum and bone.
Aetiology :
Recurrent nasal infections
Chronic sinusitis
Chronic irritation of nasal mucosa.
11. Symptoms :
Nasal obstruction
Nasal discharge : thick
and sticky.
Headache
Heaviness of head
Transient anosmia.
Signs :
Hypertrophy of
turbinates
Turbinal mucosa is
thick, does not pit on
pressure, little
shrinkage with
vasoconstrictor drugs
due to underlying
fibrosis.
Maximum changes in
the inferior turbiante.
Mulberry appearance
of inferior turbiante.
12. Treatment :
Discover the cause and remove it.
Reduction in size of turbinates by
a. Liner cauterisation
b. Submucosal diathermy
c. Cryosurgeryof turbinates
d. Partial or total turbinectomy
e. Submucous resection of turbinates bone.
f. Lasers
13. Compensatory
hypertrophic rhinitis
• In cases of marked deviation of
septum to one side.
• Roomier side of the nose shows
hypertrophy of inferior and middle
turbinates.
• To reduce the wide space to
overcome the ill effects of drying
and crusting.
14. Chronic inflammation of nose
characterized by atrophy of nasal mucosa
and turbinate bones.
Primary atrophic rhinitis :
Aetiology : Exact cause is not known,
Various theories regarding its causation
are:
a. Hereditary factors
b. Endocrinal disturbances : Starts puberty,
involves females more than males, tends to
cease after menopause.
15. c. Racial factors – White.
d. Nutritional deficiency : Deficiency of
vitamin A, D or iron.
e. Infective : Klebsiella ozaenae, (Perez
bacillus), diphtheroids, P.vulgaris, Esch.
Coli, Staphylococci and Streptococci but
they are all considered to be secondary
invaders.
f. Autoimmune process : The body reacts by
a destructive process to the antigens
released from the nasal mucosa.
16. Pathology :
Ciliated columnar epithelium is
replaced by stratified squamous type.
Atrophy of seromucinous glands,
venous sinusoids and nerve elements.
Obliterative endarteritis.
The bone of turbinates undergoes
resorption.
Paranasal sinuses are small.
17. Type 1: charecterised by endarteritis and
periarteritis of terminal arterioles
-result of chronic infection
- benefits from vasodilator effect of
oestrogen therapy
Type 2: vasodilatation of capillaries
- which might be made worse by
oestrogen therapy
18. Clinical features :
Commonly seen in females and starts around
puberty.
Foul smell from the nose.
Marked anosmia (merciful anosmia)
Nasal obstruction
Epistaxis when the crusts are removed.
Nasal cavity full of greenish or greyish black dry
crusts.
Nasal cavities appear roomy.
Nasal mucosa appear pale.
Septal perforation and dermatitis of nasal vestibule.
Nose shows saddle deformity.
19. Prognosis :
Disease persists for years
Treatment :
1. Medical :
a. Nasal irrigation and removal of crusts.
b. 25% glucose in glycerine. – Inhibits the growth
of proteolytic organisms which are responsible
for foul smell.
c. Local antibiotics – KemicetineTM
antiozaena
solution contains chloromycetin, oestradiol and
vitamin D2.
20. d. Oestradiol spray – increase vascularity of
nasal mucosa and regeneration of
seromucinous glands.
e. Placental extract injected submucosally.
f. Systemic use of streptomycin – reducing
crusting and odour. Effective against
Klebsiella organisms.
g. Potassium iodide by mouth promotes and
liquefies nasal secretion.
21. 2. Surgical :
a. Young’s operation – Both the nostrils are closed
completely just within the nasal vestibule by raising
flaps. They are opened after 6 months or later.
Modified young’s operation - Aims to partially close
the nostrils.
a. Narrowing the nasal cavities. Among the
techniques followed, some are :
Submucosal injection to teflon paste.
Insertion of fat, cartilage, bone or teflon strips
under the mucoperiosteum of the floor and lateral
wall of nose and the mucoperichondrium of the
septum.
Section and medial displacement of lateral wall of
nose.
22. SECONDARY ATROPHIC RHINITIS :
Specific infections like syphilis, lupus,
leprosy and rhinoscleroma.
Longstanding purulent sinusitis,
radiotherapy or nose or excessive
surgical removal of turbinates.
UNILATERAL ATROPHIC RHINITIS :
Extreme deviation of nasal septum.
Atrophic rhinitis on the wider side.
23. Crust-forming disease
Seen in patients who work in hot, dry and
dusty surroundings.
Confined to the anterior third of nose.
The ciliated columnar epithelium undergoes
squamous metaplasia.
Atrophy of seromucinous glands (Crusts,
epistaxis, septal perforation).
Treatment :
Bland ointment or an antibiotic and steroid.
Nasal douche.
24. Unilateral and mostly affecting males.
Nose is filled with offensive purulent
discharge and cheesy material.
Sinus mucosa becomes granulomatous. Bony
walls of sinus may be destroyed.
Treatment :
Removal of debris and granulation tissue
Free drainage of the affected sinus.
26. IgE – mediated immunologic response
to nasal mucosa to air-borne allergens.
Two clinical types
1. Seasonal. Symptoms appear in or around a
particular season.
2. Perennial. Symptoms are present throughout
the year
27. AETIOLOGY :
Inhalant allergens – Pollen from the
trees and grasses, mold spores, house
dust, debris from insects or house mite
are common offenders.
Genetic predisposition
28. Sensitized
Mast cell
Antigen
Release of mediators
Performed
• Histamine
• ECF – A
• NCF – A
• Heparin
•Others
Newly synthesized
• Prostaglandins e.g. PGD2
• Leukotrienes e.g. SRS-A
• PAG
• Thromboxane A
• TNFa
29. Clinically allergic response occurs in
2 phases :
1. Acute or early phase : Within 5-30 min,
sneeing, rhinorrhoea nasal blockagte
and/or bronchospasm. Due to release of
vasoactive amines like histamine.
2. Late or delayed phase : 2-8 hours after
exposure to allergen without additional
exposure. Due to infiltration of
inflammatory cells eosinophils, neutrophils,
basophil, monocytes and CD4+ T cells at
the site of antigen deposition.
30. No age or sex predilection
Symptoms of seasonal nasal allergy.
Paroxysmal sneezing, 10-20 sneezes at a
time, nasal obstruction, watery nasal
discharge and itching in the nose.
Symptoms of perennial allergy.
Frequent colds, persistently stuffy nose, loss
of sense of smell due to mucosal oedema,
postnasal drip, chronic cough.
Signs of allergy may be seen in the nose,
eyes, pharynx or larynx.
31. Nasal signs :
• Transverse nasal crease
• Allergic salute
• Pale and oedematous nasal mucosa
• Thin, watery or mucoid discharge
Diagnosis :
• Detailed history and physical examination.
32. Investigations :
1. Total and differential count. Peripheral
eosinophilia.
2. Nasal smear shows large number of
eosinophils.
3. Skin tests. Prick, scratch and intradermal
tests.
4. Radioallergosorbent test (RAST). Measures
specific IgE antibody concentration in the
patient’s serum.
5. Nasal provocation test.
34. Treatment :
1. Avoidance of allergen.
2. Treatment with drugs.
a. Antihistaminics
b. Corticosteorids
Oral corticosteorids
Use should be limited to acute episodes
Several systemic side effects
Topical steroids such as beclomethasone
dipropionate, budesonide, flunisolide acetate,
fluticasone are used as aerosols, very effective
in the control of symptoms.
Fewer systemic side effects.
35. c. Sodium chromoglycate
Stabilizes the mast cells and prevents them
from degraulation.
2% solution for nasal drops or spray or as an
aerosol powder.
3. Immunotherapy
Allergen is given in gradually increasing
doses till the maintenance dose is reached.
Immunotherapy suppresses the formation
of IgE.
36. Non-allergic rhinitis but clinically
simulating nasal allergy.
Condition usually persists throughout
the year.
37. Pathogenesis :
Parasympathetic stimulation causes
vasodilation and engorgement. Over activity
of parasympathetic system also causes
excessive secretion from the nasal glands.
Autonomic nervous system is under the
control of hypothalamus therefore emotions
play a great role in vasomotor rhinitis.
Nasal mucosa is also hyper-reactive and
responds to several non-specific stimuli e.g.
change in temperature, humidity.
38. Symptoms :
Paroxysmal sneezing. In the morning.
Excessive rhinorrhoea. Profuse and watery.
Nasal obstruction
Postnasal drip.
Signs :
Nasal mucosa over the turbinates is
generally congested and hypertrophic.
Complications :
Nasal polypi, hypertrophic rhinitis and
sinusitis.
39. TREATMENT :
Medical :
1. Avoidance of physical factors which
provoke symptoms.
2. Antihistaminics and oral nasal
decongestants.
3. Topical steroids.
4. Systemic steroids – for a short time in
very severe cases.
5. Psychological factors should be
removed.
40. Surgical :
1. Nasal obstruction can be relieved by
measures which reduce the size of
nasal turbinates.
2. Excessive rhinorrhoea, relived by
sectioning the parasympathetic
secretomotor fibres to nose (vidian
neurectomy).
41. Other forms of non-allergic rhinitis :
1. Drug-induced rhinitis : Several
antihypertensive drugs. Some
anticholinesterase drugs e.g. neostigmine.
Contraceptive pills because of oestrogens.
2. Rhinitis medicamentosa :Topical
decongestant nasal drops cause rebound
phenomenon.Their excessive use causes
rhinitis.Treated by withdrawal of nasal
drops, short course of systemic steroid.
42. 3. Rhinitis of pregnancy : Due to hormonal
changes. Local measures such as limited
use of nasal drops.
4. Honeymoon rhinitis
5. Emotional rhinitis : due to several
emotional stimuli.
6. Rhinitis due to hypothyroidism :
Predominance of parasympathetic activity.
7. Non air-flow rhinitis : Seen in patients of
laryngoectomy and tracheostomy.