This document discusses acute and chronic rhinitis. It defines rhinitis and rhinosinusitis. For acute rhinitis, it describes viral, bacterial, and irritative types including common cold, influenza, diphtheritic rhinitis. For chronic rhinitis it distinguishes between specific types caused by infections/diseases and non-specific types including chronic simple rhinitis, hypertrophic rhinitis, atrophic rhinitis, rhinitis sicca, and rhinitis caseosa. It provides details on causes, symptoms, complications, and treatments for each type.
inflammation of the ear, usually distinguished as otitis externa (of the passage of the outer ear), otitis media (of the middle ear), and otitis interna (of the inner ear; labyrinthitis).
inflammation of the ear, usually distinguished as otitis externa (of the passage of the outer ear), otitis media (of the middle ear), and otitis interna (of the inner ear; labyrinthitis).
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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.
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
10. Viral rhinitis
• Aetiology : Several viruses (adeno
virus,picorna virus and its sub-groups
such as rhinovirus, coxsackie, and
ECHO)
• Clinical features : Nasal stuffiness,
rhinorrhoea, sneezing, low grade fever.
• Secondary bacterial invasion may
occur.
• Treatment : Bed rest, Plenty of fluids,
Anthihistaminics, Nasal decongestants,
Analgesics & Antibiotics when
secondary infection supervenes.
Common cold
(Coryza)
11. • Sinusitis, pharyngitis,
tonsillitis,bronchitis, pneumonia and
otitis media.
Complications :
• Influenza viruses a, b or c.
• c/f are similar to common cold
Influenzal rhinitis
• Measles, rubella, chickenpox.
• Precede exanthemas by 2-3 days
Rhinitis associated
with exanthemas.
12. Bacterial 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.
Diphtheritic rhinitis
16. Chronic rhinitis
• Chronic simple rhinitis
• Hypertrophic rhinitis
• Atrophic rhinitis
• Rhinitis sicca
• Rhinitis caseosa.
Chronic non-
specific
inflammations of
nose include :
17. Chronic simple rhinitis
• 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.
• Pathology :
• Hyperaemia and oedema of mucous
membrane,
• Hypertrophy of seromucinous glands,
increase in goblet cells.
Aetiology
18. • 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.
Clinical features
19. • a. Treat the predisposing factor.
• b. Nasal irrigations with alkaline
solution.
• c. Nasal decongestants.
• d. Antibiotics help to clear nasal
infection.
Treatment
20. Hypertrophic rhinitis
Characterized by thickening of mucosa,submucosa,
seromucinous glands, periosteum and bone.
Aetiology :
• Recurrent nasal infections
• Chronic sinusitis
• Chronic irritation of nasal mucosa.
21. • Nasal
obstruction
• Nasal
discharge :
thick and
sticky.
• Headache
• Heaviness of
head
• Transient
anosmia.
Symptoms
• 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
turbinate.
• Mulberry
appearance of
inferior turbinate.
Signs
22.
23. • 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
Treatment
24. Compensatory hypertrophic rhinitis
• 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.
In cases of marked
deviation of septum
to one side.
25. Atrophic rhinitis
Chronic inflammation of nose
Characterized by atrophy of nasal mucosa and turbinate bones
• Aetiology : Exact cause is not known,
• Various theories regarding its causation
are:
• a. Hereditary factors
• b. Endocrinal disturbances : Starts at
puberty, involves females more than
males, tends to cease after menopause.
Primary atrophic
rhinitis :
26. 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.
27. • 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.
Pathology
28. • Charecterised by endarteritis and
periarteritis of terminal arterioles
• Result of chronic infection
• Benefits from vasodilator effect of
oestrogen therapy
Type 1:
• Vasodilatation of capillaries
• Might be made worse by oestrogen
therapy
Type 2:
29. • Commonly seen in
females and starts
around puberty.
• Foul smell from the
nose.(Cacosmia)
• Marked anosmia
(merciful anosmia)
• Nasal obstruction
• Epistaxis
• Nasal cavity full of
greenish or greyish
black dry crusts.
• Nasal cavities
appear roomy.
• Nasal mucosa
appear pale.
Clinical
features
30. • Disease persists for years
Prognosis :
• Medical :
• a. Alkaline 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.
Treatment
31. • Medical
• 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.
Treatment
32. • 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.
• b. Narrowing the nasal cavities.
• 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.
Treament
33.
34. • Specific infections like syphilis,
lupus,leprosy and rhinoscleroma.
• Longstanding purulent sinusitis,
• Radiotherapy of nose or excessive
surgical removal of turbinates.
SECONDARY
ATROPHIC RHINITIS
• Extreme deviation of nasal septum.
• Atrophic rhinitis on the wider side.
UNILATERAL
ATROPHIC RHINITIS
35. Rhinitis sicca
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).
• Bland ointment or an
antibiotic and steroid.
• Nasal douche.
Treatment
36. Rhinitis caseosa
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.
1)Owing to the continuity of the mucosa of the nasal mucosa and that of the sinuses some degree of inflammation is often present in the latter at the same time so constituting a rhinosinusitis
2) When the inflammation of the sinus is primary or overshadows that of the nasal fossae the condition called sinusitis
