The document describes various types of rhinitis including infective causes like the common cold from viruses like rhinovirus and influenza. It also discusses chronic rhinitis, which can be simple or hypertrophic. Non-infective causes like allergic rhinitis are mentioned. Specific conditions involving the nasal mucosa are outlined such as atrophic rhinitis, ozaena, rhinoscleroma, and nasal cholesteatoma. Causes, symptoms, examinations, and treatments are provided for each condition in the summary.
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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.
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.
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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9. CHRONIC SIMPLE RHINITIS
C/F – Nasal obstruction – worst on lying at
night
Nasal discharge – mucoid/ mucopurulent
Post nasal discharge
Headache – enlarged turbinates touch septum
Loss of smell
Signs – secretions present, enlarged
turbinates which pit on pressure and shrink
on applying vasoconstrictor
10. CHRONIC HYPERTROPHIC RHINITIS
Advanced stage
Irreversible mucosal thickening, no pitting on
pressure or no shrinkage of turbinates due to
fibrosis – permanent hypertrophied turbinates
Persistent severe nasal obstruction at night
Mouth breathing, hawking, thick voice
Diffuse hypertrophy mainly of inferior turbinate –
papillary hypertrophy anterior end, mulberry
hypertrophy posterior end (pinkish)
11. Diagnosis – DNE, X Ray PNS
Treatment
Treat the cause
Antibiotics for acute exacerbations
Alkaline nasal douching
For early stage – topical steroids, nasal
decongestants
For advanced stage – turbinoplasty –
turbinectomy, SMR, diathermy, electrocautery,
LASER
COMPENSATORY HYPERTROPHY RHINITIS – due to
marked DNS on opposite side
12. Due to prolonged use of local nasal decongestant
drops – oxymetazoline, xylometazoline – more
than 1 week
Rebound congestion
C/F
Nasal obstruction worst at night, headache due
to blockage ostia
Bloody red nasal mucosa with granulations,
turbinate hypertrophy
Treatment – stop nasal drops, oral/systemic
steroids, intranasal steroids, turbinate reduction
14. Atrophic changes affecting the anterior nasal
cavity due to dry and dusty enviroment
Etiology – farmers, miners, bakers, iron and
goldsmith, alcoholics, nutritional deficiency, post
nasal surgery
Pathology – respiratory epithelium changes to
squamous, atrophy of seromucinous glands
C/F – dirty black crusts in anterior 1/3rd of nasal
cavity which on removal can cause ulceration,
nasal bleed, perforation, dry mucosa
Non foul smelling nasal discharge
Nasal obstruction, Epistaxis
15. Treatment
Change of place of work, lifestyle
Avoid nose picking, removal of crusts
Use masks and filters at work
Lubrication with antibiotic steroid ointment
25% glucose in glycerine nasal drops – 3
drops TDS for 2-3 months
Alkaline nasal douching
16. NASAL CHOLESTEATOMA
Chronic inflammation of nose due to formation
of granulations and foul smelling offensive
cheesy material in nasal cavity
Affects nose and PNS (mainly maxillary sinus)
Etiology – nasal stenosis, adhesions, synechiae,
sinusitis, FB Nose, rhinolith, fungal infections
Pathology – stagnation of secretions,
accumulated discharge, caseous material
formation, destruction of bony walls, on
microscopy – cholesterol crystals
Males (mc), any age (3rd and 4th decade mc)
17. C/F – foul smelling nasal discharge, nasal
obstruction, loss of smell, headache, halitosis,
defective taste
Signs – cheesy material (white debris) in nasal
cavity, ulceration of nasal mucosa, perforation
and destruction of walls, external deformity
Investigations
DNE, CT PNS, X Rays
Biposy
Fungal culture
D/D – Malignancy, Fungal sinusitis
18. Complications – Intracranial spread, orbital
complications (rare)
Prognosis - good
Treatment
Oral Pencillin thrice a day for 7 days
Endoscopic removal of cause
Removal of debris and granulation tissue
FESS – for restoration of sinus drainage
19. Chronic inflammatory condition of nose associated with
progressive atrophy of nasal mucosa and turbinate bones
charaacterised by greenish yellow crusts (posterior part),
foul smell (OZAENA)
Types
Primary
Idiopathic
Endocrinal imbalance – more common in females during
menstrual age (puberty to menopause), aggravated during
menstruation and pregnancy
Nutritional deficiency – Vitamin A, D, Iron – more in poor
socio economic group, malnourished
Racial – more in whites and yellow races
Hereditary – AD
Climate - Common in tropical countries like India
22. Signs
Depression of bridge of nose, broadened nose
Nasal vestibulitis
Fetor
Roomy nasal cavities, turbinate atrophy
Pale dry mucosa
Nasopharynx visible on ant rhinoscopy
Septal perforation
Complications – atrophic pharyngitis (dry throat,
irritation, atrophic laryngitis (cough, hoarseness),
Sinusitis with small PNS, middle ear infection
(Eustachian tube obstruction), Maggots in nose
(foul smell, nerve atrophy)
23. Investigations
CBC – Hb
Serum Iron and proteins
VDRL
C/S of Nasal swab
X Ray PNS, CT PNS – hypoplasia, opacity,
thickened walls of maxillary sinus, erosion of
lateral wall
Chest X Ray – TB
Nasal smear/biopsy
D/D – Rhinitis sicca, Syphilis, leprosy,
rhinoscleroma, rhinoloith, FB, Sinusitis (no crusts)
Prognosis – life long , regress after middle age
24. Treatment
Purpose – restore hydration, minimize crusting
Medical
Alkaline nasal douching – 56.8 g (2 parts) Sodium
chloride/ salt, 28.4 g (1 part) of Sodium
bicarbonate/baking soda (loosen crusts), 28.4 g (1 part) of
Sodium biborate/washing soda (anti septic) in 280 ml (2
glasses) of warm water irrigation using 20 ml syringe , 2-3
times a day for life long
25% glucose in glycerine nasal drops/ paint after crust
removal – inhibit proteolytic organisms/ foul smell
Gauze pack soaked in liquid paraffin – lubricate nose,
loosen crusts
Kemicetene anti ozaenae solution
Potassium iodide orally – loosens secretions
25. Placental extract injections submucosally
Estrogen/ Estradiol nasal spray – increase vascularity
of nasal mucosa
Vitamin A, D, E, Iron
Chloramphenicol nasal drops
Streptomycin/ Rifampicin
Surgical
Young’s operation- both nasal apertures completely
closed for upto 2 years anteriorly
Modified young’s operation – a 3 mm opening left for
breathing
Submucosal injection of teflon paste, fat, cartilage
Section and medial displacement of lateral wall
Transfer of stenson’s duct to maxillary sinus
26. Mikulicz disease
Chronic granulomatous disease characterised by
sclerosis and stenosis of nasal passages can also
effect pharynx, larynx, trachea
Etiology
Klebsiella rhinoscleromatis
Young age – 2nd or 3rd decade
Females
Rural areas
Poor socio economic status, poor nutrition and
hygiene
North India, East Europe, Middle East, South
America, Africa
27. Pathogenesis
Air borne – droplet/ contamination material
Pathology
Begins in vestibule of nose, then spread to nose, pharynx,
larynx, trachea, bronchi
Histopathology
Mikulicz cells – large foam cells containing bacilli
Russell bodies- homogenous eosinophilic inclusion bodies
C/F
Prodromal/catarrhal stage – nasal mucosa congested, foul
smelling purulent yellowish nasal discharge, sneezing
Atrophic stage – atrophy but pink mucosa, nasal
obstruction, crusting, headache, epistaxis
Granulomatous stage – multiple painless rubbery nodule,
non ulcerative, enlarge to form hard pale granulomas
28. Broadening, thickening and woody feel of
nose (Hebra nose)
Dyspnoea and stridor (if larynx affected)
Cicatrization stage
Fibrosis of external nose (Tapir nose)
Stenosis of vestibule, nasopharynx, larynx
with adhesions leading to respiratory distress
Diagnosis – biopsy
D/D – Atrophic rhinitis (pale mucosa), tertiary
syphilis
29. Treatment
Prolonged antibiotics for 4-6 weeks
Streptomycin – DOC
Tetracycline
Amoxycillin, ciprofloxacin, rifampicin,
ampicillin, doxycycline
Steroids – to reduce fibrosis
Nasal reconstruction – to establish airway
RT – not effective
30. Chronic granulomatous disease affecting the mucous
membrane of nose, nasopharynx manifesting as vascular
polyps
Can also affect larynx, bronchi, conjuctiva, skin, genitals,
lip and palate and spread to liver and spleen through
blood
Endemic in coastal areas- india, srilanka, africa, south
america
Young age – 15 to 40 years M:F 4:1
Etiology – Rhinosporidium seeberi (aquatic protozoa)/
Kinealyi
water borne – contaminated water of ponds with animal
dung – cattle, horses, mules
Air borne – dust mixed with animal dung
Trauma is a predisposing factor
31. Pathology
Sporangia – chitinous cyst containing spores
Symptoms
Nasal obstruction U/L
Epistaxis
Blood tinged nasal discharge
Post nasal discharge, hyposmia
Signs
U/L leafy pink to purple granular polypoidal mass with
black spots bleeds on touch, pedunculated and friable
attached to nasal septum or lateral wall or nasopharynx
Avoid probe test
Biopsy – avoided as bleed, sporangia, can do DNE
D/D – Nasal growth
32. Treatment
Complete excision of mass by diathermy
knife or LASER and cauterization of base
Endoscopic examination – to identify pedicle
For larger mass – lateral rhinotomy approach
Dapsone
Amphotericin B
33. Mycobacterium tuberculosis
Secondary to pulmonary TB
Affects anterior part of nasal cavity (cartilaginous
septum), ant end of inferior turbinate
Stages
Catarrhal – inflammation and congestion
Nodular – tuberculoma formation
Ulcerative – septal perforation
Cicatrization – fibrosis, stenosis, adhesions
Pathology – acid fast bacilli, epitheloid cells,
langheran giant cells
34. C/F
Serosanginous nasal discharge, later stage –
blood stained
Nasal obstruction
Pain – due to exposed nerve endings
Signs – bright nodular thickening of septum
with perforation, adhesions, stenosis
Investigations – chest x ray, swab c/s, biopsy
, sputum for AFB, biopsy, x ray pns
Treatment – ATT, surgical reconstruction
35. Indolent and chronic form of TB
F:M 2:1
Early adult age
Nasal vestibule (mc), skin of nose and face
Pathology – granuloma formation, fibrosis,
stenosis
C/F
Foul smelling nasal discharge, crusting, nasal
obstruction, epistaxis
Butterfly appearance of nasal skin
Reddish brown APPLE JELLY NODULES – become
prominent on pressing by a glass slide
Chronic vestibulitis, septal perforation
36. Diagnosis – biopsy, c/s, mantoux test, chest
x ray
Complications – atrophic rhinitis, chronic
dacrocystitis
Treatment
ATT
Reconstructive surgery
37. Hansen’s disease
Lepromatous leprosy – nose involved in all cases
Tropical/subtropical warm/wet climate
Anterior end of inferior turbinate (mc), septum
Mycobacterium leprae
Mode of transmission – prolonged contact, droplet
infection
C/F
Catarrhal stage – coryza with bacterial infiltration following
nose picking
Nodular stage – thickening of affected part, secondary
atrophic rhinitis
Ulcerative stage – septal perforation, nasal destruction
Cicatrization stage – fibrosis, stenosis of vestibule
Saddle nose deformity, columellar retraction, AR
39. Treponema Pallidium – spirochete
ACQUIRED SYPHILIS
Primary
CHANCRE – hard, non painful, ulcerated papule most
commonly involves nasal vestibule with enlarged rubbery
LN – rare
Secondary
Simple catarrhal rhinitis- skin rash, rhinitis, fever, crusting
Tertiary – MC
Gumma – affects bony part of septum (mc), cartilage part
(rare) – swelling seen, ulcerates, scarring
Septal perforation, palatal perforation, collapse of nasal
bridge, pain, headache worst at night, crusts, bleeding,
offensive nasal discharge , vestibular stenosis
40. Congenital
Birth – 1st three months of life
Snuffles – excoriation of nasal vestibule or skin
of upper lip, features of simple catarrhal rhinitis
Delayed – puberty – Gumma formation
Diagnosis – biopsy, VDRL test
Treatment
Pencillin – DOC
Doxycycline, amoxycillin
Alkaline nasal douching
Surgical reconstruction when disease cured/free
41. Granulomatous disease associated with
abnormality of cell mediated and humoral
immunity
Resembles TB but Non caseating
Females , 3rd to 5th decade
Involves almost all organs – nose, lungs, eyes,
salivary glands, tonsils, larynx, skin, ears
Nasal features – submucosal bluish red nodules
on septum and inferior turbinate, vestibule
Crusts with nasal obstruction, pain, epistaxis
Also cause – lymphadenopathy, facial nerve
palsy, sudden deafness
42. Diagnosis
Biopsy – non caseating granuloma without myc.
Tuberculosis
Chest X Ray – diffuse pulmonary infiltrates with
hilar adenopathy
Bronchopulmonary lavage
Gallium 67 scan
Kveim test – positive
Increased serum and urinary calcium, ESR,
Alkaline phosphatase
Treatment – topical steroid nasal spray, oral
steroids
Methotrexate – for refractory cases
43. Autoimmune condition associated with necrotizing
granulomas and vasculitis of upper and lower
respiratory tract
1st site affected – nasal cavity
Also involves kidneys and skin
M=F, 40-50 years of age
Very rapid destruction but less severe
Type 1 – limited to nose
C/F – ulceration of nose with very large crusts, blood
stained nasal discharge, pain over dorsum of nose,
doesn’t respond to medical treatment
Can lead to septal perforation, saddle nose
Associated with weakness, fatigue, night sweats,
arthralgia
44. Type 2 – with pulmonary symptoms like cough,
hemoptysis, pleuritic pain and cavity in lung
Type 3 – multi organ involvement
Eyes – NLD obstruction, proptosis
Ear – serous otitis media, profound SNHL
Oropharynx – ulcers, gingival lesions
Subglottis and trachea - stenosis
Kidneys – renal failure – cause of death
Skin
Prognosis – high chances of recurrence
45. Diagnosis
CBC – anaemia, raised ESR, eosinophilia
Raised RFT
Urine – red cells, casts and albumin
X Ray chest – cavity
Biopsy (from turbinates) – vasculitis, granuloma
Anti Neutrophilic Cytoplasmic Antibody (ANCA)
C ANCA (cytoplasmic) – more specific than p
ANCA (perinuclear)
More sensitive for type 3 disease
D/D – Sinonasal lymphoma
46. Treatment
Immuno suppressive therapy –
Oral Cyclophosphamide/Azathioprine – cytotoxic
drugs
Wysolone
Cotrimoxazole – for early limited type 1
IV Ig
Plasma exchange
Nasal douching for crusts
Surgery – reconstruction when disease inactive
47. Malignant granuloma/ midline lymphoma/
stewart’s granuloma/ peripheral T cell neoplasm
Slow destruction but very severe
No pulmonary/renal involvement
No vasculitis
Autoimmune disease leading to destruction of
midline of face
Nasal – ulceration of cartilage and bone,
serosanguinous discharge, swelling of nose
Can involve upper lip, maxillary sinus, oral cavity
Can be secondary infected by bacteria
Destruction of nose and PNS
48. Diagnosis
Biopsy
Immunohistochemical studies
EBV – RNA
Treatment
Curative RT
Surgical debridement
No role of steroids or cytotoxic drugs
49. MC – children, mental retarded adults
Can enter through anterior and posterior
nares
Accidental – children – ant nares
Food particles, vomitus while coughing,
regurgitation – post nares, due to
nasopharyngeal isthmus incompetency
Iatrogenic – sponge, cotton swabs
Bullets – penetrating FB
Infection – atrophic rhinitis - maggots
50. Types
Living – maggots, leech
Non living – organic (seeds, grams), inorganic
(paper, button, pebble, rubber, chalk, beads, cell
battery)
C/F
h/o FB
Sneezing, u/l nasal blockage, u/l bleeding
u/l foul smelling nasal discharge purulent and
may be blood stained
Pain
FB seen – mc site is lower part of nasal cavity
Oedematous mucosa with granulations
51. Complications
Emergency – risk of inhalation into lower
respiratory tract
Rhinolith – long term FB with deposition of
calcium and magnesium salts
Nasal infection, sinusitis
Swallowed in oesophagus
Diagnosis
X ray PNS, Lateral view Neck – radio opaque
FB
DNE
52. Treatment
FB removal
Forceps/hook/ ET catheter – pass behind the
FB to pull it
Children – under GA
Leech – removed by putting pinch of salt/
hypertonic saline/ oxalic acid on body
53. Calculus/concretions Nose
Stone formation in nasal cavity
Formed around FB, blood clot, secretions – long
standing, thick mucus
Due to deposition of carbonates and phosphates
of calcium and magnesium
C/F
Large hard irregular but friable mass – greyish
brown or greenish black in colour, stony hard on
probing near floor of nasal cavity
U/L Nasal obstruction
u/l foul smelling blood stained nasal discharge
Head ache, epistaxis
54. Ulceration of mucosa and granulations
MC – adults
Diagnosis – X Ray PNS, DNE
Complications – Oroantral fistula
Treatment
Endoscopic removal under GA
Break the rhinolith into small pieces
Large rhinolith – lateral rhinotomy
55. Maggots in nose
Larvae of house fly – genus chrysomyia
Tropics – hot and humid climate
Months of August to November
Infest nose, nasopharynx, PNS
Also ear, tracheostoma and neck flaps
Etiology
Poor hygiene
Foul smelling nasal discharge seen in atrophic
rhintis, syphilis, leprosy, wegner’s
granulomatosis, suppurative sinusitis,
malignancy of maxilla
Immunocompromised patients - DM
56. Osteoradionecrosis after RT
Comatosed patients
Pathogenesis – foul smell attracts flies which lay
eggs, develop into larva in 24 hours (maggots)
Larva secrete proteolytic enzymes which cause
extensive destruction
C/F
Tickling sensation in nose leading to irritation
Sneezing
Lacrimation
Blood stained nasal discharge, foul smelling
Nasal obstruction
Crusting and loss of sensation
57. Headache, fever, toxemia
Cellulitis of face and nose, diffuse swelling
Pain over root of nose
Congestion, oedema and ulceration of nasal
mucosa
Complications
Intracranial complications like meningitis
Septicaemia/ infection
Destruction of nose and PNS
Palatal perforation and fistulae, septal
perforation
Psychological effect
58. Treatment
Isolate the patient – with mosquito net to avoid
contact with flies, hospitalization
Nasal hygiene to prevent recurrence
Inj TT
Broad spectrum antibiotics for secondary
infection
Irritate the maggots and plug the nasal cavity by
using cotton pledgets soaked in liquid paraffin,
chloroform, turpentine oil, ether
Topical oil, liquid paraffin drops
Nasal douching
Forceps removal
59. Acute IgE mediated immunological (type I hypersensitivity)
response of nasal mucosa to a allergen (antigen)
associated with atleast 2 of the following symptoms –
nasal discharge, nasal blockage, itching and watering from
the nose
Co exists with asthma in 45% patients, allergic dermatitis
Allergens
Inhaled – house dust mite, pollens, moulds, animal
dander, insects
Food – eggs, sea food, pea nut, milk, wheat
Drugs – aspirin, hypotensive drugs, iodide
TYPES
Seasonal – HAY FEVER – more severe, pollens –
tree/grass/weeds
Perennial – less severe – dust mite, mould, animal dander
60. Precipitating factors
Age – younger age – 15-40 years
Sex – slightly in males
Flora – geography, climate, season
Pollutants and smoke – industrialization, urbanization
Genetics – family history 50% positive
Infection – effects on tissue
Endocrine – increased in pregnancy, menstruation,
menopause
Psychological
Work place and living conditions – crowded, dirty, dusty,
damp, less sunlight
Deficiency of Vitamin C,D,Calcium and IgA
Trauma
61. Pathophysiology
Mucosa already sensitized to a allergen (priming)
Second exposure -> antibody produced against
antigen -> fixes to mast cells ->degranulation of
mast cells -> release of mediators – IMMEDIATE
RESPONSE – within 5-30 minutes of exposure
Histamine – sneezing, itching, watery discharge
PG – nasal blockage, Leukotriens – sinusitis, cold,
polyp
LATE RESPONSE – after 2-8 hours – eosinophils,
neutrophils, basophils, CD4 T cells – swelling,
thick secretions, nasal congestion
62. C/F
10-20 bouts of sneezing at a time
B/L Nasal obstruction
Watering and itching of nose
Watering and itching of eyes
Itching of palate, skin
Decreased sensation of smell
Bronchospasm
Recurrent cold in perennial AR
Signs – oedematous nasal mucosa pale blue,
oedematous turbinates pale blue, clear/mucoid
secretions, polypoidal mucosa, thickened
septum, high arched palate
63. Allergic shiners – dark circles around eyes due to
venous stasis
Allergic salute – rubs nose with the palm
Dennie Morgan/Darrier’s line – transverse nasal
crease along middle of nasal dorsum
Complications
Recurrent Sinusitis, nasal polyp
Eyes – conjuctivitis and oedema
Ears – SOM, ET blockage, retracted TM, CHL
Pharynx – granular pharyngitis, adenoid facies
Larynx – vc oedema, hoarseness of voice
64. Intermittent AR – symptoms less than 4
weeks or less than 4 days per week
Persistant AR – symptoms more than 4 weeks
or more than 4 days per week
Diagnosis
Nasal smear – nasal cytology for eosinophilia
(>10%)
CBC – TLC/DLC, AEC
DNE
X Ray PNS/ CT PNS – sinusitis/polyp
65. IN VIVO TESTS
Subcuticular test/ skin prick test/ scratch test
Preferred, reproducible, more accurate, less false
positive
Wheal more than 3 mm than negative control
10 min for histamine, 20 min for allergens
C/I – extensive dermatitis, dermatographism, on
antihistamines
Intradermal tests
High risk of anaphylaxis
Nasal provocation/ challenge test – small amount
of allergen is sniffed by the patient, applied to
mucosa, through nebulizer – anaphylaxis risk
66. IN VITRO TESTS
RAST – Radio Allergo Sorbent Test
FAST – Fluoro Allergo Sorbent Test
PRIST – Paper Immuno Allergo Sorbent Test
Specific IgE
Total IgE
No risk of systemic reaction
No affect of dermatitis, dermatographism,
antihistamines
Less sensitive
More false negative results
67. TREATMENT
Avoidance of allergen
Avoid early morning outdoors for pollen
Keep pets away for animal dander
Change bedsheets and pillow covers twice a
week, encass the mattresses, vacuum
cleaner/wet mopping, avoid carpets – dust mite
Repair leaks, damp walls – indoor moulds
Change of place, work, enviroment, AC closed
rooms, less articles in room, avoid food and
drugs causing allergy
68. DRUGS
Antihistamines
1st gen – CPM – sedation
2nd gen – cetrizine, loratidine – less sedation
3rd gen – levocetrizine, fexofenadine – minimal sedation
Relieves itching, watering and sneezing
No effect on nasal obstruction
Azelastin nasal spray – no long term sedation, safe
Steroids
Intranasal steroids – DOC , less side effects, can be used
for longer periods – fluticasone, mometasone, budesonide,
beclomethasone – rarely long term lead to fungal infection
and crusting
Oral steroids – in severe cases, for shorter periods
69. Mast cell stabilizers
Sodium chromoglycate nasal drops/spray
For prophylaxis
Decongestants
For nasal obstruction and mucosal oedema
Oral – phenylephrine, pseudoephedrine
Topical – xylometazoline, oxymetazoline, ephidrine –
use less than 7 days – Rhinitis medicamentosa
Anticholinergic drugs
Ipratropium bromide – topical
For watery rhinorrhoea, post nasal discharge
Not for sneezing, nasal obstruction, pruritus
70. Antileukotriens
Monteleukast, zafirleukast, pratileukast
For nasal obstruction, mucous secretions
Anti IgE antibody
Omalizumab
Above age of 12 years
For AR associated with moderate to severe asthma
Saline irrigation
Surgical – septoplasty, turbinate reduction, FESS
Immunotherapy – SCIT, SLIT – suppresses IgE, raise
IgG, for severe AR not responding to medical and
avoidance therapy, more effective when single or
fewer allergens
Desensitization – for specific allergens, drug allergy
71. PROTOCOL
MILD – oral antihistaminics
MODERATE/PERSISTANT – INS
SEVERE – oral antihistaminics and INS
VERY SEVERE – Oral steroids and
immunotherapy
If nasal obstructions – topic nasal
decongestants
For prophylaxis – intra nasal sodium
chromoglycate
72. Chronic condition of nasal cavity associated with
nasal blockage and rhinorrhoea due to imbalance in
autonomic nervous system with parasympathetic
overactivity and sympathetic underactivity
Parasympathetic leads to vasodilation and congestion
Etiology
Younger age, females, anxiety and depression,
psychological
Precipitated by dust, fumes, climate changes,
irritants, alcohol, exercise
Endocrinal/ hormonal causes
No cause identified - idiopathic
73. C/F
Profuse excessive rhinorrhoea, more early morning –
runners
B/L alternating nasal obstruction, more at night –
blockers
Post nasal discharge
Sneezing, itching - rare
Less oedematous pale mucosa
Turbinate hypertrophy
Mulberry inferior turbinate – posterior end
Complications
Polyps, sinusitis
D/D – Allergic rhinitis, infective rhinitis