a. Female patient.
b. Male patient.
c.Ansosmia
d Foetid smell from nose.
Ans: D
Ozaena: A chronic disease of the nose characterized by a foul-smelling nasal discharge and atrophy of nasal structures.
Atrophic rhinitis is of two types:
1. Primary and
2. Secondary.
Primary Atrophic Rhinitis
Aetiology (Remember Mnemonic HERNIA)
The exact cause is not known. Various theories advanced regarding its causation are:
The exact cause is not known. Various theories advanced regarding its causation are:
(a) Hereditary factors. Disease is known to involve more than one member in the same family.
(b) Endocrinal disturbance. Disease usually starts :Jt puberty, involves females more th an males, the
crusting and foetor associated with disease tends to cease after me nopause; these factors ha\'e r .Jl I::J the possibility of disease being an endocrina l dl ~ orde r.
(c) Racial factors. White and ye llow rae s are more susceptible than natives of equatorial Africd.
(d) Nutritional deficiency. Disease may be due to deficiency of vitamin A, D or iron or some other dietary factors. The fact that incidence of di:.ease is decreasing in western countries and is rarely seen in well-to-do families raises the possibility of some nutritional deficiency.
(e) Infective. Various organisms have been cul tureJ from cases of atrophic rhinitis such as Klebsiella ozaenae , (Perez bacillus), diphtheroids, P vulgaris, Esch. coli, Staphylococci and Streptococci but the ' are all considered to be secondary invade rs responsible for fou I smell rather than the primary ca usat ive organisms of the disease.
(f) Autoimmune process. The body reacts by a destructive process to the antigens released from the nasal mucosa. Viral infection or some other unspecified agents may trigger antigenicity of nasal mucosa.
(b) Endocrinal disturbance. Disease usually starts :Jt puberty, involves females more th an males, the
crusting and foetor associated with disease tends to cease after me nopause; these factors ha\'e r .Jl I::J the possibility of disease being an endocrina l dl ~ orde r.
(c) Racial factors. White and ye llow rae s are more susceptible than natives of equatorial Africd.
(d) Nutritional deficiency. Disease may be due to deficiency of vitamin A, D or iron or some other dietary factors. The fact that incidence of di:.ease is decreasing in western countries and is rarely seen in well-to-do families raises the possibility of some nutritional deficiency.
(e) Infective. Various organisms have been cul tureJ from cases of atrophic rhinitis such as Klebsiella ozaenae , (Perez bacillus), diphtheroids, P vulgaris, Esch. coli, Staphylococci and Streptococci but the ' are all considered to be secondary invade rs responsible for fou I smell rather than the primary ca usat ive organisms of the disease.
(f) Autoimmune process. The body reacts by a destructive process to the antigens released from the nasal mucosa. Viral infection or some other unspecified agents may trigger antigenicity of nasal mucosa.
Pathology
Ciliated columnar epithelium is lost and is replaced by strat ified squamous type. There is atrophy of seromucinous glands, ve nous blood sinusoid s and nerve elements.
Arteries in the mucosa, periosteum and bone show oblitt rati ve endarteritis. The bone of turbinates undergoes resorption causing widening of nasal chambers. Paranasal sinuses are small due to their arrested development.
Clinical Features
Disease is commonly seen in females and starts around puberty. There is foul smell from the nose making the patient a social outcast though patient himself is unaware of the smell due to marked anosmia (merciful anosmia) which accompanies these degenerative changes.
Patient may complain of nasal obstruction in spite of unduly wide nasal chambers. This is due to large crusts filling the nose. Epistaxis may occur when the crusts are removed.
Examination shows nasal cavity to be full of greenish or greyish black dry crusts covering the turbinates and septum. Attempts to remove them may cause bleeding. When the crusts have been removed, nasal cavities appear roomy with atrophy of turbinates so much so that the posterior wall of nasopharynx can be easily seen.
Nasal turbinates may be reduced to mere ridges. Nasal mucosa appears pale. Septal perforation and dermatitis of nasal vestibule may be present. Nose may show a saddle deformity.
Atrophic changes may also be seen in the pharyngeal mucosa which may appear dry and gl8zed with crusts. Similar changes may occur in the larynx with cough and hoarseness of voice (atrophic laryngitis).
Hearing-impairment may be noticed because of obstruction to eustachian tube and middle ear effusion.
Paranasal sinuses are usually small and underdeveloped with thick walls. They appear opaque on X-ray.
Antral wash is difficult to perform due to thick walls of the sinuses.
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