Diseases of the Nose _ Sinuses - DOC - DOC by keara

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									Diseases of the Nose & Sinuses

Anatomy o Nasal cavity:  Roof: nasal bones, frontal bone, CFP of ethmoid, fovea ethmoidalis, sphenoid.  Septum: PPE, vomer, quadranqular cartilage, memb. septum, columella.  Floor: maxillary & palatine bone.  Lat wall: maxilla, inf. turbinate, ethmoid bone, lacrimal bone, palatine bone. o Maxillary sinus  Largest, 10-20 cc.  Med. = lat nasal wall  Sup = orbital floor  Floor = alveolar process.  Drainage via ostium in lower infundibulum. o Frontal sinus:  Absent unilat in 12%, bilat 5%.  Drainage: into frontal recess posteromedially

Rhinitis Atrophic Rhinitis o nasal mucosal atrophy with crusting and an extremely foul odor o Cuase : uknown  Bacterial: Klebsiella ozaenae, atoxic Corynebacterium diphtheriae, and the PerezHofer bacillus  Deficiencies in vitamin A and iron  Radical surgery o Sx & Sn: halitosis, nasal obstruction, epistaxis, and headache. Offensive nasal odor, crusting, and turbinate atrophy.\ o Tx: reversing nutritional deficiencies, saline irrigations, vitamin A, & systemic or topical antibiotics. o Surgical(faliure of medical therapy): closure of the nostril and nasal vestibuloplasty to narrow the nostrils. Vasomotor Rhinitis o Overactive parasympathetic stimulation of the nasal mucosa  vasodilation, edema, and hypersecretion of mucus o Sx: nasal obstruction, profuse rhinorrhea, infrequent sneezing, stuffiness, and face pressure and headache.

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o Trigger factors: changes in weather or humidity, the presence of irritating fumes, or air conditioning or stress o Tx:  Medical: Systemic decongestants, Antihistamines, steroids, topical ipratropium bromide.  Surgical: many procedures (inf turbinectomy, submucous resection, Cryotherapy ..etc) Infectious Rhinitis o Rhinoscleroma  noncontagious, granulomatous, Klebsiella rhinoscleromatis.  4 stages: cattarrhal, atrophic, granulamatous, & sclerotic.  Mass lesions: pseudoepitheliomatous hyperplasia of the mucosa. Histologic hallmark: Mikulicz cell.  Tx: broad-spectrum antibiotics (e.g. streptomycin & tetracycline). o TB, Syphilis, leprosy. o Rhinosporidiosis, histoplasmosis, aspirgellosis. Rhinitis Medicamentosa Allergic Rhinosinusitis o Type I hypersensitivity reaction. Allergen-specific IgE bound to mast cells or basophils, then reacts with its unique allergen mast cell degranulation (release of histamine and other mediators of inflammation e.g., prostaglandins, leukotrienes). Occur 2 to 5 minutes of antigen-antibody reaction. o A second (late) phase is the result of mediator release from cells (neutrophils, eosinophils) and occurs about 4 to 6 hours after the acute phase. Allergic Rhinosinusitis o Sx: tching, sneezing, rhinorrhea, and postnasal drainage (throat-clearing and cough). Seasonal or perennial, & linkage with known exposure to allergens. o Signs:  open-mouthed “adenoid facies.”, (“allergic salute”), “allergic shiners”and puffiness around the eyes.  Pale nasal mucosa & clear rhinorrhea (in the absence of secondary infection). Polyps may be present.  high arched palate, prominent pharyngeal lymphoid o Dx  Nasal smears (Hansel’s stain)  eosinophils (> 25% of the cells).   total IgE  skin test: introducing the suspected allergen under the skin and allowing it to react with IgE bound to mast cells  wheal-and-flare response e.g. abrading or scratching, prick test, Intradermal tests, skin endpoint titration (SET). o Management:  Level I: Prevention and Control of Symptoms. Environmental Control First-line Pharmacotherapy:
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Antihistamines compete with histamine for H1-receptor sites on the target organs during the allergic response Decongestants are sympathomimetic substances that cause vasoconstriction within turbinate stroma, producing shrinkage of congested tissue (Pseudoephedrine & Phenylpropanolamine) Comolyn nasal spray stabilizes and protects mast cells from degranulation o Level II: Recognition and Management of Complicating Factors Treat other types of rhinitis: vasomotor, medicamentosa…
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o Level III: Corticosteroids for Control of Severe or Chronic Symptoms ameliorate the effects of both acute and late-phase allergic reactions Systemic Nasal intraturbinal injection !! o Level IV: Immunotherapy symptoms are not controlled with pharmacotherapy, allergens that cannot be avoided, symptoms span two or more allergy seasons, willing to cooperate in a program of immunotherapy parenteral administration of antigens  formation of allergen-specific IgGblocking antibodies  compete with IgE antibodies for target sites on mast cells or basophils.
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Paranasal Sinusitis o 3 factors essential to normal physiology of the paranasal sinuses: patency of the ostia, function of the cilia, & quality of the nasal glandular secretions. o Most significant pathophysiology that produces sinusitis: mucosal edema in and around the sinus ostium:  Hypooxygenation of the involved sinus.  Ciliary function is disturbed  stagnation of the secretion.  Local host resistance factors are diminished   darainage & perfect milieu for the growth of bacterial pathogens o Inflammation (e.g. allergic rhinitis, URTI..)  increased secretions and edema in the sinonasal mucosa. o Classification  Acute: infectious lasting from 1 day up to 4 weeks. Management is medical, and rarely surgical treatment.  Subacute: infection lasts from 4 weeks to 3 months. inflammatory process is still reversible  Medical management.  Chronic: sinusitis persists longer than 3 months. Results from acute sinusitis that has been either inadequately treated or completely untreated. The process is irreversible  surgical treatment is indicated. o Acute sinusitis:  Bacterial:

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Adults: Streptococcus pneumoniae, Staphylococcus aureus, Streptococcus pyogenes groups ABC, and Haemophilus influenzae (gram-negative). Children: S. pneumoniae, Branhamella catarrhalis (formerly known as Neisseria catarrhalis), Haemophilus influenzae, Streptococcus pyogenes groups A and C, and Streptococcus pyogenes a-hemolytic type

o Complications  Orbital complications:classification (Chandler):  Inflammatory edema—lid edema; no limitation of extraocular movement with normal acuity  Orbital cellulitis—diffuse edema of orbital contents; no discrete abscess formation  Subperiosteal abscess—purulent collection beneath periosteum of lamina papyracea; displacement of globe downward and laterally  Orbital abscess—purulent collection within orbit; proptosis and chemosis with ophthalmoplegia and decreased vision  Cavernous sinus thrombosis—bilateral eye findings; prostration; meningismus  Intra-cranial complications  direct extension through a defect in the posterior wall of the frontal sinus  Retrograde thrombophlebitis of the valveless ophthalmic vessels The subdural space abscess cerebral abscess, seizures, and neurologic deficits. Meningitis (rare). Septic thrombosis of major dural sinuses o Tx: High-dose antibiotic therapy management of increased intracranial pressure, and prevention of seizures. Surgical drainage
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Fungal Rhinosinusitis o Classification:  Acute invasive fungal sinusitis Life threatining Mucor mycosis, immunocompromised host Tx: radical resection, correct underlying medical problem, systemic antifungal.  Chronic invasive fungal sinusitis Similar to ch. Sinusitis, caused by aspergillus Endemic in hot dry climates e.g. Sudan  Mycetoma (fungus ball): concentric hyphae of aspegillus Tx: simple excision.  Allergic fungal sinusitis Most common, Demitaceous groub Nasal polyps, +ve skin test, Charcot-Layden crystals Tx: surgery & steroids  Saprophytic infection: fungal contamination
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Epistaxis o Osler-Rendu-Weber’s disease (hereditary hemorrhagic telangiectasia  autosomal dominant disease  Lack of contractile elements in the vessel walls  arteriovenous fistulae are formed.  Precipitating factors include mucosal fragility and trauma. o Blood dyscrasias  Identified early in life  Most common Factor VIII (80% of cases).  Von Willebrand’s: prolonged bleeding time, deficiency in antihemophilic Factor VIII, and impaired platelet adhesiveness. o Drugs (acetylsalicylic acid, anticoagulants), Systemic toxic agents (phosphorous, mercury), infectious diseases (scarlet fever, smallpox). Management  ABC, IV fluid, cross matching.  Silver Nitrate Cauterization  Electrical Cauterization  Cryotherapy  Nasal Packing  Anterior Nasal Packing  Posterior Nasal Packing  Greater Palatine Foramen Block  Embolization

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Surgery  Septoplasty/Submucous Resection  Internal Maxillary Artery Ligation  Transantral Sphenopalatine Artery Ligation  Anterior and Posterior Ethmoidal Artery Ligation  External Carotid Artery Ligation  Laser Photocauterization (HHT)  Septodermoplasty (HHT)  Cutaneous/Myocutaneous Flaps - Microvascular Free Flaps (HHT)

Olfactory Disorders o Olfactory bulb lies on top of the cribriform plate at the base of the brain o Olfactory epithelium: upper septum & lat nasal cavity o Epithelium:  olfactory receptor (bipolar neuron)  microvillar cell (another type of olfactory receptor cell)  supporting, or sustentacular, cells  basal cells (stem cells to replace the dying olfactory receptors)

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o Causes  Obstructive Nasal and Sinus Disease  Olfactory Loss Following Upper Respiratory Infection damage to olfactory neurons at the level of the epithelium, the bulb, or the central olfactory tracts 1/3 of patients will regain olfactory ability in 3 to 6 months  Head Trauma 5% to 10% of adults who have sustained both major and minor head trauma shearing of the delicate fila olfactoria nerves as they pass through the cribriform plate 8% to 39% of the patients  recovery of olfactory function usually within 3 months
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 Toxins
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Formalduhyde, benzene, smoking Permenant

 Aging olfactory loss in old people can occur from dementia-related diseases two dementia-related diseases: Alzheimer’s disease and Parkinson’s disease  Congenital  hypogonadotrophic hypogonadism (Kallmann’s syndrome
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Midline Nasal Masses o Anatomical Abnormalities  Deviated Nasal Septum  Turbinate Hypertrophy  Septal Perforation  Valvular Collapse  Septal Hematoma  Septal Abscess  Choanal Atresia  Foreign Bodies

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