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Non-asthmatic Immunologic Respiratory Disease (Big Picture Comparisons…
Non-asthmatic Immunologic Respiratory Disease
Immunology Review
Innate Immunity: starts and prolongs a response. Directs the type of response depending on pattern and receptor.
Adaptive Immunity: is highly specific and has a memory. Learns to not attack self (tolerance)
Mast Cells: release all sorts of mediators that ramp up the response. Only exist in peripheral tissues and are one of the only cell types to differentiate outside the bone marrow. Type 1 Hypersensitivty.
Th2: defense mechanism that activates IgE and eosinophils, starts allergic reaction. Dependent on IL-4, IL-5, and IL-13
Th1: associated with INF-gamma and IL-12. The pathway is stimulated in response to activation of dendritic cells, macrophages, and natural killer cells
Upper Airway Diseases
Rhinitis
Allergic
Presentation
Can be seasonal (mold, pollen) or perennial (dust mites, animals, cockroaches)
Normal allergy/cold symptoms
Nasal polyps: bags of eosinophils, hard to control, and will come back when removed
Associated with asthma and eczema
Pathophysiology
Most symptoms mediated by histamine or leukotrienes
Type 1 hypersensitivity
Treatment
Subcutaneous Immunotherapy
: Immune modulating, induce tolerance to allergens, switches from Th2 profile to Th1 profile, long term control with some risk for anaphylactic reaction
Pharmacologic
Nasal corticosteroids
: Most efficacious, Reduce inflammation, and Inhibit release of mediators
Other: Antihistamines, anti-leukotrienes, anti-cholinergics
Non-allergic: 1/3 of people have year round symptoms, little itching and no eye symptoms, lots of causes
Sinusitis
Pathophysiology
Blockage in the ostiomeatal unit cause infection from build up of fluid
Both Th1 and Th2 play a role
Acute (secondary to infection) or chronic
Chronic Rhinosinusitis
Pathophysiology
CRS without polyps (60%): Anatomic obstruction, infection, allergic obstruction, Th1 mediated
CRS with polyps (20-33%): Th2 mediated
Most common acute cause is viral URI
May cause superimposed bacterial infection: S. pneumo, H. infl, M. catarr
Presentation
Nasal polyps
Facial pain, pressure, congestion, fullness
Nasal obstruction/blockage
Nasal discharge, purulence, postnasal drip
Hyposmia/anosmia
Allergic Fungal Sinusitis
Pathophysiology
Hypersensitivity response to fungal colonization (NOT infections)
Most often
Aspergillus*
Presentation
Associated with nasal polyps
Associated with asthma
Produces allergic mucin
Diagnostics
Skin/Serum testing positive for
mold
Treatment
Corticosteroids
Surgical Debridement
Lower Airway Diseases
Hypersensitivity Pneumonitis
Presentation
Acute:
fever, chills, dyspnea 6-8 hours after inhalation
Subacute
: cough, dyspnea, hypoxemia insidiously over weeks
Chronic
: progressive, honeycombing, interstitial fibrosis
Pathophysiology
Th1 disease
Lymphocyte-predominant alveolitis results in
non-caseating granulomas
and pulmonary fibrosis
Caused by organic proteins: farmers lung, water related, grains, lumber, textiles
Restrictive disease
, specific precipitating antibody, interstitial disease
Risk Factors
Smoking is Protective
Wegener's Granulomatosis
Pathophysiology
Triad: granulomatous inflammation, necrosis, and small vessel vasculitis
Th1
response" IFN-gamma, TNF, IL12
Presentation
Renal disease
is common
Severe upper respiratory tract symptoms
Cough, hemoptysis, and pulmonary infiltrates
Tracheal stenosis with flat inspiratory loop
Treatment
Immunosuppresive
Diagnosis
Positive cANCA (proteinase-3)
Churg-Strauss Syndrome
Presentation
Asthma
: no asthma, no churg srauss
Allergic rhinitis
Non-specific symptoms
Pathophysiology
Systems vasculitis with eosinophilia
Granuloma formation with eosinophilic infiltrate
Th2
process: IL-4, IL-5, IL-13
Diagnosis
Peripheral blood eosinophilia
pANCA
(myeloperoxidase)
Treatment
Glucocorticoids
are the mainstay
Allergic Bronchopulmonary Aspergillosis (ABPA)
Presentation
Associated with asthma or CF
Pathophysiology
This is a colonization (NOT an infection) that when cleared improperly promotoes a strong
TH2
response
ABPA is localized
Treatment
Glucocorticoids
are mainstay
Diagnosis
Do
total serum IgE
to determine the stage
Acute or exacerbation: markedly elevated
End Stage: May be normal
Goodpasture's Disease
Pathophysiology
IgG1 antibodies directed against part of type 4 collagen
(which is also in the lung)
Antibodies bind the basement membrane and activate complement which recruits neutrophils and macrophages
Patchy diffuse or patchy bilateral infiltrates
Antiglomerular basement membrane antibodies, diffuse pulmonary hemorrhage and glomerulonephritis
Treatment
Prednisone
Plasmapheresis
Cyclophosphamide
Big Picture Comparisons
TH1
Wegener's
Hypersensitivity Pneumnitis
Allergic Rhinitis
Chronic Rhinosinusitis
TH2
ABPA
Churg-Strauss
Asthma
ABPA
Churg-Strauss
pANCA
Churg-Strauss
cANCA
Wegener's
Anti-GBM
Goodpasture's
Eosinophilia
Churgg-Strauss
Granulomatous
Wegener's
Churgg-Strauss
Hypersensitivity Pneumonitis
IgE
ABPA