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Hypersensitivity Pneumonitis Hypersensitivity Pneumonitis

Hypersensitivity Pneumonitis - PowerPoint Presentation

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Hypersensitivity Pneumonitis - PPT Presentation

HP By ziba Loukzadeh MD Occupational Medicine department Yazd University of Medical Sciences Definition Immune hypersensitive response Extrinsic allergic alveolitis granulomatous interstitial bronchiolar and alveolarfilling lung diseases caused by ID: 310826

fever lung inhalation amp lung fever amp inhalation exposure disease cxr worker exp dyspnea diagnosis pathogenesis rales thermoactinomycet farmer comparison mushroom proteins

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Slide1

Hypersensitivity Pneumonitis(HP)

By :

ziba

Loukzadeh

, M.D

Occupational Medicine department

Yazd University of Medical SciencesSlide2

DefinitionImmune (hypersensitive) response

Extrinsic allergic alveolitis: granulomatous, interstitial, bronchiolar and alveolar-filling lung diseases caused by

repeated

exposure and subsequent sensitization to a variety of organic and chemical antigensSlide3

EtiologyMicrobial agents

Animal proteins

Low molecular weight chemicalsSlide4

Microbial agents

Bacteria

-Farmer’s lung -Bagassosis -Mushroom worker’s lung

Fungi

-Wood pulp worker’s lung

-Cheese washer lung

Ameba

-Humidifier lung

Slide5

Bacteria

cause

occupation

Agent

source

Major

antigen

Farmer's lung

Agriculture worker

Moldy hay

thermoactinomycet

Mushroom worker's

Mushroom worker

Compost

thermoactinomycet

Bagassosis

Bagass worker

Moldy

sugarcane

thermoactinomycetSlide6

Animal proteinsAvian proteins : Bird breeder’s lung

Urine ,Serum ,Pelts : Animal handler’s lung

Wheat weevil : Wheat weevil lung Slide7

ChemicalsIsocyanate HP

TDI , MDI , HDI

TMA HP

Trimellitic anhydrideSlide8

PathogenesisImmunology

Repeated inhalation of antigens

sensitization immunology response(type III,IV) influx of neutrophiles shift T lymphocytes (~70%)(predominantly of CD8)

Antibodies in HP are IgG classResponse delay by 3-8 hoursSlide9

Pathogenesis (cont’)Host factors

-Non smokers > smokers

-Polymorphism in TNF-α gene -No association with HLASlide10

Pathogenesis (cont’)

Exposure factors:

-Ag concentration

-Duration of exp. -Frequency & intermittency of exp. -Particle size -Use of respiratory protection

Farmer's lung disease: winter

Bird breeder's lung: summer

Indirect exposureSlide11

Clinical features

Acute HP : fever ,chill ,myalgia ,cough & dyspnea + basilar

rales

in Ph/E (4-12 h after heavy exp. ) Recurrent febrile episodes (most frequent presentation)Subacute & chronic HP : insidious onset of respiratory symptoms ,malaise , fatigue , weight loss + basilar rales ,wheezing cyanosis ,right sided HF in Ph/E Slide12

DDxInhalation fevers

others granulomatous disorder(Sarcoidosis)

immunologic disease (Asthma)

infection fibrotic lung disease (IPF)Slide13

Comparison HP& Inhalation fever

Feature

HP

Inhalation fever

Example

Farmer`s lung disease

Metal fume fever

Etiology

Thermoactinomyces

Zinc fume fever

pathophysiology

Hypersensitive reaction

Cytokine- mediated (??)

Exposure dose

Low dose

High dose

Sensitization required

Yes

NoSlide14

Comparison HP& Inhalation fever(cont´)

Feature

HP

Inhalation fever

Fever

Yes

Yes

Flu-like syndrome

Yes

Yes

Cough

Expected

Not necessary

Dyspnea

Yes

Not typically

Chest exam

Rales

normalSlide15

Comparison HP& Inhalation fever(cont´)

Feature

HP

Inhalation fever

CXR

Alveolar infiltration

No

PFT

Decreased DLCO&volums

Minimal change

BAL

Lymocytosis

Inincreased Neutrophiles

Chronic sequle

~yes

None

Natural Hx

Reccurent or progressive

Complete recovery within 3 daySlide16

Lab. studiesPrecipitin Ab:

Helpful but not specific, not sensitive, not hallmark

Leukocytosis ,mild elevation of ESR ,CRP , IgG , IgA ,IgM ,ACE ,ANASlide17

PFT Normal (early dis.)

Restrictive

Obstructive

Mixed decreased DLCO (most sensitive physiologic test in early HP )Slide18

CXR

Acute : diffuse ground glass ,fine nodular or

reticulonodular

pattern (lower lung )Subacute : reticulonodular patternChronic : fibrosis ,reticular opacity, honey combing mediastinal lymphadenopathy (up to 50%)Slide19

HRCT

Ground glass

Centrilobular nodules

Airspace consolidation Mosaic pattenFibrosis Emphysema Slide20
Slide21

Normal CXRSlide22
Slide23
Slide24
Slide25
Slide26
Slide27
Slide28

HistopathologyClassic triad :

cellular bronchiolitis

lymphoplasmocytic interstitial infiltration

non-necrotizing granulomaSlide29

diagnosisTemporal relationship between symptoms and certain activities is often the first clue to the diagnosis of HPSlide30

diagnosisenvironmental history:

pets and other domestic animals

hobbies such as gardening and lawn care

recreational activities, for example, use of hot tubs and indoor swimming poolsuse of humidifiers, cool mist vaporizers, and humidified air conditioners moisture indicators such as leaking, flooding, or previous water damage to carpets and furnishingsSlide31

Diagnostic criteriaRequired

appropriate exposure

dyspnea on exertion inspiratory crackles lymphocytic alveolitisSupportive

recurrent febrile episodes

infiltrative on CXR

decreased DLCO

precipitating antibodies

granulomatous on lung biopsy

improvement with contact avoidanceSlide32

Treatment

Best treatment : Removal from exp.

Preferred approach : Elimination of Ag.

Oral corticosteroid : in severe or progressive diseaseO2 ,inhaled steroid & B-agonist in airflow limitationSlide33