2. HYPERSENSTITVITY PNEUMONITIS (HP) IS
REFERRED TO EXTRINSIC ALLERGIC
ALVEOLITIS,
IS A PULMONARY DISEASE OCCURS DUE TO
INHALLATION OF A VARIETY OF ANTIGENS
LEADING TO AN INFLAMMATORY RESPONSE
OF ALVEOLI AND SMALL PASSAGES.
3. THE INCIDENCE AND PREVALENCE OF HP IS
VARIABLE DEPENDING ON,
GEOGRAPHY
OCCUPATION
IN US 420-3000 PEOPLE ARE AFFECTED IN
100000 PEOPLE.
IT IS UNEXPLAINED THAT THERE IS A
DECREASED RISK OF DEVELOPING HP IN
SMOKERS.
4. HP CAN BE CAUSED BY A LARGE NUMBER OF
OFFENDING INHALLED ANTIGENS
VARIOUS ANTIGEN AND ENVIRONMENTAL
CONDITIONS IS ALSO INVOLVED
ANTIGEN DERIVED FROM BACTERIA, FUNGI,
BIRD DERIVED, CHEMICAL SOURCES IS ALSO
IMPLICATED TO CAUSE HP.
IN US FARMERS,BIRD OWNERS,INDUSTRIAL
WORKERS,HOT TUBE WORKERS IS ALSO
AFFECTED.
5. BIRD OWNERS : BIRD FEATHRES, DROP PING,
SERUM PROTEINS
FARMERS: GRAIN, MOLDY HAY, SILAGE
INDUSTRIAL WORKERS:
CHEMICAL WORKERS: FOAM,VARNISH
DETERGENT WORKERS: DETERGENT
MACHINE OPERATOR: METAL
WORKING FLUID
6. THE PATHOPHYSIOLOGY OF HP HAS NOT BEEN
CHARACTERIZED UPTO THE LEVEL OF IMMUNOLOGY.
BUT IT HAS BEEN CHARACTERIZED AS A CONDITION
WITH TH1 INFLAMMATORY PATTERN.
HOWEVER EMERGING EVIDENCES SHOW THAT TH17
LYMPHOCYTES IS ALSO INVOLVED.
THERE ARE IgG ANTIBODIES PARTICIPATING AGAINST
HP ANTIGENS IN ADAPTIVE IMMUNITY.
BUT THE ROLE OF INNATE IMMUNITY IS ALSO
IMPORTANT.
IT IS OBSERVED THAT TOLL LIKE RECEPTORS (TLR)
AND DOWN STREAM REGULATORY PROTEINS SUCH AS
MYD88 IS ALSO ACTIVATED.
MHC CLASS 2 IS ALSO OBSERVED.
7. THERE IS A HETEROGENECITY AMOUNG PATIENTS, VARAIBILITY IN
ANTIGEN EXPOSURE AND DURATION OF ANTIGEN EXPOSURE.
CLASSIFICATION
ACUTE
SUB ACUTE
CHRONIC
ACUTE HP MANIFESTS 4-8 HRS AFTER EXPOSURE TO
ANTIGEN,OFTEN INTENSE IN NATURE.
SYMPTOMS RESOLVE IN HOURS TO DAYS IF THERE IS NO
EXPOSURE TO ANTIGEN.
IN SUBACUTE HP IS TYPICALLY GRADUAL OVER A COURSE OF
WEEK 10-14 DAYS RESULTING IN ANTIGEN EXPOSURE ,ONSET OF
RESPIRATORY AND SYSTEMIC SYMPTOMS.
CHRONIC HP MAY PERSIST MORE GRADUAL SYMPTOM EXISTING
FROM MONTHS TO YEARS WITH SYMPTOMS LIKE
8. PROGRESSIVE DYSPNEA
COUGH
FATIGUE
WEIGHT LOSS
CLUBBING OF FINGERS
UNLIKE OTHER TYPE OF HP, IN CHRONIC HP
THERE IS AN IRREVERSIBLE COMPONENT TO
THE IMPAIRMENT THAT IS NOT RESPONSIBLE,
EVEN AFTER THE REMOVAL OF THE ANTIGEN.
9. PRODUCTIVE COUGH
DISCOMFORT IN CHEST
DYSPNEA
FEVER
FATIGUE
WEIGHT LOSS
10. SKIN COLOUR: A
CHARACTERISTIC RED
SPOTS IN CHEEKS IS SEEN
INSPECTION :
ASSYMETRICAL
MOVEMENT IS SEEN
PALPATION : REDUCED
TACTILE FERMITIUS IS
SEEN
PERCUSION : RESONANT
TO DIFFUSELY
HYPERRESONANT
ASCULTATION: CRACLES
SOUND IS HEARD
11. DIAGNOSIS DEPENDS ON ESTABLISHING
HISTORY OF EXPOSURE TO AN OFFENDING
ANTIGEN THAT CORRELATES WITH
RESPIRATORY AND SYSTEMIC SYMPTOMS.
A CAREFUL OCCUPATIONAL AND HOME
HISTORY MUST BE TAKEN.
IF NEEDED CLINICIAN SHOULD VISIT THE
WORK AND HOME ENVIRONMENT.
SPECIFIC ENQUIRIES MUST BE MADE ON
GEOGRAPHIC AND SOCIAL ENVIRONMENT.
12. INSTRUMENTAL DIAGNOSIS:
CHEST IMAGING
PULMONARY FUNCTION TEST
BRONCHOSCOPY
LUNG BIOPSY
LAB DIAGNOSIS:
BLOOD TEST
13. THE MAINSTRAY OF TREATMENT FOR HP IS ANTIGEN
AVOIDANCE
ONCE THE POTENTIAL ANTIGEN AND LOCATION IS
IDENTIFIED EFFORTS SHOULD BE MADE TO MODIFY
THE ENVIRONMENT TO MINIMIZE THE PATIENT
EXPOSURE.
THIS MAY BE ACCOMPLISHED WITH MESAURES SUCH
AS REMOVAL OF BIRDS AND MOULDS AND IMPROVED
VENTILLATION
ACUTE HP IS SELF LIMITING DISEASE AND HENCE NO
PHARMACOLOGICAL THERAPY IS NEEDED.
IN SUB ACUTE AND CHRONIC PHARMACOLOGICAL
THERAPY IS NEEDED WITH ADMINISTRATION OF
GLUCOCORTICOIDS.
14. PROGNOSIS IS GOOD IF THE DISEASE AND ITS
CAUSATIVE AGENT IS IDENTIFIED EARLY
HENCE FURTHER EXPOSURE CAN BE AVOIDED.
ESTABLISHING LUNG SCARRING,HOWEVER
WILL NOT RESOLVE AND THESE PATIENTS
MAY PROGRESS WITH LUNG FAILURE.
15. PROPHYLAXIS INVOLVES IDENTIFYING THE
ALLERGIC SUBSTENCES IN THE ENVIRONMENT
AND PREVENTING ITS EXPOSURE TO THE
HYPERSENSITIZED PEOPLE CAN BE THE
MEASURE TO PREVENT THE DISEASE.
16. HARRISON’S BOOK OF INTERNAL MEDICINE
VOL 2 PGS1142-1147
http://medlineplus.gov/ency/article/000109.
htm
http://www.ncbi.nlm.nih.gov/pubmed/78076
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