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HYPERSENSITIVITY PNEUMONITIS
BY
HARSHAD KHAN SIRAJ
GROUP 16
TBILISI STATE MEDICAL UNIVERSITY
 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.
 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.
 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.
 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
 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.
 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
 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.
 PRODUCTIVE COUGH
 DISCOMFORT IN CHEST
 DYSPNEA
 FEVER
 FATIGUE
 WEIGHT LOSS
 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
 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.
 INSTRUMENTAL DIAGNOSIS:
 CHEST IMAGING
 PULMONARY FUNCTION TEST
 BRONCHOSCOPY
 LUNG BIOPSY
 LAB DIAGNOSIS:
 BLOOD TEST
 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.
 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.
 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.
 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
12

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Hypersensitivity pneumonitis

  • 1. HYPERSENSITIVITY PNEUMONITIS BY HARSHAD KHAN SIRAJ GROUP 16 TBILISI STATE MEDICAL UNIVERSITY
  • 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 12