less than FEV less than by mikeholy

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									   CRIMEA STATE MEDICAL UNIVERSITY
     NAMED AFTER S.I GEORGIEVSKY
  DEPARTMENT OF INTERNAL DISEASE # 3




Pneumoconiosis
      DEBORAH AKANYA TOSIN
      Дебора Аканя Тосин
              GROUP 501




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is fibrosis and scarring of the lungs
secondary to repeated inhalation
of dust associated with some
occupations (coal miners,
construction workers, glass making
industry, cement factories).


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              Dust particles

                   Lungs

                Chronic
             inflammation
Elastic                               Fibrous
tissue                                tissue

                          Scarring of lungs
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Pneumoconiosis is usually divided
into three groups:

 Major pneumoconiosis
 Minor pneumoconiosis
 Benign pneumoconiosis

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Inhalation of some dusts results in
  “major fibrosis” of the lungs, which
  results in interference of lung
  architecture or lung function tests.

As:
  Silica  silicosis
  Asbestos  asbestosis
  Talc  talcosis
  Coal  coal workers pneumoconiosis
      (anthracosis)
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 Inhalation of some dusts results in “minor
  fibrosis” of the lungs.
 There is minimal fibrosis of the lungs
  without interference of lung architecture
  or lung function tests.
 These dusts include:
    Clay
    Koalin
    Mica
    Feldspar (non-fibrous silicates)

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There   isn't any reaction in the
 lungs, but dust deposition casts a
 shadow in x-ray of the lung. There
 is no fibrosis and no disturbance of
 lung functions.



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 It   can result from the inhalation of:
   Iron dust sidrosis
   Tin dust stannosis
   Calcium dust chalicosis
 They  are characterized by the presence of
  small rounded dense opacities on a chest
  film due to perivascular collections of
  dusts.
 Hilar lymph nodes may be prominent.
 The deposits in the lung disappear when
  exposure is discontinued.
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1.Type of pneumoconiosis according to etiology:
- Silicosis
-Silicate pneumoconiosis
-Coal-worker’s pneumoconiosis
2. Type according to current radiological sign:
- Interstitial ( diffuse sclerosis)
- Nodular.
-Tumorous.
3. Stage of growth: I, II, III
4. Current:
- Fastly progressive ( progression to another stage in 3-5 years)
- Slowly progressive (6 -15 years)
 Late (5-15 years after quitting job with hazardous agent)
5. Clinical Functional Characteristics:
- Bronchitis, Bronchectatic Disease, Emphysema, Pneumonitis, Lung
     cancer, Pleural syndrome, Silicotuberculosis, Disturbances of other
     systems (rheumatoid arthritis), decreased secretory and motoric
     function.
                  STAGE ONE                  STAGE TWO                  STAGE THREE
 DYSPNEA          After exercise           After insignificant               At rest
                                               exercise.
UPPER RESP.      Atrophy of mucus
  TRACT        membrane, decrease
               reflex of swallowing.
  LUNGS       Bronchitis, emphysema       Severe emphysema,              Emphysema,
                                          Chronic Bronchitis.          pneumosclerosis,
                                                                     bronchoectasis, often
                                                                         tuberculosis
FUNCTIONAL       Begin RF, no cvs        Increased residual lung   Severe respiratory failure.
PARAMETER           changes.            volume. Decreased vital     Decreased vital capacity
                                        Capacity (50-80%), blood   (less than 5 %), FEV1 (less
                                        gases are within normal            than 60%).
                                                 range.
 RADIOLO-       Diffusely increased     Are, more developed than    Radiological signs: abrupt
GICAL SIGNS       vascularization,       in 1st stage. Nodes 3-4          deformation of
               compression of x-ray        mm in diameter are       vascularization, enlarged
              snap of bronchial wall,           revealed.           hila. Radiological signs of
                sometimes nodular                                   pneumosclerosis – diffuse
                shadows 1-2 mm in                                      sclerosis, nodular or
              diameter are revealed.                               tumourous variant, bullous
                                                                           emphysema.
Any work that exposes you to silica dust:
    mining
    stone cutting
    quarrying
    road and building construction
    work with abrasives
    glass manufacturing
    sand blasting
    Also, some hobbies can involve exposure to
     silica (sculptor, glass blower)

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               Silicosis of the upper   Diffuse silicosis
Normal x ray   lobes
   Simple chronic silicosis From long-term exposure (10-
    20 years) to low amounts of silica dust. Nodules of chronic
    inflammation and scarring, provoked by the silica dust, form in
    the lungs and chest lymph nodes. Patients often asymptomatic,
    seen for other reasons.
   Accelerated silicosis (= PMF, progressive massive
    fibrosis) Occurs after exposure to larger amounts of silica over
    a shorter period of time (5-10 years). Inflammation, scarring, and
    symptoms progress faster in accelerated silicosis than in simple
    silicosis. Patients have symptoms, especially shortness of
    breath.
   Acute silicosis From short-term exposure to very large
    amounts of silica dust. The lungs become very inflamed,
    causing severe shortness of breath and low blood oxygen level.
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 History of significant exposure to silica dust.
  (occupational anamnesis)
 Abnormal chest X-ray (or chest CT scan)
  consistent with silicosis
 Medical evaluation to exclude other possible
  causes of abnormal chest x-ray ( sarcoidosis, TB
  and carcinoma)
 Pulmonary function tests are helpful to gauge
  severity of impairment, but NOT for diagnosis.
 Lung biopsy rarely indicated (since no effective
  treatment, biopsy is done only when other
  diagnoses are being considered)
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.   Early revealing and change of occupation to
    industry without dust.
.   Oxygen therapy to improve lung
    ventilation.
.   Corticosteroids are used in the period of
    fast progression, in Rheumatoid Silicosis.
.   Treatment of Heart failure
.   Treatment of Complication (Pleuritis,
    Pneumonia, Tuberculosis)
.   Symptomatic Therapy.
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Silicatosis (Asbestosis)
   A chronic and progressive lung disease caused by
    inhaling asbestos fibres over a long period of time.
   5- 20 years to develop
  inflammation from fibres causes scarring (fibrosis)
  and stiffening of the lung. This causes less oxygen
  exchange. Damage leads to bronchitis,
  bronhiectasis.
 Damage leads to pleural changes (pleuritis, spikes,
  enlargement of lymph nodes at the lung hila
  (containing asbestos).
 Frequent complication is lung cancer.

   Symptoms – short of breath, cough, chest tightness
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Chest X- Ray :

Interstitial pneumoscelerosis

Diagnostic Particularities:

a) In sputum - asbestos bodies
b) In skin - asbestos Warts (containing asbestos)




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Coal worker's pneumoconiosis is a lung
 disease that results from breathing in dust
 from coal, graphite, or man-made carbon
 over a long period of time.

 Necessary to differentiate from silico-
 tuberculosis, disseminated tuberculosis,
 metastatic lung cancer, and other diffuse
 infiltrative pulmonary diseases.


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1) Slow growth, benign character of
 current, active phagocytosis, saved
 lung protective mechanism.
2) Causes chronic bronchitis, lung
 emphysema
3) Radiological investigation –
 interstitial or interstitial nodular
 fibrosis of the lung.
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If coal worker's pneumoconiosis
  occurs with rheumatoid
  arthritis it is called Caplan
  syndrome.



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Caplan's syndrome (or Caplan's
 disease) is a combination of
 rheumatoid arthritis and
 pneumoconiosis that manifests as
 intrapulmonary nodules, which
 appear homogenous and well-
 defined on chest X-ray.

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Caplan's syndrome presents with
 cough
 shortness of breath
 features of rheumatoid arthritis such painful
  joints and morning stiffness.
 Examination should reveal tender,
  swollen MCP joints and rheumatoid nodules
 Auscultation of the chest may reveal
  diffuse râles that do not disappear on
  coughing or taking a deep breath.

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RHEUMATOID NODULES
Chest radiology shows multiple, round, well
  defined nodules, usually 0.5-2.0 cm in
  diameter, which may cavitate and
  resemble tuberculosis.
Lung function tests may reveal a mixed
  restrictive and obstructive ventilatory defect
  with a loss of lung volume. There may also
  be irreversible airflow limitation and a
  reduced DLCO.
Rheumatoid factor, antinuclear antibodies, and
  non-organ specific antibodies may be present
  in the serum.
Silicosis and asbestosis must be considered in
  the differential with TB.
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 Allexposure to coal dust must be stopped.
 Steroids
 Smoking cessation should be attempted.
 Rheumatoid arthritis should be treated
  normally with early use of DMARDs.




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Stage – I, II, III.
In the absence of sign – (0), In doubtful cases - (0 - I)
Nodules according to diameter are divided into 3 groups:
1) 1.5 mm; 2) 1.5 - 3 mm ; 3) 3 - 10 mm
According to distribution:
1) Small – (1)
2) Moderate – (2)
3) Large – (3)
According to type and localization of fibrosis:
1) Thin, linear, retinal – (s)
2) Sever, irregular – (t)
3) Roughly severe, cells – (u)
According to size of node
1) Small nodular, diameter - 1-5 cm
2) Large nodular, diameter - 5-10 cm (not bigger than 1/3 of lung
     field)
3) Massive nodular, diameter - more than 10cm (more than 1/3 of
     lung field).
A. Change of occupation – preventing contact with
    dust.
B. Increase of general resistance, diet.
C. Treatment of impaired lung ventilation, improve
    of airways passage – broncholytics, oxygen
    therapy.
D. Treatment of cardiac failure, ACEs, β-blockers,
    diuretics, cardiac glycosides).
E. Corticosteriods (during aggression period in
    silicosis, rheumatoid silicosis).
F. Treatment of complications (pleuritis, pneumonia
    etc).

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CRITERIA OF EFFECTIVENESS:

Stabilization of radiological changes in the
   lungs, improvement of respiratory function,
   control of respiratory and cardiorespiratory
   failure.

PROPHYLAXIS

1) Improvement of technology and emission of
    industry dust (hermitization, ventilation)
2) Sanitary – hygienic and medical control
3) Following correction of technologies and
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DEBORAH AKANYA TOSIN
           GROUP 501
  17TH NOVEMBER 2011

								
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