Spiga

Emphysema

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Diagnosis: Emphysema

Definition:

  • abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by the destruction of the walls and without obvious fibrosis
Types:

1.Centriacinar(centrilobular)
  • begins in the respiratory bronchioles and spreads peripherally
  • associated with long-standing cigarette smoking
  • predominantly involves the upper half of the lungs
2.Panacinar(Panlobular)
  • destroys the entire alveolus uniformly
  • generally is observed in patients with homozygous alpha1-antitrypsin (AAT) deficiency
  • Among smokers,focal panacinar emphysema at the lung bases may accompany centriacinar emphysema.
  • predominant in the lower half of the lungs
3.Distal acinar emphysema(paraseptal ephysema)
  • preferentially involves the distal airway structures, alveolar ducts, and alveolar sacs
  • process is localized around the septae of the lungs or pleura
  • apical bullae may lead to spontaneous pneumothorax
  • Giant bullae occasionally cause severe compression of adjacent lung tissue.

Causes:
  • Tobacco smoking (mainly)
  • Toxic chemicals
  • alpha-1-antrypsin deficiency
  • air pollution
  • genetic
  • abnormal airway reactivity
  • old age
Differential diagnosis:
  • Chronic bronchitis
  • Bronchitis
  • Bronchiectasis
Pathophysiology:

1.neutrophil and macrophage activation and retention in the lung parenchyma

  • neutrophils produce serine proteinases
  • Macrophages synthesize various metalloproteinases and cysteine proteinases.
  • neutrophils and macrophages release elastase
  • these enzymes can break down the walls of alveoli which leads to significant modifications of lung architecture.
2. alpha-1-antitrypsin deficiency

  • AAT is a glycoprotein member of the serine protease inhibitor family that is synthesized in the liver and is secreted into the blood stream
  • main function is to neutralize neutrophil elastase in the lung interstitium and to protect the lung parenchyma from elastolytic breakdown
  • AAT deficiency predisposes to unopposed elastolysis with clinical sequela of early onset of panacinar emphysema.
Symptoms:
  • productive cough or acute chest illness-cough usually is worse in the morning and produces small amounts of colorless sputum
  • Breathlessness
  • Wheezing may occur in some patients, particularly during exertion and exacerbations
Signs:
  • cyanosis
  • wheeze
  • tachpnoea
  • hyperinflation
  • cricosternal distance <3cm
  • reduce chest expansion
  • resonant or hyper-resonant percussion
  • quite breath sounds

Test:

Routine:
  • FBC=PCV increase
Imaging:
  • Chest X-ray=
-hyperinflation(> 6 ribs anterior above diaphragm,mid-clavicular line)
-Flat hemidiaphragms
-large central pulmonary arteries (due to pulmonary hypertension)
-reduce pulmonary vascular markings
-bullae
-hyperlucency of the lungs
  • CT scan
Special test:
  • Pulmonary function test
-FEV1<80%
-FEV1:FVC ration <70%
-TLC-increase
-DLCO-reduce
-RV-increase
  • ABG - PaO2 reduce±hypercapnia
  • ECG- right atrial and ventricular hypertrophy (cor pulmonale)



1 comments:

  Unknown

January 21, 2010 at 10:07 AM

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