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Organ Pathology
Respiratory System - I
Disorders of lung airiness
Jaroslava Dušková
Inst. Pathol. ,1st Med. Faculty, Charles Univ. Prague
Lung Function

oxygenation

carbon dioxide excretion
normal aeration of the lung tissue
- conditio sine qua non
Disorders of Lung Airiness
-
atelectasis / collaps
+
emphysema
coexistent in many pathology conditions !
Atelectasis / Collaps
Def.:
(cz) : A: inadequate expansion
C: secondary loss of airiness
(irrespective of age)
(eng):
A: inadequate expansion
A: loss of lung volume
Atelectasis in Children
Inadequate expansion:
immature lung tissue – insufficient
surfactant (S) production
Clinical manifestation - RDS
Regulation of (S) synthesis:
corticoids, thyroxine
insuline
The main events and outcomes in ARDS
Atelectasis (collaps) in Adults
- causes



obstruction
compression

restriction
microatelectases


contraction
chest wall
flail chest
Atelectasis (collaps) in Adults – causes I

obstruction – mucopurulent plug (infection,
mucoviscidosis), bronchomalacia –
bronchiectasis, chronic bronchitis, astma
foreign body, neoplasm (pores of Kohn)

compression – fluid, air, neoplasms in
the pleural cavity


microatelectases – loss of surfactant
contraction – loss of lung elasticity mostly
following fibrosis
Atelectasis (collaps) in Adults – causes II

chest wall restriction

flail chest
(obesity, scoliosis)
(several broken ribs)
Mucoviscidosis
cystic fibrosis, fibrocystic disease

autosomal recessive 7th chromosome
2-5% heterozygotic carriers in the caucasian
population

abnormal viscosity of mucin
– disturbance of the membrane associated
protein that serves as a calcium channel


increased concentration of chloride in sweat
decreased water content in excocrine secrets
Mucoviscidosis
cystic fibrosis, fibrocystic disease
Complications:
–
–
–
–
meconium ileus
steatorrhea
pancreatic fibrosis & cysts
bronchitis, bronchopneumonia,
bronchiectasia
– sterility
Bronchiectasis
Def.:
persistent abnormal dilation of the
bronchus.
Types:
– cylindrical
– saccular
Chronic Obstructive Airways Disease COAD
 limitation
to airflow in the lungs due to:
– airways resistence increased – narrowing
– loss of elastic recoil
Diseases of COAD type:
 chronic bronchitis
 asthma
 emphysema
Chronic obstructive pulmonary
disease (COPD)
Def.:
chronic productive cough lasting at least
three months during two subsequent
years
Causes: SMOKING, air pollution
Chronic Bronchitis
Morphology:
– hyperplasia of mucin producing goblet
cells (1GC :7CC
1GC:1CC)
– epithelial hyperplasia (& dysplasia!)
– inflammatory infiltrate
Asthma
Def.:
a chronic inflammatory disorder of the
airways in which many cells and
cellular elements play a role,
in particular, mast cells, eosinophils, T
lymphocytes, macrophages, neutrophils, and
epithelial cells.
Asthma
Clinical manifestation:




recurrent episodes of wheezing
breathlessness
chest tightness,
coughing at night or in the early morning
Prologed attack – status asthmaticus
Asthma - types
Intrinsic
Extrinsic
 abnormal

β-adrenergic reaction
 IgE normal
 causes:
–
–
–
–
coolness
effort
infection
aspirin…
type I hypersensitivity
 IgE
 causes:
–
–
–
–
–
dust
pollen
animal fur
drugs
foodsuff….
Asthma
Morphology:
bronchial lumina blocked by viscose
mucus and exudate with eosinophils
 oedema and infiltration of the mucose
 thickening of the muscle layer and
basement membrane
 Sputum:

– Charcot-Leyden crystals derived from eosinophils
– Curshman spirals – glycoproteins
– Creola bodies
Extrinsic allergic astma
Start in childhood, evidence of atopy
Allergens - household dust, organic dusts, pollens –
grasses and trees, animal fur, food products, drugs
Reagin – mediated type I hypersensitivity reaction
Serum IgE increased,
Skin tests against antigens positive
Mast cell degranulation – histamin, bradykinin
Smooth muscle contraction, hyperemia, edema,
eosinophils, mucus retention
Leukotrines, prostaglandins – brochoconstriction
vasodilatation, incr. permeability.
Intrinsic nonallergic astma
Start in adult life, no evidence of atopy
Hyperactivity of airways is response to nonspecific
stimuli
e.. Aspirin, cold, exercise…..
Constriction of bronchial wall
IgE levels normal, skin test normal
Associated with nasal polypi and bronchitis
Pathogenesis – abnormal β-adrenergic response
Emphysema
Def.:
 Increased
 Abnormal
airiness of the lung tissue
permanent enlargement of
gas exchange airways
(?
Emphysema
Types:
 non destructive (overinflation)
 destructive
–centriacinar
–panacinar
(smoking,
chronic bronchitis…)
(α1- antitrypsin
deficiency)
Smoking & Emphysema
numbers of neutrophils &
macrophages in smokers
 elastase activity
 macrophage elastase not blocked by
α1- antitrypsin
 oxygen free radicals in smoke inhibit
α1- antitrypsin

Emphysema - clinical symptoms

barrel chest, hypertrophy of
intercostal muscles

dyspnea, prolonged expiration

productive cough (if infected)
Emphysema - complications
pneumothorax
 polycytemia
 cor pulmonale

Emphysema - morphology
Macroscopy
 cushion- like
 light
 pink
 voluminous
 pericardium overlapping
 bullae
Emphysema - morphology
Microscopy
 alveolar distension
 centriacinar
 panacinar
– thinning and destruction of alveolar
septa
 reduction
of capillary bed
Interstitial emphysema
Def.:
Entrance of air into the
connective tissue of the lung,
mediastinum and soft tissue
Interstitial emphysema
Pathogenesis:

spontaneously
increased intraalveolar pressue
(cough, violent vomiting)
 iatrogenous - in patiens on respirator

traumatic - lung trauma – fractured ribs
Interstitial emphysema
Symptoms

swelling of the neck and head

crackling crepitation