ASTHMA

Bronchial biopsy specimen

from an asthmatic patient
showing sub-basement
membrane fibrosis,
eosinophilic inflammation, and
muscle hyperplasia
 IDENTIFICATION POINTS
• Goblet cell hyperplasia
• Mucus secretions
• sub-basement membrane fibrosis,
• eosinophilic inflammation,
• muscle hyperplasia.
• Mucus plugs contain whorls of shed
epithelium, which give rise to the
well-known spiral shaped mucus plugs
called Curschmann spirals.
• Numerous eosinophils and
Charcot-Leyden crystals are present.
Coiled
basophilic
mucous
pugs
found in
sputum
andtrache
al
washings
 AIRWAY REMODELING
• The other characteristic histologic findings of
asthma, collectively called “airway remodeling”
• Overall thickening of airway wall
• Sub-basement membrane fibrosis
• Increased vascularity
• An increase in size of the submucosal glands
and mucous metaplasia of airway epithelial
cells
• Hypertrophy and/or hyperplasia of the
bronchial wall muscle
 EMPHYSEMA
• Emphysema and chronic bronchitis are often
grouped as chronic obstructive pulmonary
disease (COPD),
• extrinsic trigger—cigarette smoking—is
common to both.
• Emphysema is a condition of the lung
characterized by irreversible enlargement of
the airspaces distal to the terminal bronchiole,
accompanied by destruction of their walls
without obvious fibrosis
 TYPES
• Centriaciner (central or proximal parts of
the acini, formed by respiratory bronchioles,
are affected, whereas distal alveoli are
spared )
• Panacinar( the acini are uniformly enlarged
from the level of the respiratory bronchiole
to the terminal blind alveoli)
• Distal acinar (distal portion is involved)
• Irregular(acinus is irregularly involved)
CENTRIACINAR AND PANACINAR
EMPHYSEMA
• Centriacinar emphysema. Central areas
show marked emphysematous damage (E),
surrounded by relatively spared alveolar
spaces.
• Panacinar emphysema involving the entire
pulmonary lobule.
 Enlargement of airspaces
Thinning & destruction of alveolar septa
 HONEY COMB LUNG
• Patchy interstitial fibrosis
• Fibroblastic proliferation (fibroblastic foci).
• Destruction of alveolar architecture and formation
of cystic spaces lined by hyperplastic type II
pneumocytes or bronchiolar epithelium
(honeycomb fibrosis).
• There is mild to moderate inflammation within the
fibrotic areas, consisting of mostly lymphocytes,
and a few plasma cells, neutrophils, eosinophils,
and mast cells. Foci of squamous metaplasia and
smooth muscle hyperplasia may be present.
 HONEY COMB LUNG
Usual interstitial phenumonia
leading to fibrosis in subpleural
region
Primary pulmonary
tuberculosis, Ghon
complex. The
gray-white
parenchymal focus
is under the
pleura in the
of the upper
lobe. Hilar lymph
nodes with
caseation are seen
on the
 SECONDARY PULMONARY TUBERCULOSIS. THE UPPER PARTS OF
BOTH LUNGS ARE RIDDLED WITH GRAY-WHITE AREAS OF CASEATION
AND MULTIPLE AREAS OF SOFTENING AND CAVITATION.
 GRANULOMAS
Consist of epithelioid histiocytes and multinucleate
giant cells.
 PNEUMONIA
•
The clinical presentation
may be as an acute, fulminant clinical disease
or as a chronic disease with a more protracted
course. The histologic spectrum of
pneumonia may range from fibrinopurulent
alveolar exudate seen in acute bacterial
pneumonias, to mononuclear interstitial
infiltrates in viral and other atypical
pneumonias, to granulomas and cavitation
seen in many of the chronic pneumonias.
 ACUTE PNEUMONIA
• Acute bacterial pneumonias can manifest
as one of two anatomic and radiographic
patterns, referred to as
and Bronchopneumonia
a patchy distribution of inflammation that
generally involves more than one lobe.
Gross view of
lobar
pneumonia with
gray
hepatization.
The lower lobe
is uniformly
consolidated
ETIOLOGICAL
CLASSIFICATIO
N OF
PNEUMONIA
• Pneumonia evolved through four stages: congestion, red
hepatization, gray hepatization and resolution. Early antibiotic
therapy alters or halts this typical progression.
• During the first stage, that of CONGESTION, the affected lobe(s) is
(are) heavy, red, and boggy; histologically, vascular congestion can be
seen, with proteinaceous fluid, scattered neutrophils, and many
bacteria in the alveoli.
• Within a few days, the stage of RED HEPATIZATION ensues, in which
the lung lobe has a liver-like consistency; the alveolar spaces are
packed with neutrophils, red cells, and fibrin .
In the next stage, GRAY HEPATIZATION, the lung is dry, gray, and firm,
because the red cells are lysed, while the fibrinosuppurative exudate
persists within the alveoli RESOLUTION follows in uncomplicated
cases, as exudates within the alveoli are enzymatically digested to
produce granular, semifluid debris that is resorbed, ingested by
macrophages, coughed up, or organized by fibroblasts growing into it.
 ACUTE PNEUMONIA

The congested septal

capillaries
and extensive neutrophil
exudation into alveoli
correspond to early red
hepatization. Fibrin nets
have not yet formed(RED
HEPATIZATION)
Early organization of intra-alveolar exudates, seen in areas
to be streaming through the pores of Kohn ( )(GREY
HEPATIZATION)
Advanced organizing pneumonia, featuring transformation
of exudates to fibromyxoid masses richly infiltrated by
macrophages and fibroblasts(RESOLUTION)
 A B

Fig. 3.14 Purulent inflammation. (A) Multiple bacterial abscesses (arrows) in the lung in a case of bronchopneumonia. (B) The abscess contains neutrophils and cellular debris, and is surrounded by congested blood vessels.
Thickened alveolar wall,lymphocyte and plasma cell infiltration