Chronic congestion of the lung (brown induration) (302)

spaces filled by air (might

be filled by edematous
fluids)

Coal dust (Black irregular

spots)
alveolar walls
Heart failure cells
(Single cells containing
dark dots)

Chronic LVF - impairment of the exit of the blood from the lungs
Increased pressure in the alveolar capillaries
Microhemorrhages into the alveoli, red blood cells are phagocytosed by
macrophages (heart failure cells) (macrophages laden with
hemosiderin)
Fibrosis of the interstitial spaces of the lung
Lung is brown and firm brown induration
Consequences of higher pressure in capillaries is pulmonary
hypertension, which may lead to right heart failure.

Emphysema of the lung (2)

Ruptured alveoli, forming
large airspaces (less surface
area)

Bronchus?

Pores of Kohn

Chronic lung disease

characterized by permanent
enlargement of the airspaces
Visible enlargement of the
airspaces.
major cause cigarette smoking
(protease-antiprotease theory)
Alpha-1 antitrypsin (1-AT)
deficiency 1% cases
Emphysema is classified
according to the location of the
lesions within the pulmonary
acinus:

Centriacinar (Centrilobular)

Panacinar (Panlobular)

Paraseptal

Irregular

Coal dust (smoking?)

Bronchopneumonia (303)

Bronchioles
filled with pus

Lots of rbc and neutrophils

Caused by infection of air way (trachea, bronchi)

Streptococci, staphylococci
Multifocal changes
Four stages, but we can observe different stages in every focus.

Pneumonia has 4 stages:

Congestion

Red hepatization

Gray hepatization

Resolution
macro: multifocal changes. Inflammations are yellow.
Usually complication of bronchitis.
Slide:

Normal area: some fluid in normal area (septa visible).

Inflamed area: Septa almost invisible (lots of cells in exudate

compresses the septa). Bronchi filled by pus (inflammation start
in bronchi, then involves other areas) (neutrophils, cellular
debris).

Interstitial pneumonia (305)

Artery?

Wide bronchoalveolar septa

filled with inflammatory cells
Necrotic debris on wall of
septa, forming hyaline
membranes. Serious state

No infiltration in bronchus

Enlarged capillary
in septa filled with
blood cells
Empty alveolar spaces

The most common cause is viral infection of the lung

CMV, Varicella, HSV

Viruses affect the alveolar epithelium and cause mononuclear infiltration

Children, elderly patients
Often asymptomatic, no changes in x-ray picture

Dilated interstitial parts of the lung, airspaces preserved

Symptoms: cough for a long time. Reduced lung capacity.

Necrosis of type I epithelial cells and hyaline membranes formation
Morphology: no circumscribed changes. More yellow areas suspected (in
autopsy sample). Newborn might die from interstitial pneumonia
slide: thickened septa containing cells (Inflammatory cells (lymphocytes,
plasma cells). Dilated capillaries. Hyaline membrane covers septa wall (from
necrotic debris of injured cells). Can cause death when large areas covered.
Bronchi normal with no infiltration.

Fibrocaseous tuberculosis of the lung (306)

Large area of necrotic debris

epithelioid cells
Langhans giant cell
Inflammatory infiltrates

Caused by Mycobacterium tuberculosis

Inhaled M. tuberculosis is deposited in the alveoli, usually in the

lower and middle lobes and anterior segments of upper lobes.
Generally is transmitted from person to person by aerosolized
droplets
Caseous granuloma - Classic lesion of tuberculosis

Soft, semisolid core surrounded by epithelioid cells, Langhans

giant cells, lymphocytes and peripheral fibrous tissue

Caseous necrosis in center

This is why this form of tuberculosis is called fibrocaseous

tuberculosis
Gross: large nodule (white, chalky appearance), caseous necrosis.
Granuloma at the edge.
Slide: Edges of necrosis fibrosis (fibrous connective tissue surrounds
granulomas). Lesions are large (unlike in miliary tuberculosis)

Tuberculoma (319)
Necrosis (old granuloma)

New granuloma on the edge

fibrosis

Firm, round tumor (not neoplastic)

Lung, meninges
Solitary mass with central caseous necrosis surrounded by granulomatous tissue
Encapsulated
Can form when treating tuberculosis. If treatment stops, new granuloma forms
around healing areas (fibrotic areas).

Up to 10 cm. Looks like malignant tumor.

In tumor with central necrosis, need to check border to determine cell type to
differentiate form neoplasm.
Slide: part of slide pink, other area darker. Large, light pink area = necrosis. Many
new, small granuloma around large area of necrosis. Epithelioid cells (elongated
nucleus). Can be layers of necrosis mixed with layers of fibrosis

Sarcoidosis of the lung (313)

Worldwide disease affecting all races and sexes

Causes are multifactorial environmental and genetic (BTNL gene)
lung, lymph nodes, spleen, liver, skin, uveal tract, bone marrow
Granulomatous inflammation

No caseous necrosis
multiple, sarcoid granulomas are scattered in the interstitium of the lung
granuloma lymphocytes, giant cells, epithelioid cells (macrophages)
Asteroid bodies (star shaped crystals) may be seen
Schaumann bodies (small calcifications with a laminar structure) may be present
inside Langhans cells.
slide: lymphocytes on the edges, central part with epithelioid cells (not just on the
edge like regular granuloma). Giant cells. Many granulomas.

Silicosis of the lung (323)

Whorl of collagen

Caused by the inhalation of silicon dioxide

Silica particles are ingested by alveolar macrophages

Macrophages are destroyed by silica particles

dead cells release free silica particles and fibrogenic factors

fibrogenic factors form nodules of collagen fibers.

Usually slowly progressing, nodular, fibrosing pneumoconiosis.
Silicotic nodule is composed of concentric whorls of dense, sparsely cellular collagen
Infiltration composed of lymphocytes and macrophages
At the edge of the nodule dust with carbon pigment and silica particles

silica particles are hard to see

Slide: nodule surrounded by chronic inflammatory cells (Coal dusts, macrophages,
lymphocytes). Few cells in nodule (collagen fibers).