Histopathology - Lung

Question 1

Answer 1

Hemorrhagic Infarction of Lung

 2 sharply different regions

 Hemorrhagic infarct (type of coagulative necrosis) due to venous blockage

 Infarcted area looks solid, not spongy.

 Alveolar cell nuclei are pyknotic

 Vessels disappear or contain thrombi, seen by eosinophilic fibrin

 Alveoli flooded by blood in greater amount than the interstitial blood of the anemic infarct

 Septal structure disappears

 Neutrophils at border of infarction

 Anthracosis = coal deposits

 Foamy purple parts = edema

Question 2

Answer 2

Bronchus: Metaplasia

 Columnar, ciliated, pseudrostratified, goblet cells = respiratory epithelium

 Here, normal structure is not maintained.

o stratified squamous non-keratinized epithelium (=metaplasia) can bear more irritation, but less clearing abilities

o large, clumped nuclei lacking cytoplasm = dysplasia

 Severe dysplasia indicates an in situ carcinoma

o Widening of epithelium  Metaplasia  Dysplasia

o Breaking through basal membrane = cancer

Question 3

Answer 3

Pulmonary Edema
 Acute pulmonary edema caused by LV insufficiency

o Edema is increased fluid in the interstitium

o Clinical emergency
 Increased capillary hydrostatic pressure. Dilated capillaries and blood cells in alveoli indicate

congestion in the lung
o Septa will be dark pink
o Congestion is due to passive hyperemia: pooling of venous blood results in dilation of

pulmonary capillaries  Homogenous filling of alveoli

o Transudate (lower protein content than exudate) leaks from the vessel due to hydrostatic pressure on membrane wall; Forms the faintly eosinophilic, homogenous filling

o Exudate is the darker eosinophilic spots  What causes edema in the lungs?

o L.H.F.
o Mitral stenosis
o ARDS
o Trauma
o Pulmonary hypertension

 (Macrophages eat up RBC and become hemosiderin-laden “heart failure cells” in the chronic edema slide)

 Inflammatory cells, macrophages, cellular debris of pneumocytes seen in the alveoli

 Macroscopically, lungs appear normal but weigh more

Question 4

Answer 4

Induratio brunea pulmonis: H&E and Prussian Blue

 In chronic LHF, decrease in contractility develops slowly, allowing the lungs to accommodate to the increase in hydrostatic pressure

o Venous pooling causes pulmonary congestion
o To deal with increased hydrostatic pressure, the lungs constrict their precapillary

arterioles to prevent edema and to keep the capillary pressure constant
o The pulmonary veins will be dilated and filled with blood that is fully oxygenated and

therefore appears dark red.

 Capillaries will break due to changing pressure and allow RBC into alveolar lumen

 RBC will be digested by alveolar macrophages

 Macrophages (large, purple, bean-shaped nuclei) then contain hemosiderin

o “heart failure cells” coughed up
o localized hemosiderosis
o when macrophages are saturated with hemosiderin, they appear on the surface of the

lungs in lymph vessels

 Prussian blue stains the macrophage hemosiderin blue. o The black cells are anthracotic cells.

 Macroscopically, lungs appear heavier and weigh more due to venous blood.

Question 5

Answer 5

Bronchopneumonia

 More common than lobar pneumonia (both occur when there is exudate in the alveolar spaces)

 Infection and inflammatory response spreads through bronchial tree lymph as focal adhesions

o Pneumonia originates from bronchioles
o Inflammation occurs in nodular pattern, and the nodules can be felt macroscopically

 Tissue is more solid in some regions

 Cells in alveoli instead of air

 Alveolar structure present, but wall is thick with dilated vessels due to inflammations

 PMN cells and fibrin in exudate

Question 6

Answer 6

Lobar pneumonia

 Lumen of alveoli filled with PMN exudate, not air

 Occupies entire lobe (not focal)

o Same stage of inflammation at every location

 Firm and solid consistency = “hepatization of lung”

 3 stages:

1. Hepatization rubra: blood floods lung, it will be reddish 2. Hepatization grisa: fibrin in lung turns in gray
2. Hepatization flava: leukocytes come

 Hepatization preceded by congestion. It is followed by resolution or organization.

 Surface of lung has fibrinous pleuritis. This concomitant pleuritis is a complication

 Lobar pneumonia can be caused by Strep pneumoniae and Klebsiella

Question 7

Answer 7

Pulmonary Abscess

 4 focal lesions with no alveolar septal structure

 Consequence of bronchopneumonia

 Sharply circumscribed lumen filled by necrotic tissue

 Abscess = collection of pus in non-preformed body cavity. Necrotic core.

 Core surrounded by neutrophils still in the fluid center

 Fibrinous capsule surrounds the focal lesion

 Wall of abscess is the pyogenic membrane

 Note anthracosis

Question 8

Answer 8

Tuberculosis Pulmonis

 Development of tuberculosis:
o Primary: Mycobacterium infects alveolar macrophages and survives inside, spread to

multiple sites. Induces immune system granuloma formations. Ghon complex is a combination of parenchymal and nodal involvement. T-cell mediated immunity causes spread into lymph nodes (3 weeks after exposure) and causes granuloma formation (Ranke complex)

o Secondary: typically initiated in immunosuppressed patients. Arises from reaction of dormant primary lesions. Necrotic lesions. Bacteria released from airways and ingested.

 Patches and nodules similar to pulmonary abscess or tumor on low power, but they are granulomas.

o Granulomas are 0.1-0.5 mm round structures composed of epithloid cells
o Caused by infection, foreign body, or unknown etiology (sarcoidosis, Crohn’s

Disease)
 From inside of the tuberculoma to outside:

o Eosinophilic center with causeous necrosis and the bacteria
o Pale blue ring of epitheloid cells (= type of macrophages resembling cuboidal

epithelial cells; abundant cytoplasm and central nuclei), which can fuse to form giant

cells (= multinucleated)
o Dark blue lymphocytes in an amorphous, anuclear substance; caseous necrosis

Question 9

Answer 9

To confirm that this is a tuberculoma, we use Ziehl-Neelsen (Acid Fast) Stain

 Background is pale blue, bacteria are red

 Clumped blue areas are granulomas; at higher mag, eosinophilic bacteria are seen there, too

 Chronic inflammations can be:

o Specific: e.g. tuberculoma, have characteristic morphology for the etiology

o Non-specific: majority; morphology of inflamed tissue is not characteristic for the etiology

Question 10

Answer 10

Respiratory Allergic Polyp

 Polypoid structure covered by epithelium, projects towards lumen o Respiratory epithelium covers three sides

 Edematous connective tissue structure with dilated mucous glands

 Eosinophilic exudate

 Eosinophils indicate allergic process

 Metaplastic change to stratified squamous epithelium may occur

Question 11

Answer 11

Asthma Bronchiale

 Type I Hypersensitivity

 Emphysematous parts are called “distensions”

o Septa are destroyed
o Bronchi are dilated and filled with purplish material o Expiratory dyspnea (hyperinflation)

 Lymphocytes, mucous gland hyperplasia, and destruction of wall = signs of inflammation

 Smooth muscle cells of bronchi proliferate in chronic asthma

 Exudate

 Denuded epithelium, thickened basement membrane

 Deep purple plugs filling the lumens are “Curschmann spirals” = mucin + eosinophils

Question 12

Answer 12

Infant Respiratory Distress Syndrome (PAS)

 Dense lung that looks like a solid organ (pancreas)

 PAS (+) regions are stained purple in the alveoli

o This used to be called “hyaline membrane disease”
o Waxy layer of hyaline membrane line the collapsed alveoli. Hyaline is protein and

dead cells

 Caused by prematurity (insufficient surfactant), diabetic mother, or twin pregnancy

 There is poor gas exchange, the pressure increases blood to bypass the lung

 Hyaline membranes also caused by Group B Strep or “respirator lung”

Question 13

Answer 13

Pleuritis Carcinamatosa

 Smear

 Carcinosis is a disseminated cancer

 RBC, lymphocytes, mesothelial cells can be seen

 Mesothelial cells are big and round with eccentric nuclei and vacolated cytoplasm

o Capable of phagocytosis
 Mesothelial cells form darker islands. Here there is a higher nuclei to cytoplasm ratio

Question 14

Answer 14

Emphysema H&E

 Large alveoli made by disrupting smaller

 Lack of normal septa

 Less place for oxygen exchange

 A form of COPD because exhalation is ‘obstructed’

 Larger vessels

 Macroscopically: white areas at margin

 This is panacinar type of emphysema

o destroys the entire alveolus uniformly; predominant in the lower half of the lungs

Question 15

Answer 15

Pneumocystitis Pneumonia H&E

 Less air

 Alveoli are full of eosinophilic material and desquamated, reactive cells

 Pneumocystitis is caused by the yeast-like fungus Pneumocystis jirovecii o Foamy eosinophilic material = P. jirovecii

 Large cells with deep blue nucleus with a halo are CMV inclusions, “owl eye”

 This is a P. jirovecii and CMV coinfection

 Note hemosiderin and anthracosis

Question 16

Answer 16

Pneumocystitis Pneumonia – Grocott staining

 Foamy material in alveoli stains place

 Grocott + cells are P. jirovecii

o Cell walls of these organisms are outlined

Question 17

Answer 17

Aspergillosis H&E

 Eosinophilic, dense part vs. airy part

 Airy part has thicker septa with eosinophilic material in alveoli

 Dense part has no nuclei. This is necrotized tissue

o There are rods with tree-like, septated walls with 45° bifurcation growing in the necrotized tissue

 At the left edge, normal structure is recognized better.

 Vessels are filled with collection of rods, which then penetrate the vessel rod

o Invasion of vesselinfarctionnecrosis
 This infection occurs in immunocompromised patients

Question 18

Answer 18

Aspergillosis Grocott Stain

 Septa are stained by Grocott

 Elastic fibers of vessels are also stained

Question 19

Answer 19

Chronic bronchitis H&E

 Cartilage, mucosa, glands can be seen

 Cilia is missing in some parts of the respiratory epithelium

 Few goblet cells

 Thickened basal membrane

 Lymphocyte infiltration

 Stratified squamous epithelium

 Reid Index is used post-mortally:

o Ratio between the thickness of the submucosal mucus secreting glands and the thickness between the epithelium and cartilage that covers the bronchi (i.e. glands/wall)

o Distance between epithelium and cartilage is >0.5 mm. Glands make up 0.4-0.5 mm. MetaplasiaDysplasiaplanocellular carcinoma

Question 20

Answer 20

Adenocarcinoma

 Well-delineated larger part on the left with acellular elements

 Note mucin and cholesterin crystals

 Glands are irregular, immature

o Invasive, spreading in neostroma, which is not usually in the lung

Question 21

Answer 21

Microcellular Carcinoma

 Hilus with thrombus

 Anthracosis

 Respiratory epithelium is intact

 Basophilic area has a capsule. It resembles a LN

o Higher magnification: lymphocytes, mitotic figures, loose patches of cells with irregular shape and size.

o Immature, polymorphic, highly proliferative tumor  Small cell lung cancers are immature and aggressive

o Treatment is chemo rather than operation
 It is thought to originate from neuroendocrine cells (APUD cells) in the bronchus called

Feyrter cells. They express a variety of neuroendocrine markers, and may lead to ectopic production of hormones.

Question 22

Answer 22

Mesothelioma from PLEURA H&E

 Derives from serous membrane

 Mesothelium is from the epithelial covering lining coelom

 Very variable histological picture

 Asbestos increases mesothelioma risk 1000x

o Asbestos also increases risk of bronchial carcinoma

 Slide displays tumor cells

 Large polygonal cells with large nuclei

 Cell borders well-preserved

 Mitotic figures

 Diagnosis is based on immunohistochem

o Calretinin

o WT1

 Differential diagnosis: a carcinoma that has metastasized to the pleura

o Immunohistochem

o Check for primary tumors