Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

AP reviewer > Lung > Flashcards

Lung Flashcards

1
Q

Congenital pulmonary-airway malformation: Blood supply.

A

Derived from the pulmonary circulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Congenital pulmonary-airway malformation, type 0: Gross pathology.

A

Lung parenchyma appears solid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Congenital pulmonary-airway malformation, type 0: Histology (2).

A

Disorganized proximal airways; no distal airways.

Intervening tissue consists of connective tissue, thick-walled arteries, and extramedullary hematopoiesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Congenital pulmonary-airway malformation, type 1: Gross pathology.

A

Medium and large interconnecting cysts, usually limited to one lobe.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Congenital pulmonary-airway malformation, type 1: Histology.

A

Cysts are lined by bronchial epithelium and often contain bands of smooth muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Congenital pulmonary-airway malformation, type 2: Gross pathology.

A

Back-to-back cysts, smaller than the cysts of type 1.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Congenital pulmonary-airway malformation, type 2: Histology.

A

Cysts are separated by alveolar ductlike structures, blood vessels, skeletal muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Congenital pulmonary-airway malformation, type 2: Associations.

A

Sirenomelia.

Renal malformations.

Diaphragmatic hernia.

Cardiovascular abnormalities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Congenital pulmonary-airway malformation, type 3: Gross pathology.

A

Solid mass involving the lobe or the entire lung, with hypoplasia of the other lung.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Congenital pulmonary-airway malformation, type 3: Histology.

A

Glandlike structures lined by low cuboidal epithelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Congenital pulmonary-airway malformation, type 3: Associations.

A

Male sex.

Polyhydramnios.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Congenital pulmonary-airway malformation, type 4: Gross pathology.

A

Peripherally located cysts of variable size.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Congenital pulmonary-airway malformation, type 4: Histology.

A

Cysts can have thick walls and are lined by a single layer of pneumocytes.

Capillary beds beneath the epithelial lining.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Congenital pulmonary-airway malformation, type 4: IHC.

A

Pneumocytes express TTF-1 and surfactant proteins A and B.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Congenital pulmonary-airway malformation: Limitations on diagnosis.

A

Diagnosis cannot be made when there is chronic inflammation and fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Bronchopulmonary sequestration: Definition (2).

A

Anomalous segment of lung has no connection with the normal tracheobronchial tree.

Blood supply comes from the systemic circulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Bronchopulmonary sequestration: Types (2).

A

Intralobar.

Extralobar.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Bronchopulmonary sequestration, intralobar type: Typical location.

A

Lower lobe.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Bronchopulmonary sequestration, intralobar type: Gross pathology (3).

A

No pleural covering.

Sharply demarcated from the normal lung tissue.

May have vascular pedicle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Bronchopulmonary sequestration, intralobar type: Histology (3).

A

Marked chronic inflammation.

Mucus accumulation and microcyst formation.

Dense fibrosis surrounds remnants of bronchioles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Bronchopulmonary sequestration, extralobar type: Typical location.

A

Left side.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Bronchopulmonary sequestration, extralobar type: Gross pathology (2).

A

Covered with visceral pleura.

Separate from normal lung tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Bronchopulmonary sequestration, extralobar type: Histology (3).

A

Enlarged bronchi, bronchioles, alveoli.

No significant inflammation or fibrosis.

Dilated subpleural lymphatics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Bronchopulmonary sequestration, extralobar type: Association.

A

Congenital pulmonary-airway malformation, type 2, is present in up to half of cases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Bronchogenic cyst: Origin.

A

Anomalous budding of the tracheobronchial anlage during development.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Bronchogenic cyst: Most common site.

A

Mediastinum.

No communication with the tracheobronchial tree.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Bronchogenic cyst: Radiography.

A

May have an air-fluid level.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Bronchogenic cyst: Histology (3).

A

Epithelial lining and wall (smooth muscle, cartilage) resemble those of a normal bronchus.

Squamous metaplasia or chronic inflammation may occur.

No alveolar tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Congenital lobar emphysema: Definition.

A

Hyperinflation of one or more lobes of the lung.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Congenital lobar emphysema:

A. Age at presentation.
B. Most common site.

A

A. Within 6 months after delivery.

B. Left upper lobe.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Congenital lobar emphysema: Radiography.

A

Compression of contralateral lung and mediastinal shift.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Congenital lobar emphysema: Histology.

A

Alveolar distention without fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Congenital lobar emphysema: Etiologies.

A

Idiopathic: Most cases.

Intrinsic compression of the bronchus supplying the affected lobe: Structural defect of bronchus.

Extrinsic compression: Mass.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Chronic bronchitis: Histology.

A

Reid index >0.5 (glands make up more than half the thickness of the bronchial wall).

Mild chronic inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Asthma: Gross pathology (3).

A

Hyperinflated lungs.

Mucous plugging of airways.

Saccular bronchiectasis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Asthma: Histology (3).

A

Mucous plugs containing eosinophils.

Fibrosis beneath the basement membrane with patchy loss of epithelium.

Thickened walls of airways due to edema, hyperplasia of smooth muscle, increased mucous glands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Asthma vs. chronic bronchitis.

A

Chronic bronchitis: Few or no eosinophils.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Bronchiectasis: Definition.

A

The bronchus is wider than its bronchial artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Bronchiectasis: Clinical presentation.

A

Persistent cough.

Copious, foul-smelling sputum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Bronchiectasis: Causes (8).

A 
Primary ciliary dyskinesia.
Rheumatoid arthritis.
Immunodeficiency.
Cystic fibrosis.
Inflammatory bowel disease.
No known cause (30%).
Graft-versus-host disease.

Infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Bronchiectasis: Histology (2).

A

Mucosa: Variable inflammation, reactive changes, necrosis.

Wall: Chronic inflammation, fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Middle-lobe syndrome:

A. Definition.
B. Causes.

A

A. Recurrent or persistent atelectasis of the right middle lobe.

B. Lymphadenopathy, malignancy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Type of emphysema associated with

A. Cigarette smokers (2).
B. α₁-Antitrypsin deficiency.

A

A. Proximal acinar or centrilobular.

B. Panacinar or panlobular.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Types of emphysema associated with bullous disease and idiopathic spontaneous pneumothorax (2).

A

Distal acinar, paraseptal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Emphysema: Histology (2).

A

Alveolar distention without fibrosis.

Club-shaped septa may project into the alveolar spaces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Interstitial emphysema.

A

Presence of air outside the airways, e.g. in the connective tissue and around bronchovascular bundles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Constrictive bronchiolitis: Site.

A

Terminal conducting airways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Constrictive bronchiolitis: Associations (8).

A

Collagen-vascular disease.
Hypersensitivity pneumonitis.
Inhalational injury.
Neuroendocrine hyperplasia/tumors.

Viral infection.
Organ transplantation.
Inflammatory bowel disease.
Drugs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Constrictive bronchiolitis: Histology (4).

A

Fibrosis.

Chronic inflammation with epithelial metaplasia.

Smooth-muscle hyperplasia.

Luminal obliteration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Acute bronchiolitis:

A. Age group.
B. Associations (2).

A

A. Infants and children.

B. Viral infection, bacterial infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Acute bronchiolitis: Histology (3).

A

Intense acute and chronic inflammation of small bronchioles.

Epithelial necrosis and sloughing.

Edema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Diffuse bronchiolitis:

A. Epidemiology.
B. Associations (4).

A

A. Affects Asian adults.

B. HLA Bw54; cold agglutinin, increased ESR, leukocytosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Diffuse bronchiolitis: Histology (3).

A

Lymphocytes, plasma cells, foamy macrophages.

Many intraluminal neutrophils.

Organization of exudate to form polypoid plugs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Respiratory bronchiolitis: Association.

A

Cigarette smoking.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Respiratory bronchiolitis: Histology (4).

A

Interstitial inflammation.

Many intraluminal pigmented macrophages.

Smooth-muscle hypertrophy.

Mild fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Mineral-dust bronchiolitis: Type of lung disease.

A

Restrictive, due to fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Mineral-dust bronchiolitis: Histology (3).

A

Fibrosis.

Deposits of dust mainly around respiratory bronchioles.

Luminal narrowing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Follicular bronchiolitis: Type of lung disease.

A

Obstructive, due to external compression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Follicular bronchiolitis: Histology.

A

Lymphoid hyperplasia with reactive germinal centers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Follicular bronchiolitis: Associations.

A

Anything that causes lymphoid hyperplasia, e.g. chronic inflammation, infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Diffuse alveolar damage: Clinical equivalents (3).

A

Acute respiratory-distress syndrome.

Acute interstitial pneumonia.

Acute lung injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Diffuse alveolar damage: Relevance to autoimmune disease (2).

A

Various collagen-vascular diseases cause DAD-type inflammation.

Various vasculitides can resemble AIP clinically.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Diffuse alveolar damage: Distribution of lesions (2).

A

Patchy involvement of the lung, but concentrated in the lower lobes.

Diffuse involvement of the alveolus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Diffuse alveolar damage: Radiography.

A

Ground-glass opacities that spare the lobules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Diffuse alveolar damage: Phases.

A

Exudative: First week.

Proliferative: Second week.

Fibrotic: Late.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Diffuse alveolar damage, exudative phase: Histology.

A

Hyaline membranes and interstitial edema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Diffuse alveolar damage, proliferative phase: Histology.

A

Interstitium and airspaces: Florid proliferation of fibroblasts, myofibroblasts, type 2 pneumocytes.

Arteries: Intimal proliferation, medial hypertrophy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Diffuse alveolar damage, fibrotic phase: Histology.

A

Dense interstitial fibrosis with microcysts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Diffuse alveolar damage vs. usual interstitial pneumonia (3).

A

UIP:

− No hyaline membranes.
− Temporal heterogeneity of fibrosis.
− Fibrosis has more collagen and fewer cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Acute respiratory-distress syndrome: Prognosis.

A

Most patients regain near-normal lung function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Acute interstitial pneumonia:

A. Clinical presentation.
B. Prognosis.

A

A. Resembles severe community-acquired pneumonia but does not respond to antibiotics.

B. Death in 6 months in 78% of cases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Cryptogenic organizing pneumonia:

A. Clinical presentation.
B. Duration.

A

A. Cough, dyspnea, and flulike symptoms.

B. Subacute.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Cryptogenic organizing pneumonia: Prognosis.

A

Usually responds to steroids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Cryptogenic organizing pneumonia: Distribution of lesions.

A

Subpleural.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Cryptogenic organizing pneumonia: Radiography.

A

Peribronchial consolidation and nodularity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Cryptogenic organizing pneumonia: Histology (2).

A

Masson bodies: Intraluminal plugs consisting of young fibrous tissue.

Interstitial mild chronic inflammation with foci of foamy macrophages.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Cryptogenic organizing pneumonia: Special stain.

A

Movat’s stain: Masson bodies appear green; dense fibrosis would appear yellow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Cryptogenic organizing pneumonia vs. usual interstitial pneumonia.

A

UIP:

− Dense fibrosis (not seen in COP).
− Fibroblastic foci are interstitial, not intraluminal.
− Temporal heterogeneity of fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Cryptogenic organizing pneumonia vs. nonspecific interstitial pneumonia.

A

NSIP: Interstitial chronic inflammation without Masson bodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Usual interstitial pneumonia:

A. Clinical presentation.
B. Duration.

A

A. Progressive dyspnea and cough.

B. Chronic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Usual interstitial pneumonia:

A. Associated environmental agents (3).
B. Associated inherited diseases (2).

A

A. Cigarettes, asbestos, drugs.

B. Familial idiopathic pulmonary fibrosis, Hermansky-Pudlak syndrome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Usual interstitial pneumonia: Association that imparts a better prognosis.

A

Collagen-vascular disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Usual interstitial pneumonia: Prognosis.

A

Median survival is 3 years.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Usual interstitial pneumonia: Distribution of lesions (2).

A

Subpleural.

Lower lobes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Usual interstitial pneumonia: Radiography (3).

A

Honeycombing.

Ground-glass opacities.

Traction bronchiectasis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Usual interstitial pneumonia: Histology.

A

Temporal heterogeneity: The same area may contain both mature fibrosis and subepithelial young fibrosis (fibroblastic foci).

Spatial heterogeneity: Some areas are affected, some not.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Usual interstitial pneumonia: Histologic findings associated with poor prognosis (4).

A

Diffuse alveolar damage.

Infection.

Capillaritis.

Organizing pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Usual interstitial pneumonia vs. hypersensitivity pneumonitis with fibrosis.

A

Hypersensitivity pneumonitis:

− Mainly upper lobes.
− Centered on bronchioles.
− More cellular inflammation, including giant cells or poorly formed granulomas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Usual interstitial pneumonia vs. Langerhans’ cell histiocytosis.

A

Langerhans’ cell histiocytosis:

− Centered on bronchioles.
− Few or no fibroblastic foci.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Usual interstitial pneumonia: How to diagnose cases that contain findings of other interstitial lung diseases.

A

As usual interstitial pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Nonspecific interstitial pneumonia:

A. Clinical presentation.
B. Duration.

A

A. Dyspnea, cough, fever.

B. Subacute.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Nonspecific interstitial pneumonia: Associations (5).

A

Cigarettes.

Drugs.

Immunodeficiency.

Collagen-vascular diseases.

Hypersensitivity pneumonitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Nonspecific interstitial pneumonia: Distribution of lesions.

A

Subpleural.

Lower lobes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Nonspecific interstitial pneumonia: Radiography.

A

Peribronchial ground-glass opacities.

Reticular opacities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Nonspecific interstitial pneumonia: Long-term prognosis.

A

Cellular type: Excellent.

Fibrotic type: Poor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Nonspecific interstitial pneumonia, cellular type: Histology (3).

A

Diffuse interstitial infiltrate of lymphocytes and plasma cells.

Preservation of the pulmonary architecture.

Hyperplasia of type 2 pneumocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Nonspecific interstitial pneumonia, fibrotic type: Histology (4).

A

Loose to dense interstitial fibrosis that thickens the alveolar walls.

Fibrosis shows temporal homogeneity.

Preservation of the pulmonary architecture.

Mild or moderate chronic inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Nonspecific interstitial pneumonia: Histological clue to an association.

A

Abundance of lymphoid aggregates suggests collagen-vascular disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Nonspecific interstitial pneumonia: What should not be seen histologically (3).

A

Significant honeycombing.

Many fibroblastic foci.

Granulomas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Nonspecific interstitial pneumonia vs. lymphoid interstitial pneumonia.

A

LIP:

− Denser inflammatory infiltrate.
− Architectural distortion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Desquamative interstitial pneumonia: Clinical presentation.

A

Dyspnea, cough, chest pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Desquamative interstitial pneumonia: Duration.

A

Subacute.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Desquamative interstitial pneumonia: Distribution of lesions.

A

Subpleural.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Desquamative interstitial pneumonia:

A. Frequent association.
B. Infrequent associations (2).

A

A. Cigarette smoking, even years after cessation.

B. Sirolimus; mutations in SP-C, the gene for surfactant protein C.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Desquamative interstitial pneumonia: Radiography.

A

Ground-glass opacities.

Thin-walled cysts.

Reticular opacities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Desquamative interstitial pneumonia: Histology (3).

A

Pigmented macrophages (originally thought to be “desquamated” pneumocytes) fill alveoli.

Intraalveolar laminated basophilic concretions (“blue bodies”) sometimes present.

No significant fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Desquamative interstitial pneumonia: Special stain.

A

Prussian blue highlights the finely granular pigment within the macrophages.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Desquamative interstitial pneumonia vs. respiratory bronchiolitis-interstitial lung disease.

A

RB-ILD: Macrophages fill the bronchioles but not the distal airspaces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Lymphoid interstitial pneumonia: Associations.

A

Children: AIDS.

Adults: Immunocompromise, including AIDS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Lymphoid interstitial pneumonia: Clinical presentation in children.

A

Manifestations of AIDS: Recurrent infections, parotiditis, failure to thrive.

Respiratory failure occasionally.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Lymphoid interstitial pneumonia: Radiography (2).

A

Children: Miliary reticulonodular infiltrates.

Adults: The same plus alveolar consolidation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Lymphoid interstitial pneumonia: Histology (2).

A

Dense mononuclear inflammation of the interstitium, sometimes with germinal centers.

Partial obliteration of architecture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Lymphoid interstitial pneumonia: Microbiological association.

A

ISH detects EBV in most cases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Lymphoid interstitial pneumonia: Clinical course.

A

No progression to fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Hypersensitivity pneumonitis:

A. Associations.
B. Distribution of lesions.

A

A. Various organic antigens, esp. those of thermophilic actinomycetes and birds.

B. Upper lobes, peribronchiolar.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Hypersensitivity pneumonitis: Phases (3).

A

Acute: Exposure to high concentrations of antigen; onset in 4-8 hours; resolution in 24-48 hours.

Subacute: Continuous or intermittent exposure to low concentrations of antigen; responds to steroids or to withdrawal of antigen.

Chronic: Subacute plus fibrosis; worse prognosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Hypersensitivity pneumonitis, subacute phase: Histology (2).

A

Small, poorly formed granulomas and mononuclear inflammation next to bronchioles.

Foamy histiocytes in alveoli and interstitium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Hypersensitivity pneumonitis, chronic phase: Histologic patterns (3).

A

NSIP-like pattern: Homogeneous fibrosis with architectural preservation.

UIP-like: Patchy subpleural fibrosis with architectural distortion.

Irregular peribronchiolar pattern: UIP-like plus peribronchiolar fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Hypersensitivity pneumonitis vs. usual interstitial pneumonia.

A

UIP:

− No giant cells, no granulomas.
− Mainly subpleural and in lower lobes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Hypersensitivity pneumonitis vs. nonspecific interstitial pneumonia.

A

NSIP: No giant cells, no granulomas.

Clinical history may be required to make the distinction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Hypersensitivity pneumonitis vs. sarcoidosis.

A

Sarcoidosis:

− Well-formed granulomas with hyalinized rim and location along bronchovascular bundles.
− No UIP- or NSIP-like changes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Eosinophilic lung diseases: Unknown etiology (3)

A

Simple eosinophilic pneumonia.

Acute eosinophilic pneumonia.

Chronic eosinophilic pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Eosinophilic lung diseases: Known etiology (4).

A

Allergic bronchopulmonary aspergillosis.

Bronchocentric granulomatosis.

Parasitic infections.

Drugs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Eosinophilic lung diseases: Vasculitic causes (2).

A

Allergic angiitis.

Churg-Strauss syndrome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Eosinophilic lung disease: How to diagnose without tissue or cytology.

A

Demonstrate pulmonary opacities and peripheral eosinophilia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Acute eosinophilic pneumonia:

A. Clinical presentation.
B. Associations (2).

A

A. Acute respiratory distress that mimics infectious pneumonia.

B. Cigarettes, dust.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Acute eosinophilic pneumonia: Histology (3).

A

Resembles acute phase of DAD but with alveolar and interstitial eosinophils.

Hypertrophied and detached type 2 pneumocytes.

Intact basal lamina.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Acute eosinophilic pneumonia: Prognosis.

A

Rapid and complete response to corticosteroids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Acute eosinophilic pneumonia: Degree of eosinophilia.

A

BAL: More than 25%.

Peripheral blood: Often no eosinophilia at first.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Chronic eosinophilic pneumonia: Radiography.

A

Peripheral consolidation mainly involving middle and lower zones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Chronic eosinophilic pneumonia: Laboratory abnormalities (2).

A

Peripheral eosinophilia.

Elevated IgE in 7% of patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Chronic eosinophilic pneumonia: Histology.

A

Intraalveolar and interstitial eosinophils (single or in aggregates) and eosinophilic giant cells.

Damage to basal lamina, leading to fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Parasites that can cause eosinophilic lung disease: Allergic reaction (3).

A

Entamoeba.

Toxocara.

Clonorchis sinensis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Parasites that can cause eosinophilic lung disease: Direct invasion (4).

A

Ascaris lumbricoides.

Ankylostoma duodenale.

Paragonimus westermani.

Schistosomes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Parasites that can cause eosinophilic lung disease: Others (3).

A

Strongyloides stercoralis.

Microfilariae.

Dirofilaria immitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Sarcoidosis: Frequency of pulmonary disease.

A

90-95%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Pulmonary sarcoidosis: Clinical course (2).

A

Abrupt, acute illness with a better prognosis.

Chronic, insidious illness with persistent, progressive course.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Pulmonary sarcoidosis: Distribution of lesions (3).

A

Around the lymphatic vessels in the pleura, the interlobular septa, and the bronchovascular bundles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Histology of pulmonary sarcoidosis:

A. Periphery of granulomas.
B. Tissues involved by granulomas.

A

A. Concentric fibrosis often; usually no cuff of lymphocytes.

B. Vessels, pleura.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Histology of pulmonary sarcoidosis: Inclusions that can be confused for microorganisms (2).

A

Hamazaki-Wesenberg bodies: GMS (+), AFB (+); mimic fungi.

Microcalcifications: Mimic fungi or P. jiroveci.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Sarcoidosis vs. hypersensitivity pneumonitis.

A

Hypersensitivity pneumonitis:

− Granulomas are less well formed.
− More inflammation in the interstitium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Types of disease associated with a sarcoidosis-like disorder (2).

A

Malignancies.

Collagen-vascular disorders.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Idiopathic pulmonary hemosiderosis: Age group.

A

Children and adolescents.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Idiopathic pulmonary hemosiderosis:

A. Clinical manifestations (4).
B. Clinical course.

A

A. Cough, hemoptysis, iron-deficiency anemia, weight loss.

B. Subject to spontaneous remission or exacerbation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Idiopathic pulmonary hemosiderosis: Associations (3).

A

IgA nephropathy.

Dermatitis herpetiformis.

Celiac disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Idiopathic pulmonary hemosiderosis: Gross pathology.

A

Heavy, red-brown lung tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Idiopathic pulmonary hemosiderosis: Histology (2).

A

Intraalveolar dense groups of hemosiderin-laden macrophages, or frank hemorrhage.

Loss or hyperplasia of alveolar epithelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Idiopathic pulmonary hemosiderosis: Pertinent negative findings (5).

A

Granulomas.

Vasculitis.

Infarction.

Infection.

Immune complexes or immunoglobulins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Idiopathic pulmonary hemosiderosis: Treatment.

A

Immunosuppression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Goodpasture’s syndrome: Relevance of epidemiology to presentation (2).

A

Young white males: Pulmonary symptoms often precede renal symptoms.

Elderly women: Glomerulonephritis and renal failure precede pulmonary disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Goodpasture’s syndrome: Pulmonary manifestation.

A

Hemoptysis, which may be mild or life-threatening.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Goodpasture’s syndrome: Histology of pulmonary disease (3).

A

Intraalveolar hemorrhage with many hemosiderin-laden macrophages.

Fibrous thickening of alveolar septa.

Hyperplasia of pneumocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Goodpasture’s syndrome: Ancillary tests (2).

A

Immunofluorescence: Linear IgG, IgM, or IgA and complement along the alveolar basement membrane.

Serology: Circulating autoantibodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Goodpasture’s syndrome: Electron microscopy.

A

Fragmented capillary basement membranes.

Widened gaps between endothelial cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Goodpasture’s syndrome: Antibodies (2).

A

Anti-GBM against the non-collagenous domain of the α₃ chain of type IV collagen.

Concurrent c-ANCA or p-ANCA in one third of patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Goodpasture’s syndrome: Associated HLA type.

A

DR2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Pulmonary silicosis: Classification according to timing.

A

Acute: Symptoms within 3 years after exposure.

Accelerated: Within 3-10 years.

Chronic: At least 20 years.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Pulmonary silicosis: Classification according to gross pathology.

A

Simple: Nodules up to 1 cm.

Progressive massive: Nodules >1 cm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

Pulmonary silicosis, acute: Histology (3).

A

Pulmonary edema.

Interstitial inflammation.

PAS-positive granular substance fills alveoli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Pulmonary silicosis, chronic: Histology.

A

Discrete fibrous nodules of variable size, mainly in the upper lobes and subpleural regions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Pulmonary silicosis, chronic: Structure of nodules.

A

Center: Amorphous.

Middle zone: Layers of dense collagen with focal calcification and necrosis.

Periphery: Particle-laden macrophages, lymphocytes, fibroblasts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Microbiological association of pulmonary silicosis:

A. Organism.
B. Histology.

A

A. Mycobacterium tuberculosis (silicotuberculosis).

B. Silicotic nodules with central necrosis and epithelioid granulomas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

Pulmonary silicosis vs. pulmonary alveolar proteinosis.

A

Pulmonary alveolar proteinosis:

− Little inflammation or fibrosis.
− Protein is reactive for antibodies to surfactant apoptotein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Pulmonary alveolar proteinosis: Associations (3).

A

Inorganic dust.

Hematological malignancy.

Immunodeficiency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

Pulmonary alveolar proteinosis: Complication.

A

Secondary infection by

− Fungi.
− Viruses.
− Pneumocystis jiroveci.
− Nocardia.
− Mycobacteria.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Pneumoconiosis: Particles that induce fibrosis (5).

A

Silica.

Coal dust.

Asbestos.

Beryllium.

Talc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Pneumoconiosis: Particles that induce little or no fibrosis (3).

A

Iron oxide.

Tin.

Barium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

Asbestosis:

A. Timing.
B. Clinical presentation (3).

A

A. Symptoms appear 15-20 years after exposure.

B. Dyspnea, clubbing, restrictive lung disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Asbestosis: Location of lesions.

A

Mostly in the lower lobes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

Asbestosis: How the inhaled fibers get to the pleura.

A

Through the lymphatic channels (carried in macrophages) or by direct penetration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

Asbestos: Chemical composition.

A

Hydrated magnesium silicates.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

Asbestosis: Appearance of fibers in tissue (2).

A

Asbestos body: Brown (due to hemosiderin), beaded, two bulbous ends, clear core.

Ferruginous body: No clear core.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

Asbestosis: Histology of tissue reaction (3).

A

Diffuse interstitial fibrosis with chronic inflammation.

Hyperplasia of type 2 pneumocytes.

Alveolar epithelial cells may contain a substance that resembles Mallory’s hyaline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

Asbestosis: Preferred sample for recovery of asbestos bodies.

A

Bronchioloalveolar lavage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

Asbestosis: Related cancers.

A

Mesothelioma.

Lung cancer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

Radiation pneumonitis, acute:

A. Timing.
B. Clinical presentation.

A

A. Symptoms begin between 6 weeks and 6 months after exposure.

B. Cough, dyspnea on exertion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

Radiation pneumonitis: Exacerbating factors (3).

A

Chemotherapy.

Prior irradiation.

Infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Radiation pneumonitis, acute: Histology.

A

Hyaline membranes as in diffuse alveolar damage.

Interstitial proliferation of atypical fibroblasts within young fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

Radiation pneumonitis, fibrotic stage: Histology.

A

Resembles NSIP but with hyperplasia and cytologic atypia of type 2 pneumocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

Radiation pneumonitis: Typical cells (2).

A

Foam cells: Lipid-rich cells with features of macrophages and smooth-muscle cells.

Radiation fibroblasts: Stromal cells with atypical nuclei and much blue cytoplasm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

Radiation pneumonitis: Prognosis (2).

A

Acute pneumonitis usually responds to corticosteroids.

Carcinoma may arise after >10 years.

182
Q

Bleomycin toxicity:

A. Incidence.
B. Mechanism.

A

A. Less than 5%.

B. The lungs are relatively deficient in hydrolase, which detoxifies bleomycin.

183
Q

Bleomycin toxicity: Exacerbating factors (3).

A

Oxygen.

Cyclophosphamide and other drugs.

Radiation.

184
Q

Bleomycin toxicity: Radio-recall phenomenon

A

Bleomycin can unmask damage to lungs caused by previous irradiation.

185
Q

Bleomycin toxicity: Histology.

A

Diffuse alveolar damage.

Atypia of pneumocytes.

Progression to nonuniform fibrosis in some patients.

186
Q

Amiodarone toxicity: Histology.

A

Diffuse alveolar damage.

Hyperplasia of type 2 pneumocytes.

Foamy histiocytes in airspaces.

187
Q

Amiodarone toxicity: Electron microscopy.

A

Lamellar inclusions in alveolar macrophages.

188
Q

Methotrexate toxicity: Histology.

A

Poorly formed granulomas.

Interstitial inflammation that includes eosinophils.

189
Q

Wegener’s granulomatosis: Clinical triad.

A

Disease of upper airways (e.g. sinusitis).

Disease of lower airways.

Glomerulonephritis.

190
Q

Wegener’s granulomatosis: Affected sites (3).

A

Head and neck.

Lungs.

Kidneys.

191
Q

Wegener’s granulomatosis: Autoantibody.

A

c-ANCA in most: Usually against proteinase 3.

192
Q

Wegener’s granulomatosis in the lungs: Distribution of lesions.

A

Mostly in the lower lobes.

193
Q

Wegener’s granulomatosis in the lungs: Gross pathology.

A

Many nodules of variable size.

Cavitation in half of cases.

194
Q

Wegener’s granulomatosis in the lungs: Histology (5).

A

Geographic necrosis.

Granulomatous inflammation.

Palisades of histiocytes.

Microabscesses.

Vasculitis of small vessels.

195
Q

Wegener’s granulomatosis in the lungs: Special stain.

A

Elastic stain: Destruction of elastic lamina.

196
Q

Wegener’s granulomatosis vs. Churg-Strauss syndrome (5).

A

Churg-Strauss syndrome:

− Eosinophilia in blood and tissues is typical.
− Asthma is typical.
− Cardiac disease is common.
− Renal disease is mild.
− Sinus disease is mild.
197
Q

Churg-Strauss syndrome: Clinical tetrad.

A

Asthma.

Rhinitis.

Peripheral eosinophilia.

Systemic vasculitis.

198
Q

Churg-Strauss syndrome: Autoantibody.

A

p-ANCA in some: Usually against myeloperoxidase.

199
Q

Churg-Strauss syndrome in the lungs: Gross pathology (4).

A

Multifocal consolidation.

Eosinophilic pleural effusion.

Stellate peripheral pulmonary arteries.

Cavitation is rare.

200
Q

Churg-Strauss syndrome in the lungs: Histology (4).

A

Eosinophilic pneumonia.

Diffuse hemorrhage.

Vasculitis.

Extravascular granulomas with central necrosis.

201
Q

Churg-Strauss syndrome in the lungs: Pharmacological differential diagnosis.

A

Carbamazepine-induced vasculitis.

202
Q

Churg-Strauss syndrome in the lungs: Microbiological differential diagnoses.

A

Parasitic infection.

Fungal infection.

203
Q

Pulmonary arterial hypertension: Associations with systemic diseases (4).

A

Scleroderma.

Sickle-cell disease.

Rheumatoid arthritis.

Systemic lupus erythematosus.

204
Q

Pulmonary hypertension: Symptoms (5).

A

Dyspnea.

Chest pain.

Syncope.

Cough.

Hemoptysis is rare.

205
Q

Pulmonary hypertension: Leading cause.

A

Left-sided heart failure.

206
Q

Pulmonary hypertension:

A. Definition.
B. Gross pathology.

A

A. Pulmonary systolic pressure >25 mmHg.

B. Pulmonary atherosclerosis.

207
Q

Grading scheme for pulmonary hypertension: Use.

A

Applies only to idiopathic pulmonary hypertension and to certain types of secondary pulmonary hypertension (“APAH”).

208
Q

Grading scheme for pulmonary hypertension: Histology of Grade I (2).

A

Medial hypertrophy of pulmonary arteries.

Extension of muscle into walls of pulmonary arterioles.

209
Q

Grading scheme for pulmonary hypertension: Histology of Grade II.

A

Grade I plus proliferation of intimal cells.

210
Q

Grading scheme for pulmonary hypertension: Histology of Grade III (3).

A

Grade I plus subendothelial fibrosis.

Small arteries and arterioles: Concentric masses of fibrous tissue, reduplication of elastic lamina, occlusion of vascular lumens.

Large arteries: Atherosclerosis.

211
Q

Grading scheme for pulmonary hypertension: Histology of Grade IV (3).

A

Medial hypertrophy is less apparent.

Progressive dilatation of small arteries.

Plexiform lesions.

212
Q

Grading scheme for pulmonary hypertension: Histology of Grade V (2).

A

Plexiform and angiomatoid lesions.

Intraalveolar hemosiderin-laden macrophages.

213
Q

Grading scheme for pulmonary hypertension: Histology of Grade VI (2).

A

Necrotizing arteritis with thrombosis.

Transmural infiltrates of neutrophils and eosinophils.

214
Q

Grading scheme for pulmonary hypertension: Which grades are reversible?

A

Grades I, II, and III.

215
Q

Grading scheme for pulmonary hypertension: Which grades are associated with secondary pulmonary hypertension?

A

Grades I, II, and III.

216
Q

Pulmonary hypertension due to chronic thrombotic or embolic disease: Histology (3).

A

Little or no medial hypertrophy.

Eccentric intimal fibrosis with focal obliteration.

Organizing thrombi with recanalization.

217
Q

Pulmonary hypertension: Mutation.

A

Familial pulmonary arterial hypertension: BMPR4 on 2q33-q34.

218
Q

Pulmonary veno-occlusive disease: Age group.

A

Mostly in children and young adults.

219
Q

Pulmonary veno-occlusive disease: Distribution of lesions.

A

Pulmonary venules and small veins in the lobular septa.

220
Q

Pulmonary veno-occlusive disease: Histology of veins.

A

Occlusion of affected veins by intimal fibrosis.

Medial hypertrophy (“arterialization”) and increase in elastic fibers.

Usually no plexiform lesions or vascular inflammation.

221
Q

Pulmonary veno-occlusive disease: Additional histology.

A

Capillaries may be dilated and tortuous, mimicking pulmonary capillary hemangiomatosis.

Hemosiderin may be abundant, mimicking idiopathic pulmonary hemosiderosis.

222
Q

Pulmonary capillary hemangiomatosis.

A

Proliferation of capillaries causes thickening of alveolar septa.

223
Q

CMV pneumonia: Infected cells (4).

A

Fibroblasts.

Endothelial cells.

Respiratory epithelial cells.

Macrophages.

224
Q

CMV pneumonia: Effect of ganciclovir on histology.

A

Makes the intranuclear inclusions redder and rounder.

225
Q

Herpes simplex virus: Respiratory infections.

A

Necrotizing tracheobronchitis.

Necrotizing bronchiolocentric pneumonia.

Interstitial pneumonitis resembling DAD.

226
Q

Measles virus: Respiratory infections.

A

Necrotizing bronchiolitis.

Giant-cell pneumonia.

227
Q

Parainfluenza virus:

A. Cytopathic effects.
B. Respiratory infection.

A

A. None or multinucleate giant cells.

B. Giant-cell pneumonia (genotypes 2 and 3).

228
Q

Hantavirus:

A. Cytopathic effect.
B. Histology of respiratory infection (2).

A

A. None; virus is identified by IHC or PCR.

B. Marked alveolar edema; immature leukocytes in alveolar capillaries.

229
Q

Legionella pneumonia: Type of inflammation (3).

A

Neutrophilic.

Monocytes and macrophages.

All of the above.

230
Q

Legionella pneumonia: Other histologic features (3).

A

Intraalveolar fibrin and hemorrhage.

Abundant nuclear debris.

Vasculitis occasionally.

231
Q

Legionella pneumonia:

A. Special stain.
B. Other method of detection.

A

A. Silver stain.

B. Urinary antigen test detects serogroup 1 only.

232
Q

Nocardia pneumonia: Main route of infection.

A

Inhalation of bacteria in soil and decaying organic matter.

233
Q

Nocardia pneumonia: Sites of concurrent infection (4).

A

Skin.

Bone.

Kidney.

Brain.

234
Q

Nocardia pneumonia: Histology (3).

A

Necrosis.

Microabscesses.

Immunocompromised: Poorly formed granulomas rather than abscesses.

235
Q

Nocardia pneumonia: Special stains (3).

A

Gram stain.

Fite’s stain.

Silver stain.

236
Q

Ghon lesion of pulmonary tuberculosis:

A. Size.
B. Consistency.
C. Location.

A

A. 1-2 cm.

B. Necrotic center.

C. Lower upper lobe or upper lower lobe, near the pleura.

237
Q

Pulmonary tuberculosis: Ghon complex.

A

Consists of a Ghon lesion and enlarged hilar lymph nodes.

238
Q

Pulmonary tuberculosis: Ranke complex.

A

Fibrosis and calcification of the Ghon complex due to cell-mediated immunity.

239
Q

Pulmonary tuberculosis: Characteristic cell.

A

The Langhans cell: A giant cell with peripherally arranged nuclei, formed by the fusion of the histiocytes that surround the granuloma.

240
Q

Pulmonary tuberculosis: Complications of growth of lesion (4).

A

Cavitation.

Empyema.

Bronchopneumonia.

Embolization.

241
Q

Mycobacterium tuberculosis: Virulence factors (3).

A

Proteins of the cell envelope.

Lipopolysaccharide.

Mycobacterial cell-entry protein (Mcep).

242
Q

Mycobacterium tuberculosis: Proteins of the cell envelope that impart virulence (3).

A

Peptidoglycan.

Arabin-galactan.

Mycolic acids.

243
Q

Mycobacterium tuberculosis:

A. Lipopolysaccharide.
B. Gene for the cell-entry protein.

A

A. Lipoarabinomannan.

B. mce1A.

244
Q

Mycobacterium avium complex: Most likely portal of entry.

A

The gastrointestinal tract.

245
Q

Atypical mycobacterial infections: Histology (3).

A

Necrotizing granulomas.

Non-necrotizing granulomas.

Immunocompromised patients: Poorly organized infiltrates of histiocytes, nonspecific inflammation.

246
Q

Pulmonary disease due to rapidly growing mycobacteria: Leading causes (2).

A

M. abcessus.

M. fortuitum.

247
Q

Hyphae of Aspergillus spp.:

A. Branching.
B. Septa.

A

A. Dichotomous; acute-angle.

B. Frequent.

248
Q

Hyphae of Fusarium spp.:

A. Branching.
B. Septa.

A

A. Right-angle mostly.

B. Frequent.

249
Q

Hyphae of Pseudallescheria boydii.:

A. Branching.
B. Septa.

A

A. Haphazard.

B. Frequent.

250
Q

Hyphae of zygomycetes:

A. Branching.
B. Septa.
C. Differences from other fungal hyphae (2).

A

A. Haphazard; obtuse-angle.

B. Inconspicuous.

C. Wider (up to 25 μm); non-parallel sides.

251
Q

Zygomycosis: Most common genus.

A

Rhizopus.

252
Q

Zygomycosis: Portal of entry.

A

Inhalation of spores.

253
Q

Zygomycosis: Predisposing factors (6).

A

Breach of skin or mucosa.

Iatrogenic immunosuppression.

Neutropenia.

Diabetes mellitus.

Antibiotics, broad-spectrum.

Severe malnutrition.

254
Q

Zygomycosis: Vascular lesions (2).

A

Invasion of vessels.

Granulomatous vasculitis.

255
Q

Growth of zygomycetes in tissue:

A. Facilitating enzyme.
B. Role of iron.

A

A. Ketone reductase permits growth in acidic, glucose-rich environments.

B. Essential for growth; deferroxamine increases susceptibility to zygomycosis.

256
Q

Pulmonary aspergillosis: Patterns of disease (3).

A

Colonization of old cavity lesion (fungus ball).

Hypersensitivity reactions.

Invasion.

257
Q

Pulmonary aspergillosis: Target lesion.

A

Necrotic center surrounded by hemorrhagic rim or infarct.

258
Q

Pulmonary aspergillosis: Classic tissue reaction.

A

Hemorrhagic infarct with sparse inflammation.

259
Q

Bronchocentric granulomatosis: Causes.

A

Infection.

Noninfectious process such as allergy.

260
Q

Bronchocentric granulomatosis: Histology (2).

A

Necrotizing granulomatous inflammation destroys small bronchi and bronchioles.

Palisading histiocytes replace the airway walls.

261
Q

Histoplasmosis: Clinical forms (3).

A

Acute pulmonary histoplasmosis.

Chronic pulmonary histoplasmosis.

Disseminated histoplasmosis.

262
Q

Acute pulmonary histoplasmosis: Clinical presentations (2).

A

Self-limiting illness in a young child with first exposure to H. capsulatum.

Acute, severe illness similar to ARDS, resulting from exposure to a large inoculum of the fungus.

263
Q

Chronic pulmonary histoplasmosis: Clinical presentation.

A

Cavitary lesions in an adult with underlying lung disease.

264
Q

Disseminated histoplasmosis: Risk factors (3).

A

Infancy.

Immunosuppression.

Congenital T-cell deficiency.

265
Q

Histoplasmosis: Histology (3).

A

Necrotizing granulomas with thick fibrous capsule.

Concentric calcification may impart “tree-bark” appearance.

Immunocompromised: Organisms within foamy macrophages.

266
Q

Pulmonary histoplasmosis: Complications (5).

A

Granulomatous mediastinitis: Matting and caseous necrosis of mediastinal lymph nodes.

Mediastinal fibrosis: Young adults; often lethal.

Pericarditis, pleural disease, broncholithiasis.

267
Q

Primary pulmonary coccidioidomycosis: Usual clinical presentation.

A

Asymptomatic or subclinical; self-limited.

268
Q

Pulmonary coccidioidomycosis: Cutaneous manifestations (2).

A

Erythema nodosum.

Erythema multiforme.

269
Q

Blastomycosis: Initial clinical presentation.

A

Flulike illness.

270
Q

Blastomycosis: Histology.

A

Abscesses at first.

Necrotizing granulomas later.

Disseminated infection: “Yeast lakes” with little inflammation.

271
Q

Blastomycosis: Radiography.

A

Can be indistinguishable from primary pulmonary malignancy.

272
Q

Pulmonary cryptococcosis:

A. Usual clinical presentation.
B. Usual radiography.

A

A. Asymptomatic.

B. Inapparent.

273
Q

Pulmonary cryptococcosis:

A. Diagnosis (2).
B. Population at risk for severe disease.

A

A. Culture or cytology of bronchioloalveolar lavage.

B. Immunocompromised.

274
Q

Pulmonary cryptococcosis: Gross pathology.

A

Focal consolidation with gelatinous cut surface.

275
Q

Pulmonary cryptococcosis: Histopathology in the immunocompetent (2).

A

Granulomas with fibrosis.

Organisms within giant cells and macrophages.

276
Q

Pulmonary cryptococcosis: Histopathology in the immunocompromised (3).

A

Organisms may fill alveoli and cause minimal inflammation.

Dense aggregation of fungi may induce a fibrohistiocytic reaction.

Organisms may lack capsules.

277
Q

Pneumocystis jiroveci: Four types of infection.

A

Asymptomatic.

Infantile pneumonia.

Pneumonia in the immunocompromised.

Extrapulmonary infections.

278
Q

Pneumocystis jiroveci: Risk factors for infantile pneumonia (2).

A

Malnutrition.

Prematurity.

279
Q

Pneumocystis jiroveci: Sites of extrapulmonary infection (4).

A

Bone marrow.

Lymph nodes.

Spleen.

Liver.

Others.

280
Q

Pneumocystis jiroveci: Radiography.

A

CT: Bilateral alveolar and interstitial infiltrates radiating from the hilum.

281
Q

Pneumocystis jiroveci: Life cycle.

A

Trophozoites conjugate to form cysts, which contain sporozoites, which develop into trophozoites.

282
Q

Pneumocystis jiroveci: Microscopy of cysts in vivo.

A

Spherical and contain up to 8 sporozoites that measure 1-2 μm.

Empty cysts resemble cups or helmets.

283
Q

Pneumocystis jiroveci: Special stains used in identifying cysts (2).

A

GMS: Best stain; dots within cysts are not sporozoites.

Toluidine blue.

284
Q

Pneumocystis jiroveci: Special stains used in identifying trophozoites and sporozoites (3).

A

Wright, Giemsa, and Wright-Giemsa.

285
Q

Pneumocystis jiroveci: Another stain.

A

Immunofluorescence: Monoclonal antibody against the wall of the cyst.

286
Q

Pneumocystis jiroveci: Targets of PCR (4).

A

Better: Mitochondrial 23S RNA (mtLSUrRNA), internal transcribed spacers.

Others: Cytoplasmic 5S RNA, dihydrofolate reductase regions.

287
Q

Pneumocystis jiroveci: Peak incidence of pneumonia in children with HIV.

A

At 3-6 months after delivery.

288
Q

Lung transplantation: Early complications (5).

A

Acute rejection.

Bacterial infection.

Pulmonary edema.

ARDS.

Diffuse alveolar hemorrhage.

289
Q

Acute cellular rejection: Timing.

A

Usually between 3 and 6 months, but sometimes as early as 1 week or not until years later.

290
Q

Acute cellular rejection:

A. Incidence.
B. Helpful clinical test.

A

A. More than 80%.

B. Forced exploratory volume in 1 second (FEV₁) is the most sensitive clinical test.

291
Q

Criteria of an ideal transbronchial biopsy to be examined for transplant rejection.

A

At least 3-5 fragments.

At least 100 alveoli and 1 bronchiole.

292
Q

Acute rejection of lung transplant: Possibly associated histologic finding.

A

Lymphocytic bronchitis / lymphocytic bronchiolitis.

293
Q

Chronic rejection of lung transplant:

A. Possibly associated histologic finding.
B. Timing of this finding.
C. Recognition of this finding.

A

A. Bronchiolitis obliterans (fibrous obliteration).

B. Usually within a year.

C. Pulmonary-function tests; biopsy not required.

294
Q

Grading of rejection of lung transplants: A0.

A

No infiltrate of leukocytes.

No hemorrhage.

No necrosis.

295
Q

Grading of rejection of lung transplants: A1.

A

Perivascular lymphoid cuff, at least two cell layers thick.

Infiltrate is hard to detect at low power.

296
Q

Grading of rejection of lung transplants: A2.

A

Perivascular lymphoid cuff is at least 3 cell layers thick.

No neutrophils, but eosinophils may be seen.

297
Q

Grading of rejection of lung transplants: A3.

A

Expansion of lymphoid infiltrate into the interstitium.

Neutrophils may be apparent.

Endothelialitis may be seen.

298
Q

Grading of rejection of lung transplants: A4.

A

Diffuse alveolar damage.

299
Q

Grading of rejection of lung transplants: B0.

A

No inflammation of airways.

300
Q

Grading of rejection of lung transplants: B1.

A

Minimal inflammation of the airways.

301
Q

Grading of rejection of lung transplants: B2.

A

Cuff of mononuclear cells, with occasional eosinophils, in the submucosa of bronchi or bronchioles.

302
Q

Grading of rejection of lung transplants: B3.

A

Expansion of the infiltrate into a dense band.

Lymphocytic satellitosis with necrosis of epithelial cells of the airway.

303
Q

Grading of rejection of lung transplants: B4.

A

Severe inflammation with ulceration of the airway epithelium and fibrinopurulent exudate.

304
Q

Alveolar adenoma: Histology.

A

Cystic spaces: Lined by bland type 2 pneumocytes; filled with PAS-positive granular matter.

Stroma: Rich in spindle cells; shows focal myxoid change.

305
Q

Papillary adenoma of the lung: Histology.

A

True papillae lined by cuboidal or columnar cells.

Ciliated or oxyphilic cells may be present.

306
Q

Papillary adenoma of the lung: Which features should be minimal or absent (3)?

A

Intracellular mucin.

Atypia.

Mitotic activity.

307
Q

Mucous-gland adenoma:

A. Clinical presentation.
B. Histology.

A

A. Obstructive symptoms.

B. Bland mucin-producing cells line cysts, glands, microacini, tubules, and papillae.

308
Q

Mucinous cystadenoma:

A. Size.
B. Histology.

A

A. 1-5 cm.

B. Cystic spaces lined by incomplete layer of mucinous cells; giant-cell reaction to extravasated mucin.

309
Q

Bronchogenic squamous dysplasia or squamous-cell carcinoma in situ:

A. Clinical detection.
B. Clinical appearance.

A

A. Facilitated by autofluorescence bronchoscopy.

B. Flat or superficial (75%); nodular or polypoid (25%).

310
Q

Bronchogenic squamous-cell carcinoma in situ: Typical location.

A

Near bifurcations in segmental bronchi.

311
Q

Bronchogenic squamous dysplasia: Grades.

A

Mild, moderate, severe.

312
Q

Bronchogenic severe squamous dysplasia vs. squamous-cell carcinoma in situ.

A

SCC in situ: Extreme atypia involving full thickness of epithelium.

313
Q

Basal-cell hyperplasia of the airways: Definition.

A

Respiratory epithelium with more than three layers of basal cells; otherwise normal.

314
Q

Squamous-cell carcinoma in situ vs. invasive carcinoma in a transbronchial biopsy:

A

SCC in situ:

− Smooth edges of the fragments.
− Flat epithelial surface.
− Smooth basement membrane.

315
Q

Putative order of progression to bronchogenic squamous-cell carcinoma.

A

Basal cell hyperplasia, squamous metaplasia, squamous dysplasia, SCC in situ, invasive SCC.

316
Q

Atypical adenomatous hyperplasia: Situation.

A

Almost always found incidentally in lungs with preexisting adenocarcinoma (invasive or in situ).

317
Q

Atypical adenomatous hyperplasia: Size.

A

Up to 5 mm in diameter.

318
Q

Atypical adenomatous hyperplasia: Histology (3).

A

Atypical pneumocytes line discrete area of thickened alveolar septa.

Gaps between cells.

Essentially no ciliated or mucous cells.

319
Q

Atypical adenomatous hyperplasia: Immunohistochemistry.

A

Demonstrates surfactant protein A (PE10) in up to 25% of cases.

320
Q

Atypical adenomatous hyperplasia vs. adenocarcinoma in situ (2).

A

Adenocarcinoma in situ:

− At least 5 mm (usually >10 mm) in diameter.
− May show central collapse with fibrosis or scar.

321
Q

Atypical adenomatous hyperplasia vs. diffuse interstitial lung disease.

A

Diffuse interstitial lung disease: Accompanying interstitial inflammation.

322
Q

Atypical adenomatous hyperplasia vs. peribronchiolar metaplasia.

A

Peribronchiolar metaplasia consists of ciliated cells.

323
Q

Atypical adenomatous hyperplasia vs. papillary adenoma.

A

Atypical adenomatous hyperplasia has no true papillae.

324
Q

Atypical adenomatous hyperplasia: Mutated genes.

A

KRAS and EGFR.

325
Q

Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia: Histology.

A

Increase in individual cells or in groups of neuroendocrine cells in the bronchial epithelium.

326
Q

Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia: Progression.

A

Breach of basement membrane to form carcinoid tumorlets.

327
Q

Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia: Significance.

A

May be the precursor of low-grade, peripheral carcinoids.

328
Q

Carcinoid tumorlet vs. carcinoid tumor.

A

Carcinoid tumor: More than 5 mm in diameter.

329
Q

Bronchogenic adenocarcinoma in situ: Former name.

A

Bronchioloalveolar carcinoma.

330
Q

Bronchogenic adenocarcinoma in situ: Subtypes.

A

Nonmucinous (more common).

Mucinous.

331
Q

Bronchogenic adenocarcinoma in situ: How to report on a biopsy.

A

As lepidic pattern (could be either adenocarcinoma in situ or invasive adenocarcinoma).

332
Q

Bronchogenic adenocarcinoma in situ: Mutated genes.

A

KRAS and EGFR.

333
Q

Bronchogenic adenocarcinoma: Frequency of metastatic disease at presentation.

A

About 50%.

334
Q

Bronchogenic adenocarcinoma: Important feature of gross pathology.

A

Tumor is usually singular but can be multiple.

335
Q

Minimally invasive adenocarcinoma of the lung:

A. Definition.
B. Histology.

A

A. Tumor is no more than 3 cm in size, with an invasive component of no more than 5 mm.

B. Mucinous or nonmucinous.

336
Q

Bronchogenic adenocarcinoma: Overall importance of growth patterns.

A

Their percentages should be estimated in the report.

337
Q

Bronchogenic adenocarcinoma in situ: Histology.

A

Noninvasive growth of cells along alveolar septa.

No gaps between cells.

Possible slight thickening of septa with desmoplasia.

338
Q

Bronchogenic adenocarcinoma: Acinar pattern.

A

Acini and tubules resembling bronchial glands.

339
Q

Bronchogenic adenocarcinoma: Papillary pattern.

A

True papillae lined by large, atypical cells.

Papillary may form secondary or tertiary branches.

There may be psammoma bodies.

340
Q

Bronchogenic adenocarcinoma: Lepidic pattern.

A

Noninvasive growth along alveolar septa.

Often seen at the edge of an invasive adenocarcinoma.

341
Q

Bronchogenic adenocarcinoma, solid pattern: Criterion for diagnosis.

A

At least 5 mucin droplets per 2 high-power fields.

342
Q

Significance of specific patterns of bronchogenic adenocarcinoma:

A. Solid pattern.
B. Clear-cell pattern.

A

A. More likely to have the EML4−ALK mutation if there is >10% signet-cell change.

B. If extensive, must be distinguished from renal-cell carcinoma.

343
Q

Bronchogenic adenocarcinoma: Other patterns.

A

Micropapillary.

Signet-ring.

344
Q

Fetal adenocarcinoma of the lung: Histology.

A

Resembles fetal lung in the pseudoglandular stage; reminiscent of endometrioid adenocarcinoma.

345
Q

Bronchogenic adenocarcinoma: Helpful immunohistochemical marker.

A

Napsin A is expressed by pulmonary adenocarcinomas but not by other carcinomas except those of the kidney.

346
Q

Invasive mucinous adenocarcinoma of the lung: Immunohistochemistry.

A

Usually negative for TTF-1 and may also lack CK7.

347
Q

Use of BG8 in immunohistochemistry.

A

As a marker of epithelial cells; not expressed by mesothelial cells.

348
Q

Mutations of KRAS in bronchogenic adenocarcinoma:

A. Exons (3).
B. Frequent clinical association.

A

A. 12, 13, 61.

B. Smoking.

349
Q

Mutations of EGFR in bronchogenic adenocarcinoma:

A. Exons.
B. Clinical associations (3).

A

A. 18-21.

B. Female sex; never having smoked; Asian ethnicity.

350
Q

Bronchogenic adenocarcinoma in situ: Diagnostic criteria (5).

A

Three of the following:

− Stratification of cells is marked.
− Coarse chromatin with large nucleoli.
− Height of cells is increased.
− Mitotic figures.
− Overlap of nuclei due to crowding of cells.
351
Q

Bronchogenic adenocarcinoma: Mutated genes (3).

A

KRAS: 30% (most common).

EGFR.

EML4−ALK.

352
Q

Bronchogenic squamous-cell carcinoma: Variants (5).

A

Papillary.

Clear-cell.

Small-cell.

Basaloid.

Non-keratinizing.

353
Q

Bronchogenic squamous-cell carcinoma: Variant associated with a better prognosis.

A

Papillary variant.

354
Q

Bronchogenic squamous-cell carcinoma: Histology of the small-cell variant.

A

Cytoplasm: Moderately abundant; distinct intercellular boundaries.

Nuclei: Irregular; large nucleoli; no molding; no salt-and-pepper chromatin.

355
Q

Bronchogenic squamous-cell carcinoma: Differential diagnosis of the basaloid variant.

A

Adenoid-cystic carcinoma:

− Younger patients.
− Better prognosis.

356
Q

Use of p40 in the immunohistochemistry of lung carcinomas.

A

Positive in SCC, negative in adenocarcinoma.

357
Q

Bronchogenic squamous-cell carcinoma: Most common mutation.

A

Gain of 3q26.

358
Q

Bronchogenic squamous-cell carcinoma: Important molecular prognostic marker.

A

Loss of p16INK4A correlates with shorter survival.

359
Q

Bronchogenic squamous-cell carcinoma: Molecular targets of therapy (4).

A

PIK3CA, SOX2, DDR2, BRF2.

360
Q

Small-cell carcinoma of the lung: Consistent mutation.

A

−3p, which may cause loss of FHIT (fragile histidine triad gene).

361
Q

Small-cell carcinoma of the lung: Less consistently mutated genes (3).

A

Bcl-2.

p53.

Rb.

362
Q

Small-cell carcinoma of the lung: Importance of immunohistochemistry.

A

The diagnosis of small-cell carcinoma is made by light microscopy, even if all neuroendocrine markers are negative (which occurs in <10% of cases).

363
Q

Small-cell carcinoma of the lung: Paraneoplastic syndromes (4).

A

Lambert-Eaton syndrome.

Cerebellar degenerative syndromes.

Cushing’s syndrome.

SIADH.

364
Q

Large-cell carcinoma: Cytology.

A

Nuclei: Large, vesicular; large nucleolus.

Cytoplasm: Moderately abundant; discrete cell borders.

365
Q

Adenocarcinomas of the lung that are usually negative for TTF-1 by immunohistochemistry (3).

A

Mucinous adenocarcinoma.

Squamous-cell carcinoma.

Large-cell carcinoma.

366
Q

Large-cell neuroendocrine carcinoma: Histology.

A

Nuclei: Large nucleolus.

Cytoplasm: Abundant.

Arrangement of cells: Nests, trabeculae, rosettes.

367
Q

Large-cell neuroendocrine carcinoma: Immunohistochemistry (2,2).

A

Positive: Cytokeratin, CEA.

Variable: TTF-1.

Staining for neuroendocrine markers is often patchy and weak.

368
Q

Pulmonary carcinoid tumor: Environmental association.

A

Atypical carcinoid is associated with smoking.

369
Q

Pulmonary carcinoid tumor: Sites.

A

Bronchial (most tumors): May cause obstructive symptoms.

Peripheral: Usually asymptomatic.

370
Q

Pulmonary carcinoid tumor: Stroma.

A

Vascular; may contain metaplastic bone or cartilage.

371
Q

Pulmonary carcinoid tumor: Typical.

A

> 0.5 cm in diameter.

Fewer than 2 mitotic figures per 10 hpf.

No necrosis.

372
Q

Pulmonary carcinoid tumor: Atypical.

A

2-10 mitotic figures per 10 hpf.

  • or -

Focal necrosis.

373
Q

Pulmonary carcinoid tumor: Prognosis (2).

A

Typical: Five-year survival rate is 90%.

Atypical: Five-year survival rate is 50%.

374
Q

Expression of neuroendocrine markers by neuroendocrine tumors.

A

Typical carcinoid: Strong expression.

Atypical carcinoid: Slightly weaker.

Small-cell carcinoma and large-cell neuroendocrine carcinoma: Weakest.

375
Q

Pulmonary carcinoid tumor: Features that are not used to distinguish typical from atypical tumors (2).

A

Nuclear atypia and pleomorphism.

Intensity of staining for neuroendocrine markers.

376
Q

Carcinoid tumors: Positive non-neuroendocrine markers (3).

A

Cytokeratin.

CD99.

S100 (sustentacular cells).

377
Q

Pulmonary hamartoma: Typical location.

A

Peripheral (90%).

378
Q

Pulmonary hamartoma: Radiography.

A

Fat and calcification on high-resolution CT.

379
Q

Pulmonary hamartoma: Histology.

A

Nodules of mature cartilage, fat, smooth muscle, fibromyxoid tissue, and/or bone.

Benign respiratory epithelium lines the clefts that separate the nodules.

380
Q

Pulmonary hamartoma: Associated chromosomal regions (2).

A

12q15 and 6p21: High-mobility-group loci.

381
Q

Pulmonary hamartoma vs. pulmonary chondroma (2).

A

Pulmonary chondroma:

− No clefts between nodules.
− Often multiple.

382
Q

Carney’s triad.

A

Pulmonary chondromas.

Epithelioid gastrointestinal stromal tumor.

Extraadrenal paraganglioma.

383
Q

Pulmonary lipoma: Typical site (2).

A

Within central bronchi.

Left side.

384
Q

Lymphangioleiomyomatosis: Gender (2).

A

Sporadic: Females.

Associated with tuberous sclerosis: Both sexes.

385
Q

Lymphangioleimyomatosis: Clinical behavior.

A

Destructive and metastatic; considered a low-grade tumor.

386
Q

Lymphangioleiomyomatosis: Associated tumors (5).

A

Lymphangioleimyomas of the lungs.

Lymphangioleimyomas of lymph nodes.

Renal angiomyolipomas.

Hamartomas.

Uterine leiomyomas.

387
Q

Lymphangioleimyomatosis: Clinical presentation (5).

A

Progressive dyspnea.

Cough.

Chylous pleural effusion.

Recurrent pneumothorax.

Hemoptysis.

388
Q

Lymphangioleimyomatosis: Gross pathology.

A

Hyperaerated lungs containing many cysts, 0.5-2 cm, that distort the pleural surface.

389
Q

Lymphangioleimyomatosis: Types of lesion (2).

A

Disordered proliferation of smooth-muscle cells near bronchi and vessels.

Air-filled cyst with a wall of disordered smooth muscle.

390
Q

Lymphangioleimyomatosis: Types of cell (2).

A

Small spindle cells that express proliferating-cell nuclear antigen.

Larger, epithelioid cells that express HMB-45.

391
Q

Lymphangioleimyomatosis histology score.

A

LHS-1: Less than 25% of the lung tissue is replaced by cysts and nodules of LAM.

LHS-2: 25% to 50%.

LHS-3: More than 50%.

392
Q

Lymphangioleimyomatosis: Immunohistochemistry (4).

A

Positive: HMB-45, estrogen receptor, bcl-2; D2-40 (often).

393
Q

Lymphangioleimyomatosis: Abnormal gene, its location, and its product.

A

TSC2 on 16p13 encodes tuberin.

394
Q

Lymphangioleimyomatosis: Possible origins of pulmonary lesions.

A

Migration or metastasis of LAM cells from

  • Angiomyolipomas.
  • Lymph nodes.
395
Q

Lymphangioleimyomatosis: Associated tumor of the central nervous system in sporadic cases.

A

Meningioma.

396
Q

Inflammatory myofibroblastic tumor: Viral associations (2).

A

Pulmonary: HHV-8.

Splenic and nodal: EBV.

397
Q

Inflammatory myofibroblastic tumor: Histology (4).

A

Fascicles or whorls of spindle cells.

Inflammatory cells.

Variable stroma.

Tumor cells may invade vessel walls and adjacent structures.

398
Q

Inflammatory myofibroblastic tumor: Cytology (2).

A

Rare cells may have vesicular nuclei and large nucleoli.

Mitotic figures are usually (but not always) few.

399
Q

Inflammatory myofibroblastic tumor: Inflammatory component.

A

Consists of plasma cells, lymphocytes, histiocytes, occasional Touton-type giant cells, granulocytes.

May obscure the spindle cells.

400
Q

Inflammatory myofibroblastic tumor: Immunohistochemistry (3,3,2).

A

Positive: Vimentin, SMA, MSA.

Negative: S-100, CD117, myogenin.

ALK and p80 are positive in 45% of cases, more likely in the larger cells with vesicular nuclei.

401
Q

Inflammatory myofibroblastic tumor vs. inflammatory fibrosarcoma.

A

Inflammatory fibrosarcoma has more nuclear atypia.

402
Q

Inflammatory myofibroblastic tumor: Putative cell of origin.

A

The fibroblastic reticulum cell.

403
Q

Pleuropulmonary blastoma: Location.

A

Arises in parenchyma of lung but involves pleura or mediastinum.

404
Q

Types of pleuropulmonary blastoma: Age groups.

A

Type I: Infants.

Type II: Toddlers.

Type III: Pre-schoolers.

405
Q

Type of pleuropulmonary blastoma: Relevance.

A

Type III has the worst prognosis.

Tumors of type I may progress to type III unless resected.

406
Q

Types of pleuropulmonary blastoma: Gross pathology.

A

Type I: Purely cystic.

Type II: Solid and cystic.

Type III: Solid.

407
Q

Pleuropulmonary blastoma: Cellular components.

A

Small, blue blastemal cells.

Large, spindle-shaped, often rhabdomyoblastic cells.

No epithelial cells.

408
Q

Pleuropulmonary blastoma: Histology (3).

A

Sheets of blastemal cells.

Sarcomatous foci: Malignant cartilage, fat, skeletal muscle, or undifferentiated sarcoma.

Multifocal necrosis.

409
Q

Pleuropulmonary blastoma: Possibly associated gene.

A

DICER1, which encodes an endoribonuclease that generates small non-encoding regulatory RNAs.

410
Q

Pleuropulmonary blastoma vs. metastatic Wilms’ tumor.

A

Wilms’ tumor: Positive for cytokeratin (epithelial component) and WT-1.

411
Q

Adult pulmonary blastoma: Epidemiology.

A

More common in females.

412
Q

Adult pulmonary blastoma: Histology.

A

Biphasic, sarcomatoid carcinoma:

− Epithelium: Resembles pseudoglandular stage of fetal lung development (or endometrioid carcinoma with subnuclear or supranuclear vacuoles).
− Stroma: Blastema with occasional sarcomatous differentiation.

413
Q

Pulmonary MALT lymphoma: Histology (4).

A

Centrocyte-like monomorphic cells form nodules that infiltrate alveolar septa.

Lymphoepithelial lesions involve bronchial epithelium.

Tumor cells may colonize follicles or mantle zones.

Plasma cells and plasmacytoid lymphocytes may be seen.

414
Q

Pulmonary MALT lymphoma: Mutations (4).

A

Trisomy 3.

t(11;18)(q21;q21).

t(14;18)(q32;q21).

t(1;14)(q22;q32).

415
Q

MALT lymphoma: Frequently involved gene.

A

JH region of immunoglobulin heavy chain.

416
Q

Pulmonary MALT lymphoma vs. CLL: Histology.

A

CLL: Infiltrate does not involve the lung parenchyma.

417
Q

Pulmonary Langerhans’-cell histiocytosis:

A. Age group.
B. Association.

A

A. Ages 30-50.

B. Smoking.

418
Q

Pulmonary Langerhans’-cell histiocytosis: Difference from extrapulmonary LCH.

A

Pulmonary LCH is a reactive proliferation.

Extrapulmonary LCH is a neoplasm.

419
Q

Pulmonary Langerhans’-cell histiocytosis: Radiography (2).

A

Early: Many subcentimeter nodules, esp. in the upper and middle lobes.

Later: Nodules are larger and have central lucency due to cavitation or bronchiolar dilatation.

420
Q

Pulmonary Langerhans’-cell histiocytosis: Histology (4).

A

Stellate or Medusa-head nodules centered on bronchioles.

Nodules consist of Langerhans’ cells (grooved nuclei), eosinophils, lymphocytes, plasma cells.

Nodules may invade vessels.

Progression from cellular nodules to fibrotic scars.

421
Q

Pulmonary Langerhans’-cell histiocytosis: Associated histologic finding.

A

Respiratory bronchiolitis.

422
Q

Pulmonary Langerhans’-cell histiocytosis: Expressed cytokines (2).

A

TGF-β₁.

GM-CSF.

423
Q

Langerhans’ cells: Immunohistochemistry.

A

Positive: S-100, CD1a, Langerin.

Negative: CD68.

424
Q

Reactive eosinophilic pleuritis:

A. Cause.
B. Histology.

A

A. Pneumothorax.

B. Eosinophils mixed with proliferating mesothelial cells and mononuclear cells.

425
Q

Post-transplantation lymphoproliferative disorder: Definition.

A

Abnormal lymphocytic proliferation (benign or malignant) occurring during immunosuppression and often involving the transplanted organ.

426
Q

Post-transplantation lymphoproliferative disorder: Origin of proliferating cells.

A

Bone marrow: The donor.

Solid organs: The recipient.

427
Q

Post-transplantation lymphoproliferative disorder: Timing.

A

Occurs 1 month to 4 years after the transplantation.

428
Q

Post-transplantation lymphoproliferative disorder: Viral association.

A

EBV.

429
Q

Post-transplantation lymphoproliferative disorder in the lung: Types.

A

Plasmacytic hyperplasia.

Polymorphic lymphoproliferative disorder.

Malignant lymphoma or multiple myeloma.

430
Q

PTLD of the lung: Association of type with age.

A

Plasmacytic hyperplasia is the most common type in children and young adults.

431
Q

PTLD of the lung: Histology of plasmacytic hyperplasia.

A

Proliferation of small polyclonal T and B lymphocytes, plasma cells, occasional immunoblasts.

Preserved pulmonary architecture.

432
Q

PTLD of the lung: Histology of polymorphic lymphoproliferative disorder.

A

Clonal lymphocytes, plasmacytoid cells; immunoblasts that may resemble Reed-Sternberg cells.

Distorted pulmonary architecture.

433
Q

PTLD of the lung: Most common type of lymphoma.

A

Diffuse large B-cell lymphoma.

434
Q

Post-transplantation lymphoproliferative disorder: Treatment.

A

Reduction in immunosuppression during the first year after transplantation.

435
Q

Malignant mesothelioma: Prognosis (2).

A

Death in <1 year; a few months later for epithelioid mesothelioma.

436
Q

Malignant mesothelioma: Relation to smoking.

A

Smoking does not increase the risk of mesothelioma.

Smoking + asbestos = greatly increased risk for lung carcinoma.

437
Q

Malignant mesothelioma: Variants.

A

Epithelioid.

Sarcomatoid.

Biphasic.

438
Q

Epithelioid mesothelioma: Cytology.

A

Bland, homogeneous.

Nuclei: Round, vesicular; large nucleolus.

439
Q

Epithelioid mesothelioma: Histology.

A

Grows in tubules, papillae, glands or acini, solid sheets, or a combination of patterns.

440
Q

Desmoplastic mesothelioma:

A. Definition.
B. Frequency.

A

A. A collagenous subtype of sarcomatoid mesothelioma.

B. Makes up about 10% of malignant mesothelioma.

441
Q

Biphasic mesothelioma: Criterion.

A

The tumor must be at least 10% epithelioid and at least 10% sarcomatoid.

442
Q

Malignant mesothelioma: Most common variant.

A

Epithelioid.

443
Q

Malignant mesothelioma: “Specific” markers (4).

A

Calretinin.

CK5/6.

WT-1.

D2-40.

444
Q

Malignant mesothelioma: Nonspecific markers (2).

A

Pancytokeratin.

CK7.

445
Q

Malignant mesothelioma: Mutation.

A

Homozygous deletion of CDKN2A/ARF at 9p21.

446
Q

Malignant mesothelioma: Best immunohistochemical marker and its interpretation.

A

Calretinin:

  • Stains cytoplasm of all mesothelial cells.
  • Stains nuclei of malignant mesothelioma.
447
Q

Malignant mesothelioma vs. reactive mesothelial hyperplasia: Histology.

A

Reactive mesothelial hyperplasia does not invade the parietal pleural fat.

448
Q

Malignant mesothelioma vs. reactive mesothelial hyperplasia: Immunohistochemistry (4).

A

Reactive mesothelial hyperplasia: Cytoplasmic desmin.

Malignant mesothelioma: Linear EMA, strong p53, GLUT1.

449
Q

Desmoplastic mesothelioma vs. chronic fibrosing pleuritis.

A

Chronic fibrosing pleuritis: Combinations of cytokeratins demonstrate orderly growth and absence of invasion of pleural fat.

450
Q

Solitary fibrous tumor of the pleura: Histology (3).

A

Uniform spindle cells in a collagenous stroma.

Alternating hypocellular and hypercellular areas.

Hemangiopericytoma-like vascular pattern.

451
Q

Solitary fibrous tumor of the pleura: Immunohistochemistry.

A

Positive: CD34, CD99, bcl-2.

Negative: Cytokeratins (usually).

452
Q

Congenital pulmonary-airway malformation: Definition.

A

Malformation of part of the lung parenchyma, with abnormal direct connections to the normal tracheobronchial tree.

AP reviewer (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions