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MHD 1 > L73-76 Pulmonary Pathology I-IV > Flashcards

L73-76 Pulmonary Pathology I-IV Flashcards

1
Q

Describe the lining of the trachea.

A
  1. Cartilage
  2. Mucosa (epithelium and submucosal glands)
  3. Transverse muscle bundles
  4. Longitudinal muscle bundles
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2
Q

How do the trachea and bronchi differ?

A

Bronchial cartilage is discontinuous vs. Tracheal cartilage is continuous

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3
Q

Describe the primary bronchial epithelium.

A

Pseudostratified ciliated columnar epithelium with some goblet cells (More ciliated than goblet normally)

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4
Q

How do the tertiary bronchi and bronchioles differ?

A

Tertiary bronchi have cartilage and submucosal glands vs. Bronchioles lack cartilage and submucosal glands

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5
Q

What types of cells line the bronchioles?

A

Ciliated and non-ciliated (clara) cells

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6
Q

What are the types of cells in the alveoli?

A
  1. Type I (squamous pneumocytes): gas exchange
  2. Type II (granular pneumocytes): secrete surfactant
  3. Alveolar macrophages
  4. Endothelial cells (line blood vessels)
  5. Fibroblasts (structural support)
  6. Rare lymphocytes and mast cells
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7
Q

The lungs develop from the ___.

A

Foregut

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8
Q

What are the 4 common congenital lung abnormalities?

A
  1. Agenesis
  2. Hypoplasia
  3. Atresia and tracheoesophageal fistula
  4. Congenital Cystic Adenomatoid Malformation (CCAM/CPAM)
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9
Q

Acute lung injury is a spectrum of bilateral pulmonary damage (epithelial and endothelial) which manifests as what three things?

A
  1. Acute onset dyspnea (may also be tachypnic)
  2. Hypoxemia (may lead to cyanosis)
  3. Development of bilateral pulmonary infiltrates in the absence of cardiac failure
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10
Q

What are clinical causes of ALI?

A

A: Aspiration, acute pancreatitis, air/amniotic fluid embolism
R: Radiation
D: Drug overdose, DIC< drowning
S: Shock, sepsis, smoke inhalation

Also: pneumonia, trauma, fat embolism, inhalation injury, reperfusion injury, uremia

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11
Q

If ALI is severe, it can progress to ___.

A

ARDS (Acute Respiratory Distress Syndrome)

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12
Q

Describe the pathogenesis of ALI.

A

Injury occurs. Macrophages secrete IL-1, IL-8, TNF, leading to neutrophil margination, sequestration, and migration into the alveolus. Local tissue damage occurs, edema enters the alveoli, surfactant is inactivated, and hyaline membrane forms.

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13
Q

How is ARDS treated?

A

Supportive care, treat underlying condition

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14
Q

What are the phases of ARDS?

A
  1. Early exudative phase (acute)
  2. Subacute proliferative phase (organizing)
  3. Fibrotic phase (late)
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15
Q

What is the primary histological finding in ARDS?

A

Diffuse alveolar damage

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16
Q

What are some causes of respiratory distress syndrome in newborns?

A
  1. Fetal injury during delivery
  2. Aspiration
  3. Cord compression
  4. Excessive sedation of the mother
  5. Hyaline membrane disease/RDS (most common)
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17
Q

What is the fundamental abnormality in respiratory distress syndrome?

A

Insufficient pulmonary surfactant production by immature lungs, resulting in failure of lungs to inflate after birth

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18
Q

Surfactant, synthesized in ___ cells, can be secreted as early as ___ weeks, but is not produced in sufficient amounts until ___ weeks.

A

Type II pneumocytes; 20; 34

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19
Q

Discuss how prematurity leads to hyaline membrane formation.

A
  1. Reduced surfactant synthesis, storage, and release
  2. Increased alveolar surface tension
  3. Atelectasis
  4. Uneven perfusion and hypoventilation
  5. Hypoxemia and CO2 retention
  6. Acidosis
  7. Pulmonary vasoconstriction
  8. Pulmonary hypoperfusion
  9. Endothelial and epithelial damage
  10. Plasma leak into alveoli
  11. Hyaline membrane formation
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20
Q

What modulates surfactant synthesis?

A
  1. Glucocorticoids (increase production)
  2. Insulin (decrease production)
  3. Labor (induces production)
  4. Prolactin
  5. Thyroxine
  6. TGF-beta
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21
Q

What is atelectasis?

A

Complete or partial collapse of a lung or lobe of a lung

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22
Q

What are the three types of acquired atelectasis and where does the mediastinum shift?

A
  1. Resorption/obstruction - shifts toward affect lung
  2. Compression - shifts away from affect lung
  3. Contraction
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23
Q

What can cause resorption/obstruction atelectasis?

A

Excessive secretions (asthma, COPD, bronchiectasis)

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24
Q

What can cause compression atelectasis?

A

Effusions, tumors, CHF

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25
Q

What can cause contraction atelectasis?

A

Fibrosis

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26
Q

What is pneumothorax?

A

Air or gas in the pleural cavity that causes compression and atelectasis

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27
Q

Broadly, what is the problem in obstructive vs. restrictive lung diseases?

A

Obstructive: increased resistance to airflow due to obstruction at any level

Restrictive: reduced expansion of lung parenchyma with decrease in total lung capacity

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28
Q

What are the major pathologic features of asthma?

A
  1. Chronic bronchial inflammation with eosinophils
  2. Bronchial smooth muscle hyperreactivity
  3. Increased mucus production
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29
Q

What are the symptoms of asthma?

A

Wheezing, breathlessness, chest tightness, cough

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30
Q

What is atopic asthma?

A

Immune-mediated, type I hypersensitivity reaction

Begins in childhood, triggered by environmental allergens

Family history of asthma, atopy

Positive skin and serum tests

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31
Q

What is non-atopic asthma?

A

Non-immune triggering mechanisms

Negative skin and serum tests

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32
Q

When should we suspect drug-induced asthma?

A

Patients with recurrent rhinitis and nasal polyps (particularly aspirin)

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33
Q

Describe the pathogenesis of asthma.

A

APC presents antigen to Th2 cells. These produce IL-3, IL-5, GM-CSF, which recruit eosinophils. These degranulate and lead to increased mucus production and smooth muscle hyperactivity.

IgE also binds to mast cells, creating memory.

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34
Q

Which chromosome has several susceptibility genes for asthma? What are the genes?

A

5q: IL-13 CD-14

Also 20q: ADAM 33

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35
Q

What is status asthmaticus?

A

Prolonged bout of asthma lasting for days, responding poorly to treatment

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36
Q

What can be seen on microscopy in asthma?

A

Curschmann spirals

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37
Q

What can be seen on histology in asthma?

A

Eosinophils

Charcot Leydon Crystals (degranulated eosinophils)

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38
Q

What are the 2 types of COPD? Compare them briefly.

A

Chronic bronchitis: tends to affect larger airways, results in mucus hypersecretion and inflammation

Emphysema: tends to affect lower airways, lose elastic recoil due to destruction of septa

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39
Q

What is the clinical definition of chronic bronchitis?

A

Persistent productive cough for at least three consecutive months in at least two consecutive years

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40
Q

What is at risk for chronic bronchitis?

A
  1. Smokers
  2. Urban dwellers
  3. Middle aged men
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41
Q

What are the 4 types of emphysema?

A
  1. Centriacinar (centrilobular)
  2. Panacinar (panlobular)
  3. Distal acinar (paraseptal)
  4. Irregular
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42
Q

Centriacinar emphysema:

  1. Location
  2. Population
  3. Associations
A
  1. Respiratory bronchioles, upper lobes
  2. Male smokers
  3. Chronic bronchitis, coal-workers pneumoconiosis
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43
Q

Panacinar emphysema:

  1. Location
  2. Associations
A
  1. Lower lobes

2. Alpha-1-anti-trypsin deficiency

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44
Q

Distal acinar emphysema:

  1. Location
  2. Can lead to ___ in young adults
A
  1. Along pleura and lobular septa, adjacent to areas of fibrosis, scarring, atelectasis
  2. Spontaneous PT
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45
Q

Discuss the pathogenesis of emphysema.

A

Tobacco generates ROS. These inactivate antiproteases (functional alpha-1-AT deficiency). Neutrophils produce elastase that cannot be broken down. This causes tissue damage.

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46
Q

Discuss the gross lung appearance in emphysema.

A

Hyperinflated lungs with formation of bullae

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47
Q

Discuss the histologic appearance in emphysema.

A

Destruction of septal walls, loss of elastic recoil, destruction of vascular bed, cystically dilated spaces

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48
Q

Alpha-1-AT is encoded by codominantly expressed genes on chromosome ___.

A

14

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49
Q

Compare the age of bronchitis vs. emphysema.

A

40-45 vs. 50-75

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50
Q

Compare the dyspnea of bronchitis vs. emphysema.

A

Mild/late vs. Severe/early

51
Q

Compare the cough of bronchitis vs. emphysema.

A

Early/copious sputum vs. Late/scanty sputum

52
Q

Compare the frequency of infections of bronchitis vs. emphysema.

A

Common vs. Occasional

53
Q

Compare the airway resistance of bronchitis vs. emphysema.

A

Increased vs. Normal/slightly increased

54
Q

Compare the elastic recoil of bronchitis vs. emphysema.

A

Normal v. Low

55
Q

Compare the CXR of bronchitis vs. emphysema.

A

Prominent vessels/large heart vs. Hyperinflation/small heart

56
Q

Compare the appearance of bronchitis vs. emphysema.

A

Blue bloater (R heart failure, water weight gain) vs. Pink puffy (skinny, lanky)

57
Q

What is bronchiectasis?

A

Permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue caused by chronic necrotizing inflammation

58
Q

What are causes/predisoposing conditions of bronchiectasis?

A
  1. Obstruction
  2. Infection (TB, aspergillus)
  3. Congenital/Hereditary (CF, Kartagener’s, immunodeficiency)
  4. Other (RA, Lupus, Graft vs. Host disease)
59
Q

What are the 4 parts of Kartagener syndrome?

A
  1. Sinusitis
  2. Bronchiectasis
  3. Situs inversus
  4. Infertility
60
Q

What causes Kartagener syndrome?

A

Primary ciliary dyskinesia caused by absence/shortening of dynein arms

61
Q

What are the symptoms of restrictive/infiltrative lung disease?

A
  1. Dyspnea
  2. End inspiratory crackles
  3. Hypoxia
62
Q

What are the CXR findings of restrictive/infiltrative lung disease?

A
  1. Nodules
  2. Irregular lines
  3. Ground glass shadows
63
Q

What is the primary gross end stage pathology of restrictive/infiltrative lung disease?

A

Honeycomb lung

64
Q

What is the common pathogenesis of infiltrative lung disease?

A

Inflammation and fibrosis of the interstitium

65
Q

Sarcoidosis predominates in the ___ lobes of the lung.

A

Upper

66
Q

What CXR abnormalities are seen in 90% of patients with sarcoidosis?

A

Bilateral hilar lymphadenopathy

67
Q

What is seen on histology in sarcoidosis?

A
  1. Non-caseating granulomas (rim of lymphocytes, found along lymphatic routes)
  2. Multi-nucleated giant cells with cytoplasmic inclusions (Schaumann bodies, asteroid bodies)
68
Q

Sarcoid granulomas may include this cell, seen on histology.

A

Epithelioid histiocytes (flip flop cell)

69
Q

What are some lab abnormalities seen in sarcoidosis?

A
  1. Elevated serum ACE
  2. Hypercalcemia
  3. Systemic immune abnormality markers
70
Q

Why is hypercalcemia seen in sarcoidosis?

A

Granulomas promote conversion of 25-OH Vitamin D to 1,25-OH Vitamin D, which promotes absorption of calcium from the gut

71
Q

What is the histologic pattern seen in idiopathic pulmonary fibrosis (IPF)?

A

Usual interstitial pneumonia

72
Q

Describe the pathogenesis of idiopathic pulmonary fibrosis.

A
  1. Repeated cycles of epithelial activation/injury
  2. Abnormal epithelial repair
  3. Fibroblastic proliferation
73
Q

Describe the gross morphology of IPF.

A
  1. Cobblestoning - pleural surface scarring
  2. Firm, rubbery, white surface - fibrosis
  3. Honeycombing (peripheral cysts)
74
Q

What are the symptoms of IPF?

A
  1. Dyspnea on exertion
  2. Dry cough
  3. Velcro crackles
75
Q

What is a miscellaneous group of disorders characterized by the accumulation of dust in the lungs and the tissue reaction to its presence?

A

Pneumoconioses

76
Q

What happens in anthracosis?

A

Smokers, urban dwellers, coal miners, etc. inhale carbon pigment, which is engulfed by macrophages

77
Q

What is the difference between simple coal workers pneumoconiosis and progressive massive fibrosis?

A

In simple coal workers pneumoconiosis, accumulations of dust-laden macrophages lead to fibrosis. In progressive massive fibrosis, coal nodules coalesce, leading to fibrotic bulky black tissue masses - “black lung”

78
Q

What is Caplan Syndrome?

A

Rheumatoid pneumoconiosis - form of coal worker pneumoconiosis associated with RA; cavitating nodules on radiology

79
Q

In addition to fibrosis, what can asbestos cause?

A

Pleural effusions, pleural plaques, bronchgenic carcinoma, malignant mesothelioma, and laryngeal carcinoma

80
Q

What is seen on histology in asbestosis?

A

Ferruginous bodies

81
Q

Discuss the risks associated with asbestos exposure, lung cancer, malignant mesothelioma, and smoking.

A

Lung cancer: 5x increase risk for asbestos workers, 55x for those who also smoke
Malignant mesothelioma: 1000x increase for asbestos workers, no additional increase for those who also smoke

82
Q

What is the most prevalent chronic world occupational disease?

A

Silicosis

83
Q

What is seen on histology in silicosis?

A
  1. Nodules with concentric hyalinzed collagen and a whorled appearance
  2. Coalesced nodules
  3. Progressive massive fibrosis
  4. Fibrotic lesions in hilar lymph nodes, pleura
84
Q

What happens to the lymph nodes in silicosis?

A

Eggshell calcification

85
Q

Those who have silicosis are at increased risk for ___. Why?

A

TB - silica depresses cell-mediated immunity

86
Q

What is the most common benign lung tumor and what is it?

A

Hamartoma; benign neoplasm with various disorganized mesenchymal tissues; contains clefts and cartilage

87
Q

What are the dominant oncogenes involved in lung cancer?

A

C-MYC, KRAS, EGFR, c-Met, C-KIT

88
Q

What are the tumor suppressor genes involved in lung cancer?

A

p53, RB1, p16, other genes on chromosome 3

89
Q

Smokers tend to develop what kind of lung cancers and where?

A

Small cell and squamous cell carcinomas; central airway compartments (airway conducting system, proximal bronchus)

90
Q

Non-smokers tend to develop what kind of lung cancers and where? What genes are involved?

A

Adenocarcinoma; terminal respiratory units (gas exchange system, distal parenchyma)

91
Q

What gene is implicated in the development of adenocarcinoma in smokers? In non-smokers?

A

Smokers: KRAS

Non-smokers: EGFR

92
Q

What are the 4 common complaints involved with lung cancer?

A
  1. Cough
  2. Weight loss
  3. Chest pain
  4. Dyspnea
93
Q

What are other clinical features of lung cancer?

A
  1. Pneumonia, abscess
  2. Pleural effusion
  3. Pericardial tamponade
  4. Hoarseness (recurrent laryngeal nerve)
  5. Dysphagea
  6. Diaphragm paralysis (phrenic nerve)
  7. Rib destruction
94
Q

What is SVC syndrome?

A

Facial swelling, cyanosis, dilation of veins in head and neck when SVC is involved in lung cancer

95
Q

What are pancoast tumors?

A

Apical tumors

96
Q

What can pancoast tumors cause?

A
  1. Destruction of 1st/2nd rib

2. Horner syndrome

97
Q

What are the symptom of Horner syndrome?

A 
Ptosis
Anhidrosis
Miosis
Enopthalmos
Loss of ciliospinal reflex
98
Q

What are 3 common paraneoplastic syndromes?

A
  1. SIADH
  2. Cushings
  3. Calcitonin
99
Q

What are some other systemic manifestations of lung cancer?

A
  1. Eaton-Lambert
  2. Sensory neuropathy
  3. Acanthosis nigricans
  4. Clubbing
100
Q

What happens in Eaton-Lambert?

A

Muscle weakness due to autoantibodies against calcium channels

101
Q

What cancer is Eaton-Lambert most commonly associated with?

A

Small cell carcinoma

102
Q

What are the 2 types of lung carcinoma?

A
  1. Small cell carcinoma (20%)

2. Non-small cell carcinoma (80%)

103
Q

What are the 3 types of non-small cell carcinoma?

A
  1. Squamous cell carcinoma (25-30%)
  2. Adenocarcinoma (30-40%)
  3. Large cell carcinoma (10-15%)
104
Q

Squamous cell carcinoma is more common in ___ (men v. women) and is associated with ___. It tends to arise ___ (centrally vs. peripherally).

A

Men; smoking; centrally

105
Q

What are some histologic features of squamous cell carcinoma?

A

Intercellular bridges and keratinization

106
Q

Squamous cell carcinoma has a high frequency of ___ mutations.

A

p53 (rarely EGFR and KRAS)

107
Q

Adenocarcinoma is more common in ___ (men v. women) and is less associated with smoking. It tends to arise ___ (centrally vs. peripherally).

A

Women; peripherally

108
Q

Describe the gross mass in adenocarcinoma.

A

Spiculated mass and central scarring

109
Q

What are the three precursor lesions in adenocarcinoma?

A
  1. Atypical Adenomatous Hyperplasia (AAH)
  2. Adenocarcinoma in situ (AIS)
  3. Minimally invasive adenocarcinoma
110
Q

Describe the AAH lesions.

A
  1. Well-demarcated focus
  2. <5 mm
  3. Lined by cuboidal to low columnar epithelium
111
Q

Describe the AIS lesions.

A
  1. 3cm or less
  2. Grow along pre-existing structures
  3. Preservation of alveolar architecture
  4. No invasion
112
Q

Describe the MIA lesions.

A
  1. 3cm or less AND
  2. Invasive focus <5 mm
  3. No invasion into pleura, lymphatics, or blood vessels
113
Q

Adenocarcinomas are often ___ positive and 80% contain ___.

A

TTF-1; mucin

114
Q

What happens in the EGFR mutations?

A

Mutations occur in the kinase receptor of the tyrosine kinase domain resulting in constitutive activation

115
Q

What is the targeted therapy available for EGFR mutations?

A

Erlotinib

116
Q

What is the targeted therapy available for ALK mutations/gene fusions?

A

Crizotinib

117
Q

What is the targeted therapy available for KRAS mutations?

A

No specific targeted therapy

118
Q

Describe small cell carcinoma on histology.

A

Oat cells, densely packed small blue tumor, scant cytoplasm, finely dispersed chromatin, high mitotic activity, necrosis

119
Q

What 2 genes are inactivated in 100% of cases of small cell carcinoma?

A

p53 and RB

120
Q

Where does mesothelioma originate from?

A

Pleura (mesothelial cells)

121
Q

Which tumor suppressor genes are involved in mesothelioma?

A

p16/CDKN2A

NF2

122
Q

What are the 2 histologic types of mesothelioma?

A
  1. Epithelioid

2. Sarcomatoid

123
Q

What is seen on EM in mesothelioma?

A

Microvilli

MHD 1 (58 decks)

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