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Pathology > Tumours of the Lung > Flashcards

Tumours of the Lung Flashcards

1
Q

Lung cancer’s ranking in terms of commonly diagnosed cancers?

A

Most frequently diagnosed cancer in the world

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2
Q

Lung tumors etiology?

A

Carcinogenic in nature

172,000 in US, vs 18,000 in 1950s

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3
Q

What is the age of diagnosis of lung cancer?

A

40-70 years of age

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4
Q

Survival rate of lung cancer?

A

41%= 1 year survival

15% after 5 years (regardless of stage)

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5
Q

What are common carcinogens involved in lung cancer?

A
  1. Tobacco: 87% relationship, women, higher incidence with higher pack years.
  2. Industrial hazards: radiation, asbestos, etc.
  3. Air pollution
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6
Q

What are precursor lesions involved in lung cancer?

A
  1. Squamous dysplasia and carcinoma in-situ.
  2. Atypical adenomatous hyperplasia.
  3. Diffuse neuroendocrine cell hyperplasia.
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7
Q

Histological classifications of lung tumours

A
  1. Squamous cell carcinoma (SCC): 25%-40%
  2. Small cell (oat cell) carcinoma: 20-25%
  3. Adenocarcinoma: 25-40%
  4. Large cell carcinoma (large cell neuroendocrine: 10-15%
    - Adenosquamous
    - Carcinoid (typical and atypical)
    - Salivary gland-type (carcinomas)
    - Pleomorphic/sarcomatoid/sarcomatous
    - Unclassified
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8
Q

Most common lung tumour locations:

A
  1. Hilum: 1st-3rd order bronchi

2. Alveoli/terminal - adenocarcinomas (bronchiolaveolar type)

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9
Q

What is the progression of lung cancer in bronchial mucosa?

A

Goes from a dysplastic lesion to a small, wart-like nodule of bronchial mucosa.

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10
Q

What is the progression in terms of the bronchial lumen?

A

Fungate into bronchial lumen (aka Intraluminal mass)

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11
Q

What is the progression of lung tumours in terms of the tissue?

A

Penetrates bronchial wall and extend into peribronchial tissue.
*Carina and mediastinum

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12
Q

Shape of intraparenchymal mass in lung tumour progression?

A

Creeps along to form a cauliflower-like intraparenchymal mass

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13
Q

Characteristics of small cell cancer (SCC)

A
  1. Men
  2. Smoking history >98%
  3. Central location (smokers): segmental and subsegmental bronchi
    **peripheral incidence is increasing
    (Slide 9 for photo)
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14
Q

What role does P53 play in the genetics of SCC?

A
  1. NO bearing on prognosis
  2. Early alterations (overexpression and mutations, less common)
  3. Increases throughout precursor development.
    * 10-50% dysplasias
    * 60-90% high grade dysplasia
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15
Q

RB in SCC?

A

Tumour suppressor gene

15%

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16
Q

P16 in SCC?

A

CDK-inhibitor

It’s inactivated 65% of the time

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17
Q

Allelic losses in SCC?

A

Tumor suppressor genes lost
Precede dysplasia ***
3p, 9p, 17p

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18
Q

EGFR role in SCC?

A

Overexpressed 80% of the time
RARELY mutated
*Epidermal growth factor

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19
Q

Her-2/neu role in SCC?

A

30%
Without gene amplification (breast)
*Human epidermal growth factor 2, oncogene

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20
Q

What happens in adenocarcinoma?

A

Glandular differentiation/mucin

foto slide 12

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21
Q

Growth patterns of adenocarcinoma?

A
  1. Pure or mixed
  2. Acinar
  3. Papillary
  4. Bronchioalveolar**
  5. Solid with mucin
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22
Q

What is the etiology of adenocarcinoma?

A
  1. Most common tumor in women and non-smokers (75%)
  2. Peripheral location: smaller
  3. 80% with mucin
  4. Slow growing
  5. Metastasize early and widely***
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23
Q

KRAS’ role in Adenocarcinoma (ACa) genetics?

A

5% in non-smokers
30% smokers
*RAS subfamily, control of growth factors, mutated in cancers

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24
Q

Other genetic markers found in ACa?

A

P53
RB
P16

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25
Q

Characteristics of bronchioalveolar cancer?

A

Found in bronchioalveolar regions

1-9% lung tumours

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26
Q

General location of bronchioalveolar cancer (BAC)? (photo slide 15)

A

Peripherally located
Can be single or
Multiple nodules (MC): coalesce–>pneumonia-like (slide

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27
Q

Morphology of BAC?

A

Solid, grey-white with translucent secretions

Rarely: atelectasis/emphysema

28
Q

Where does BAC arise?

A

From atypical, adenomatous hyperplasia (monoclonal)*

29
Q

Kind of spread of BAC?

A

Lepidic (along alveolar/BA walls); scaly
Like butterflies on a fence
Non-destructive (doesn’t invade underlying architecture).

30
Q

Cells affected by BAC?

A

Bronchiolar cells
Clara cells (protect lining, secrete GAGs)
Type II pneumo’s

31
Q

What is mucinous BAC like?

A

Tall columnar cells filled with mucin.

Aerogenous spread with: satellite tumors, coalesce.

32
Q

What is non-mucinous BAC like?

A

Columnar/peg-shaped/cuboidal cells.
Grow along alveolar septae
Rare aerogenous spread: resectable*

33
Q

Small cell carcinoma epidemiology ?

A

1% non-smokers
No pre-invasive phase*
**Most aggressive, earliest to metastasize, and no surgical option
15-25% cure with chemo and radiation

34
Q

SCC location ?

A

Major bronchi and peripheral

35
Q

SCC histologic characteristics? (photo A slide 19)

A

Highly malignant

  1. Clustered growth
  2. Scant cytoplasm imparting blue cells appearance
  3. Ill-defined cell borders
  4. Granular (salt and pepper)
  5. Absent nucleoli
  6. Neurosecretory granules
36
Q

Histologic characteristics of SCC (slide 20, b)

A
  1. Round, oval, or spindle-shaped cells
  2. Nuclear molding
  3. Apoptosis
  4. Smaller than resting lymphocytes
  5. Necrosis
37
Q

SCC genetics?

A

P53: mutated 50-8-%
RB: mutated 80-100%
BCL2 by IHC in 90%

38
Q

Large cell carcinoma characteristics (slide 22)?

A 
Undifferentiated
Lacks squamoid, glandular, or SCC features
Large nuclei
Nucleoli
Moderate cytoplasm
39
Q

Secondary pathology of tumours of the lung

A
  1. Partial obstruction: focal emphysema
  2. Total obstruction: atelectasis
  3. Suppurative/ulcerative bronchitis
  4. SVC compression
  5. Pericarditis
  6. Pleuritis
40
Q

Lung tumours: paraneoplastic syndromes

A
  1. ADH: SCC
  2. ACTH: SCC
  3. PTH, PTH-related peptide, prostaglandin E, cytokines
  4. Calcitonin (hypocalcemia)
  5. Gonadotropins (gynecomastia)
  6. Serotonin and bradykinin (carcinoid)
41
Q

Pleural effusions are seen in what?

A

Primary or secondary disease

42
Q

Normal pleural effusions:

A

15 cc serous lubricating fluid

Acellular and clear

43
Q

Pleural effusions with increased hydrostatic pressure?

A

CHF

44
Q

Pleural effusions with increased vascular permeability?

A

Pneumonia

45
Q

Pleural effusions with decreased osmotic pressure?

A

Nephrotic syndrome

46
Q

Pleural effusions with increased negative pressure (intrapleural)?

A

Atelactasis

47
Q

Pleural effusions with decreased lymphatic drainage?

A

Mediastinal carcinomatosis

48
Q

Characteristis of pleural effusions in inflammatory conditions?

A
  1. Serous, serofibrinous, fibrinous: infections, SLE, uremia, metastases.
  2. Empyema: bacterial or mycotic seeding.
    - ->loculated, yellow-green creamy pus
    - ->small to large volume
    - ->exudate: usually organizes (adhesions)
  3. Hemorrhagic pleuritis: sanguineous inflammatory exudate.
    - -> look for exfoliated tumour cells
49
Q

Non-inflammatory pleural effusions ?

A
  1. Hydrothorax (serous)
  2. Hemothorax
  3. Chylothorax
50
Q

Hydrothorax (serous) effusions

A
  1. Cardiac failure (congestion and edema)
  2. Uni or bilateral
  3. Without loculations (bridging fibrosis)
  4. Basal (atelectasis/compression)
  5. Resorbed with underlying cause
51
Q

Hemothorax effusions:

A

ruptured AA, or vascular trauma

52
Q

Chylothorax effusions:

A 
milky fluid: lymphatics
Emulsified fats
Usually left-sided
Smaller
Thoracic duct trauma (MCC)
Tumour
53
Q

Pneumothorax: details

A
  1. Air or gas in the pleural cavity
  2. MC- emphysema, asthma, and TB
  3. Spontaneous (rupture of alveolus): abscess cavity (interstitial emphysema)
  4. Traumatic: perforating chest wall injury
54
Q

Spontaneous idiopathic pneumothorax:

A

young ppl
Blebs*: apical/subpleural
Recurrent

55
Q

Tension pneumothorax:

A 
flap valve (inspiration w/out exit)=pressure pump. 
May compress vital organs and functions
56
Q

Pleural tumours: types?

A
  1. Primary (RARE): solitary, fibrous tumours; malignant mesothelioma
  2. Secondary (WAY more common): lung, breast
57
Q

Solitary fibrous tumours: what are they?

A

Soft-tissue tumours: pedicle attachment to pleura.
Do NOT produce effusion
Dense fibrous tissue with occasional cysts.
Rarely malignant: mitoses, necrosis, pleomorphism.
IHC: CD34+, KERATIN –

58
Q

What is mesothelioma?

A 
Happens in visceral or parietal pleura. 
Due to asbestos
7-10% in high-exposure (life-time) groups. 
Latent period :25-40 years
Smokers and non-smokers
59
Q

Gross characteristics of mesothelioma? Slide 33

A

Plaques
Effusions
Invasion

60
Q

Mesothelioma epithelioid characteristics? Slide 44

A
  1. Tubular or papillary structures
  2. +acid mucopolysaccharide
  3. +CEA/epithelial GAGs (ACa)
  4. Strong keratin staining: perinuclear vs. peripheral
  5. Calretinin, WT1, CK 5/6, mesothelin, thrombodulin
61
Q

Upper airway inflammation: infections

A

Adenovirus, echovirus, rhinovirus

Bacterial: mucopurulent to suppurative exudate

62
Q

Upper airway inflammation due to allergies/hay fever

A 
Pollen 
Fungi
Animals
Dust mites
IgE mediated
63
Q

Upper airway inflammation due to nasal polyps:

A

Cumulative bouts

Ulceration

64
Q

Chronic upper airway inflammation:

A

origin independent

deviation

65
Q

Sinusitis:

A

impaired drainage
Frontal> anterior, ethmoid
Mixed flora
Kartagener syndrome

66
Q

Necrotizing upper airway due to :

A

Fungal infection (mucormycosis)
Wegener’s
Lymphoma

67
Q

Laryngeal issues:

A

Laryngitis
Laryngeoepiglottitis: H. influenza or B-strep
Croup: inspiratory stridor, heavy smokers

Pathology (5 decks)

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