Tumours of the Lung Flashcards

(67 cards)

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
Characteristics of bronchioalveolar cancer?
Found in bronchioalveolar regions | 1-9% lung tumours
26
General location of bronchioalveolar cancer (BAC)? (photo slide 15)
Peripherally located Can be single or Multiple nodules (MC): coalesce-->pneumonia-like (slide
27
Morphology of BAC?
Solid, grey-white with translucent secretions | Rarely: atelectasis/emphysema
28
Where does BAC arise?
From atypical, adenomatous hyperplasia (monoclonal)*
29
Kind of spread of BAC?
Lepidic (along alveolar/BA walls); scaly Like butterflies on a fence Non-destructive (doesn't invade underlying architecture).
30
Cells affected by BAC?
Bronchiolar cells Clara cells (protect lining, secrete GAGs) Type II pneumo's
31
What is mucinous BAC like?
Tall columnar cells filled with mucin. | Aerogenous spread with: satellite tumors, coalesce.
32
What is non-mucinous BAC like?
Columnar/peg-shaped/cuboidal cells. Grow along alveolar septae Rare aerogenous spread: resectable*
33
Small cell carcinoma epidemiology ?
1% non-smokers No pre-invasive phase* **Most aggressive, earliest to metastasize, and no surgical option 15-25% cure with chemo and radiation
34
SCC location ?
Major bronchi and peripheral
35
SCC histologic characteristics? (photo A slide 19)
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
Histologic characteristics of SCC (slide 20, b)
1. Round, oval, or spindle-shaped cells 2. Nuclear molding 3. Apoptosis 4. Smaller than resting lymphocytes 5. Necrosis
37
SCC genetics?
P53: mutated 50-8-% RB: mutated 80-100% BCL2 by IHC in 90%
38
Large cell carcinoma characteristics (slide 22)?
``` Undifferentiated Lacks squamoid, glandular, or SCC features Large nuclei Nucleoli Moderate cytoplasm ```
39
Secondary pathology of tumours of the lung
1. Partial obstruction: focal emphysema 2. Total obstruction: atelectasis 3. Suppurative/ulcerative bronchitis 4. SVC compression 5. Pericarditis 6. Pleuritis
40
Lung tumours: paraneoplastic syndromes
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
Pleural effusions are seen in what?
Primary or secondary disease
42
Normal pleural effusions:
15 cc serous lubricating fluid | Acellular and clear
43
Pleural effusions with increased hydrostatic pressure?
CHF
44
Pleural effusions with increased vascular permeability?
Pneumonia
45
Pleural effusions with decreased osmotic pressure?
Nephrotic syndrome
46
Pleural effusions with increased negative pressure (intrapleural)?
Atelactasis
47
Pleural effusions with decreased lymphatic drainage?
Mediastinal carcinomatosis
48
Characteristis of pleural effusions in inflammatory conditions?
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
Non-inflammatory pleural effusions ?
1. Hydrothorax (serous) 2. Hemothorax 3. Chylothorax
50
Hydrothorax (serous) effusions
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
Hemothorax effusions:
ruptured AA, or vascular trauma
52
Chylothorax effusions:
``` milky fluid: lymphatics Emulsified fats Usually left-sided Smaller Thoracic duct trauma (MCC) Tumour ```
53
Pneumothorax: details
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
Spontaneous idiopathic pneumothorax:
young ppl Blebs*: apical/subpleural Recurrent
55
Tension pneumothorax:
``` flap valve (inspiration w/out exit)=pressure pump. May compress vital organs and functions ```
56
Pleural tumours: types?
1. Primary (RARE): solitary, fibrous tumours; malignant mesothelioma 2. Secondary (WAY more common): lung, breast
57
Solitary fibrous tumours: what are they?
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
What is mesothelioma?
``` 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
Gross characteristics of mesothelioma? Slide 33
Plaques Effusions Invasion
60
Mesothelioma epithelioid characteristics? Slide 44
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
Upper airway inflammation: infections
Adenovirus, echovirus, rhinovirus | Bacterial: mucopurulent to suppurative exudate
62
Upper airway inflammation due to allergies/hay fever
``` Pollen Fungi Animals Dust mites IgE mediated ```
63
Upper airway inflammation due to nasal polyps:
Cumulative bouts | Ulceration
64
Chronic upper airway inflammation:
origin independent | deviation
65
Sinusitis:
impaired drainage Frontal> anterior, ethmoid Mixed flora Kartagener syndrome
66
Necrotizing upper airway due to :
Fungal infection (mucormycosis) Wegener's Lymphoma
67
Laryngeal issues:
Laryngitis Laryngeoepiglottitis: H. influenza or B-strep Croup: inspiratory stridor, heavy smokers