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Pathology Term 1 > Week 6 - RESP > Flashcards

Week 6 - RESP Flashcards

Lung Cancers

1
Q

What is the pathogenesis of lung cancer?

A
  1. smoking/carcinogens
  2. 3p/EGFR mutations
  3. dysplasia
  4. more mutations (Kras/C-myc)
  5. infiltration
  6. spread
  7. metastases (p53 mutation)

*normal –> hyperplasia –> metaplasia –> mild dysplasia –>severe dysplasia –> MALIGNANCY

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2
Q

What are the gross and microscopic features of small cell carcinomas?

A

Gross:

  • grey/white, diffuse, infiltrating tumour at hilar region
  • spread around bronchi
  • infiltrative
  • early/rapid spread

Micro:

  • irregular, small, dark blue/hyperchromatic cells in sheets
  • pleomorphic cells with irregular large nuclei
  • scanty cytoplasm
  • neuroendocrine cells –> paraneoplastic syndromes
  • OAT CELLS
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3
Q

What are the gross and microscopic features of squamous cell carcinomas?

A

Gross:

  • expanding tumour (NOT infiltrating)
  • grey/white, nodular, central (hilum)
  • spread to LNs/extrapulmonary structures

Micro:

  • pleomorphic cells with irregular nuclei forming irregular clusters
  • keratin pearl formation/keratinisation of cells
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4
Q

What are the gross and microscopic features of adenocarcinomas?

A

Gross:

  • grey/white, nodular, peripheral tumours
  • expanding (NOT infiltrating)
  • increase in F/non-smokers
  • central scar
  • spread to LNs/extrapulmonary structures

Micro:

  • pleomorphic cells with irregular dark nuclei forming irregular glands
  • areas of necrosis
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5
Q

Which mutations are commonly seen in squamous cell carcinomas vs. adenocarcinomas?

A 
SCC = 3p deletion (increase in males/smokers)
Adeno. = EGFR mutation (increase in previous scar pts.)
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6
Q

Compare grade 1 vs. grade 4 cancers?

A

Grade 1:

  • well differentiated
  • slow growing
  • still gland formation (some cells functioning normally)

Grade 4:

  • poorly differentiated (very irregular/pleomorphic)
  • fast growing
  • NO gland formation
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7
Q

True or False?

3p deletion mutation is seen in normal bronchial epithelium of smokers

A

True

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8
Q

What are local and systemic clinical features of lung cancer?

A

Local:

  • obstruction (effusions, pneumonias, atelectasis)
  • hemoptysis
  • bronchiectasis
  • SVC obstruction/syndrome
  • pancoast tumour
  • horner’s syndrome

Systemic:

  • cachexia
  • paraneoplastic syndromes
  • clubbing
  • bone pain/epilepsy –> metastases
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9
Q

What is pancoast tumour?

A
  • destructive lesions of thoracic inlet (destruction of ribs 1 + 2)
  • involvement of brachial plexus + cervical sympathetic nerves –> severe shoulder pain radiating to axilla/scapulae, atrophy of hand/finger muscles, wrist tenderness, horner’s syndrome, SVC syndrome
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10
Q

What is horner’s syndrome?

A
  • seen in pts. with pancoast tumours
  • 3 features:
  1. Ptosis
  2. Meiosis
  3. Anhydrosis
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11
Q

What sign is seen in SVC syndrome? How do you test for it and what indicates a positive sign?

A

Pemberton’s Sign:

  • raise patient’s arms above head for 30s
  • a positive test will give rise to flushing/facial swelling, plethora, inspiratory stridor, raised JVP
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12
Q

What is the pathogenesis of hemoptysis in lung cancer?

A

Cancer proteases break down surrounding tissue and vessels causing haemorrhage

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13
Q

What are Ix. for lung cancer?

A

Imaging
-CXR, US, MRI, CT, PET scan

Cytology

  • sputum
  • bronchial lavage

Bronchoscopy/Thoracotomy

Biopsy
-needle/excision

Tumour markers
-epithelial; neuroendocrine

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14
Q

Outline lung cancer cytology for the “big 3”

A

Adenocarcinoma:

  • gland formation
  • mucin

Squamous cell carcinoma:

  • pink cytoplasm
  • keratin pearl formation

Small cell carcinoma:

  • little cytoplasm
  • nil glands/keratin
  • oat cells
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15
Q

True or False?

Carcinoid tumours continuously produce hormones

A

True

-they have neuroendocrine cells which secrete serotonin and other hormones

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16
Q

What is carcinoid syndrome?

A
  • intermittent diarrhoea
  • facial flushing –> dry (no sweating)
  • palpitations
  • abdominal cramps
  • SOB/wheezing

*result of carcinoid tumour

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17
Q

What is a lung hamartoma?

A
  • NOT a true tumour
  • it is an embryonic disorganisation
  • consists of normal lung tissue BUT in a hapazard arrangement
  • round or nodular
  • benign behaviour
18
Q

What are the 2 types of embryonic disorganisation?

A
  1. Hamartoma:
    - normal tissue in normal place (hapazard arrangement)
    - e.g. lung hamartoma
  2. Choristoma:
    - normal tissue in abnormal place (ectopic)
    - e.g. gastric tissue in appendix
19
Q

True or False?

There is a latent period of roughly 25-40yrs for mesothelioma to manifest

A

True

  • preceded by fibrous pleural plaques caused by asbestos bodies
  • chronic pleural irritation
  • encases lung from pleura (literally “squeezes” the lung)
20
Q

What is broncho-alveolar carcinoma?

A
  • in-situ adenocarcinoma (low grade)
  • pneumonic spread –> NO invasion/tissue damage
  • tumour cells line alveolar walls
  • presents clinically like pneumonia
21
Q

What is paraneoplastic syndrome?

A

Clinical symptoms due to “chemical product” released by tumour

*NOT as a result of the tumour itself

22
Q

What % of lung cancers produce substances which cause paraneoplastic syndromes and which type are they commonest in?

A

3-10%

-common in small cell lung cancers

23
Q

What substance can be released by some squamous cell carcinomas?

A

Parathyroid hormone related peptide (PTH-rp)

-results in paraneoplastic syndrome causing lysis of bone and hypercalcemia!

24
Q

What paraneoplastic syndromes commonly occur in adenocarcinomas?

A

Haematologic syndromes
- mucin from tumour causes coagulation of blood

e.g. migratory thrombophlebitis, non-bacterial endocarditis

25
Q

What paraneoplastic syndromes commonly occur in small cell lung cancer?

A

ACTH –> cushings syndrome
ADH –> hyponatremia, SIADH, Diabetes insipidus
Gastrin releasing peptide –> peptic ulcer
Calcitonin –> hypocalcemia
Myasthenic syndrome –> autoimmune damage

26
Q

Compare NSCLC vs. SCLC

A

NSCLC:

  • expansive tumours
  • squamous + adeno.
  • better prognosis
  • later spread
  • less paraneoplastic syndromes
  • early –> surgical resection

SCLC:

  • infiltrating tumours
  • small cell/oat cell cancer
  • poor prognosis
  • early spread
  • more paraneoplastic syndromes
  • surgery NOT an option
27
Q

What is the commonest type of lung cancer?

A

NSCLC

-adenocarcinoma

28
Q

Why are cells so dark in small cell lung cancer?

A
  • scanty cytoplasm

- increase nucleus size

29
Q

Why do small cell cancers secrete increased hormones?

A
  • cells involved are neuroendocrine cells

- increase chance of paraneoplastic syndromes

30
Q

p53/Rb gene mutations are more commonly seen in?

A

small cell carcinomas

31
Q

Multiple large, rounded tumours scattered all over lungs is likely?

A

metastases

32
Q

What is the common route of spread of tumour –> lungs (metastases)?

A
  • lungs = most common site of metastases
  • haematogenous spread
  • tumour invades veins –> R heart –> lungs

*veins increase risk of tumour invasion than arteries as they are thinner

33
Q

What is silhouette sign?

A
  • loss of normal silhouette of a structure

- due to change of differing densities to similar densities of 2 adjacent structures

34
Q

What are air bronchograms?

A
  • radiological feature of consolidation
  • patent, air-filled airways within the opacity which stand out as dark, linear +/or branching structures against the opacified lung
35
Q

What are the most common causes of consolidation?

A
  • pneumonia

- neoplasm

36
Q

What are the 2 types of atelectasis?

A
  1. Resorption:
    - mucous
    - tumour
    - foreign body
  2. Relaxation
    - pleural effusion
    - pneumothorax
    - round atelectasis
37
Q

Where do adenocarcinomas, squamous cell carcinomas and small cell carcinomas typically arise from?

A

Adenocarcinoma:
-peripheral tumour

Squamous:
-central tumour (hilum)

Small cell:
-central tumour (hilum)

38
Q

What are the 2 types of bronchogenic carcinomas?

A
  1. SCLC (20%)
  2. NSCLC (80%)
    - adenocarcinomas (50%)
    - squamous cell carcinomas (30%)
39
Q

What is the etiology of lung cancer?

A
  • smoking
  • occupational exposures (asbestos, fumes, etc.)
  • fibrosis/scarring (TB, pneumoconioses, etc.)
  • radioactive gases
  • genetics
  • idiopathic
40
Q

What % of heavy smokers develop lung cancer?

A

11%

-BUT, 90% of lung cancer incidence is smokers

41
Q

True or False?

95% of lung cancers in smokers is bronchogenic carcinoma

A

True

-5% = carcinoid, hamartoma, mesothelioma

42
Q

What is the most common internal cancer?

A

Lung cancer

Pathology Term 1 (6 decks)

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