7 Respiratory Pathology: Lung Cancer Flashcards Preview

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Flashcards in 7 Respiratory Pathology: Lung Cancer Deck (47)
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1
Q

Q: In terms of most common cause of death in the UK, what place is cancer? What’s mortality within 1 year of diagnosis? 5 yr survival? What needs to happen for better prognosis? How do lung cancer rates vary globally?

A

A: 3rd

80%

5.5%

detect early

decreasing in developed world by increasing in non

2
Q

Q: Name causative factors of cancer. (5) What do lung cancer trends follow? Therefore?

A
A:  tobacco (++ carcinogens in smoke)
radiation (e.g.) radon
asbestos
genetic predisposition
other (e.g. heavy metals)
  • lung cancer trends follow smoking prevalence
  • ++ health outcomes with earlier cessation of smoking
3
Q

Q: What are the clinical features of cancer? (6)

A

A: - haemoptysis: coughing up blood

  • unexplained or persistent (3+ wks): cough
  • unexplained or persistent (3+ wks) chest/ shoulder pain
  • ” dyspnoea
  • ” hoarseness
  • finger clubbing
4
Q

Q: What occurs if someone is thought to have lung cancer?

A

A: urgent referral for a chest X ray (CXR)

5
Q

Q: Clinical history: 74 yr old male; 6 month h/o weight loss, lethargy, – appetite; haemoptysis; good performance status; smoker equivalent of 70 pack yrs; no occupational risk factors; clubbing of finger nails, nicotine staining, cachexia, diminished air entry right base.

What should happen next? (7) Finally?

A

A: 1. CXR
2. bronchoscopy/ CT/ lymph node biopsy (take samples when do bronchoscopy); PET scan

staging TNM classification (tumour (T1-4)- location and size, 1-4; lymph nodes (N0-3), 0-3; metastases (M0-1), 0-1)

fitness

treatment

6
Q

Q: What does histopathology involve? (5) Aim?

A

A: confirm diagnosis;

type; stage; molecular pathology; cytology; histology (biopsy/ surgical biopsy)

7
Q

Q: Summarise the type of system the airways are? How wide are bronchi? bronchiole? small airways? Role of small airways? What prevents the collapse of trachea?

A

A: - airway conductive system (asymmetrical dichotomous branching tubular system up to 24 times)

bronchi >1mm; bronchiole <1mm; small airways <2mm (conduct to alveoli)

cartilage prevents collapse

8
Q

Q: What does the gas exchange compartment contain? (4) Where do tumours occur?

A

A: (alveoli)

airways; alveolar parenchyma (epithelium/ interstitium); vasculature (arteries/ veins/ lymphatics); pleura

anywhere

9
Q

Q: By which type of pathway do carcinomas develop? Result in? (4) Where do mutations occur? (2)

A

A: multistep accumulation of mutations resulting in:

o disordered growth
o loss of cell adhesion (less organised structures)
o invasion of tissue by tumour
o simulation of new vessel formation around tumours

  • mutations occur in epithelial cells and stem cells
10
Q

Q: What is reflected in the histology of tumours?

A

A: different tumour types

11
Q

Q: Which cells in the lung do tumours tend to arise from? (3) What are the 2 types? How do these types differ? (2) 2 examples. What is the most common type of lung cancer?

A

A: epithelial, mesenchymal (soft tissue), lymphoid

  • benign: do not metastasise; can cause local complications (e.g. airway obstruction); e.g. chondroma
  • malignant: potential to metastasise; variable clinical behaviour; commonest: epithelial tumours->carcinomas
12
Q

Q: What is the most common type of lung cancer? What percentage of all lung cancer cases does it make up? 3 subtypes? Give occurrence rate of 2 of them.

A

A: Non-small cell lung cancer

about85%

Squamous cell carcinoma, adenocarcinoma, and large cell carcinoma

  • squamous cell carcinoma (20-40%)
  • adenocarcinoma (20-40%)
13
Q

Q: What is the 5 year survival rate for early stage non-small cell carcinoma? Late stage? What can some people be offered if they have early stage non-small cell carcinoma? reason?

A

A: early stage 1: 60% 5 yr survival

late stage: 5% 5 yr survival

20-30% have early stage tumours suitable for surgical resection
o less chemosensitive

14
Q

Q: What type of pathway leads to the development of squamous cell carcinoma? What is this a subtype of? What is squamous cell carcinoma closely related to? What is a key feature that means early detection is beneficial?

A

A: multi-step pathway of development

Non-small cell lung cancer

closely associated with smoking

local spread, metastasise late

15
Q

Q: Where does squamous cell carcinoma manifest? (traditionally and now) Explain the pathway for development. (5) What can it lead it? What type of treatment can you get? downside?

A

A: proximal airways- traditionally central arising from bronchial epithelium, but recent increase in peripheries (smoking changes)

  1. ciliated respiratory epithelium exposed to recurrent irritation
  2. metaplasia
  3. squamous epithelium (X mucous clearing) -> more unstable
  4. dysplasia -> ability to invade surrounding tissue
  5. carcinoma
  • keratinisation
  • may develop fatal haemorrhage with anti-angiogenic therapy
16
Q

Q: In what group of people is adenocarcinoma most common? How does this vary? (3) How has incidence changed over time? Where does it manifest itself in terms of airways?

A

A: commonest type in non-smokers
- commoner in far east, females and non-smokers

  • increasing incidence
  • distal airways and alveolar epithelium; more often multicentric
17
Q

Q: What is specific to adenocarcinomas? (3) When is this form of cancer curative? What is common and early? What does histology show?

What is the target for treatment?

A

A: atypical adenomatous hyperplasia: proliferation of atypical cells lining the alveolar walls -> ++ size -> invasive
• early resection before invasion -> curative
• commoner in far east, females and non-smokers
• extrathoracic metastases common and early
• histology shows evidence of glandular differentiation
• variety of molecular abnormalities provide targets for treatment

18
Q

Q: Describe the incidence of large cell carcinoma. How has incidence changed over time? What can cause it? Describe it.

A

A: uncommon
• decreasing in incidence
• occupational exposure etc.
• poorly differentiated tumours of large cells

19
Q

Q: What does incidence of large cell carcinoma show? reason? What is prognosis?

A

A: no histological evidence of glandular or squamous differentiation
• probably v. poorly differentiated adeno/ squamous cell carcinomas
• poorer prognosis (the likely course of a medical condition)

20
Q

Q: Apart from non small cell lung cancer, give another type of lung cancer. What percentage of lung cancer cases does it make up? What is the rate of survival if untreated? if treated? What is the current treatment offered? why?

A

A: small cell carcinoma (20%)

• survival 2-4 months untreated (10-20 months with current therapy); chemoradiotherapy (very chemosensitive)

21
Q

Q: What is affected with small cell carcinoma? where? Describe the differentiation of these cells. What is it closely related to?

A

A: small cells
• often central near bronchi
• poorly differentiated (often just nuclei)
• very close association with smoking

22
Q

Q: What percentage of those with small cell carcinoma, present with advanced disease? Describe. Prognosis? What can this type of cancer lead to?

A

A: 80%

divide very rapidly -> often necrotic (outgrow their blood supply)- all energy is put into proliferation

poor

paraneoplastic syndromes

23
Q

Q: What are paraneoplastic syndromes? Pathogenesis? (2)

A

A: symptoms that occur at sites distant from a tumour or its metastasis

pathogenesis remains unclear, but these symptoms may be secondary to substances secreted by the tumour or may be a result of antibodies directed against tumours that cross-react with other tissue

(systemic effect of tumour from abnormally expressed tumour cells of factors (e.g. hormones/ other factors) not normally expressed by tissue from which tumour arose)

24
Q

Q: What are the local effects of lung cancer?

A

A: - bronchial obstruction

  • invasion of local structures
  • inflammation/ irritation/ invasion of pleura/ pericardium
25
Q

Q: What can inflammation be caused by in lung cancer? What can this cause? (2)

A

A: invasion of pleura / pericardium

pleuritis/ pericarditis -> breathlessness/ cardiac compromise

26
Q

Q: What can invasion of local airways and vessels lead to in lung cancer? (4)

A

A: haemoptysis, cough; invasion around large vessels; oesophagus -> dysphagia;
chest wall -> pain;
nerves -> Horners syndrome

27
Q

Q: What can bronchial obstruction lead to in terms of lung cancer? (4)

A

A: collapse of distal lung -> SOB (Shortness of breath); impaired drainage of bronchus -> chest infection- pneumonia/ abscess

28
Q

Q: What are 5 systemic effects of bronchogenic carcinoma?

A

A: - distant spread -> brain, skin, liver, bones

- paraneoplastic syndromes

29
Q

Q: What does smoking do to be a lung cancer risk factor? (2)

A

A: inhibits p53 gene -> housekeeping does not occur -> cells that should’ve been destroyed live on = cancer cells

also promotes oncogenic fusion protein production (as do viruses)

30
Q

Q: What does it mean for finger nails to club?

A

A: nail bed angle is more than 180 degrees (obtuse)

31
Q

Q: How do you measure the extent of cancer? Describe (3).

A

A: TNM classification
tumour (includes location)
lymph nodes
metastasise

  • T staging is based on location, size and proximity to other organs
  • If the tumour is closer to the mediastinum or the chest wall then it has a HIGHER T STAGING irrespective of its size

-If the tumour spreads to the lymph nodes in the neck then there is higher staging

32
Q

Q: What does it mean if cancer has spread to the lymph nodes? What can be done if the cancer is early and has not spread to lymph nodes?

A

A: Surgery is not practical-> chemo first

surgically remove

33
Q

Q: What kind of metastasise can occur that is classed as a medical emergency? how do patients feel? (2) what is done?

A

A: superior vena cava obstruction

  • headache
  • congested

put stent in to recanalise the SVC-> allow normal blood flow

34
Q

Q: What are the order of events with lung cancer? (5)

A

A: 1. suspected lung cancer

  1. CT thorax (better than Xray- use Xray for small suspicions)
  2. diagnosis // 4. staging => cell type?
  3. tests: PET-CT, PFTS(pulm function tests), MRI brain
  4. treatment plan (are they fit enough/smokers etc)-> have multidisciplinary meeting
35
Q

Q: How do you check if cancer has spread from the lung to other organs?

A

A: given FDG

do PET-CT

rapidly acting cells pick it up and since it’s radioactively labelled-> visualise

36
Q

Q: Describe a method of extracting a sample from cancer. Benefits? Risks? What’s an alternative?

A

A: trans thoracic CT biopsy
-put needle through chest wall into lung

  • real time
  • sensitivity 70-100%
  • risk of pneamothorax 25-30%
  • small sample size
  • fine needle aspiration can be used to sample a few cells which are then looked at by pathologists -> sample the highest staged area
37
Q

Q: What is cancer treatment based on? (4)

A

A: Treatment is based on the cell type of the tumour, the extent of the tumour (TNM), how fit the patient is (are there co-morbidities, are they fit for surgery)

38
Q

Q: What are the 2 compartments of the lung?

A

A: airway conductive system, gas exchange compartment

39
Q

Q: In the formation of an adenocarcinoma, what is the most common mutation in smokers? (3) in non smokers? What is the precursor?

A

A: -K ras mutation

  • DNA methylation
  • p53

EGFR mutation/amplification

clara cell/type 2 pneumocyte

40
Q

Q: Explain the Importance of Histological Tumour Type. (1,2)

A

A: Small Cell Lung Carcinoma
-Chemoradiotherapy (surgery is very rare as it has usually spread by the time it’s identified)

Non-Small Cell Lung Carcinoma

  • 20-30% have early stage tumours suitable for surgical resection
  • Less chemosensitive
41
Q

Q: What does New data suggest? (4)

A

A: that it is becoming increasingly important to SUB-TYPE non-small cell carcinoma for treatment

  • some patients with squamous cell carcinoma develop fatal haemorrhage with Bevacizumab
  • some chemo works better in adenocarcinoma (pemetrexed)
  • variety of molecular abnormalities provide targets for treatment only found in adenocarcinomas eg EGFR, ALK, ros, ret mutations
42
Q

Q: What is EGFR? Where is it found? role? What can happen to it? causes? predominantly in? What is EGFR the target of?

A

A: Targets of Treatment - EGFR (Epidermal Growth Factor Receptor= type of membrane receptor TYROSINE KINASE)

EGFR sits on the surface of cells and signals a variety of downstream pathways that make the cell divide: regulates angiogenesis, proliferation, apoptosis and migration

You can get mutation or amplification of EGFR, mainly in adenocarcinoma (predominantly among non-smokers) which makes receptor permanently on

EGFR is the target of a TYROSINE KINASE INHIBITOR

43
Q

Q: What is immunemodulatory therapy?

A

A: helping your body fight the tumour

44
Q

Q: How have tumours evolved to evade the immune system? effectively? Treatment?

A

A: express protein PDL1= inhibits cytotoxic T cells

effectively hides tumour from immune response

can block that expression

45
Q

Q: What cells can be analysed by histopathologists? (4) Called?

A

A: (Cytology)

Sputum

Bronchial washings and brushings

Pleural fluid (if the tumour is peripheral it can irritate the pleura and make it produce fluid)

Endoscopic fine needle aspiration of tumour/enlarged lymph nodes

46
Q

Q: What tissues can be analysed by histopathologists? (5) Called?

A

A: (histology)

Biopsy at bronchoscopy - central tumours

Percutaneous CT guided biopsy - peripheral tumours

Mediastinoscopy and lymph node biopsy - for staging

Open biopsy at time of surgery if lesion is not accessible otherwise - frozen section

Resection specimen - confirm excision and staging

47
Q

Q: What are the 2 types of paraneoplastic syndromes? Include examples.

A

A: endocrine- eg syndrome of inappropriate ADH causing hyponatremia (especially in small cell carcinoma)

Non-Endocrine - Haematologic/Coagulation defects