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Resp week 4 > Pathology of lung cancers > Flashcards

Pathology of lung cancers Flashcards

1
Q

Is lung cancer the commonest cause of cancer death?

A

Yes

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2
Q

How many people in Scotland are diagnosed each year with lung cancer? Is it equal men/women?

A

Approx 5000, pretty much equal now men/women

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3
Q

What are the causes of Lung Cancer?

A 
Tobacco!
Environmental radon
Occupational exposure - Chromates/hydrocabons/nickel
Air pollution/urban environment
Radiation
Pulmonary fibrosis
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4
Q

What percentage of lung cancers can be attributed to tobacco?

A

85%

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5
Q

What percentage of smokers will get lung cancer?

A

10%

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6
Q

Is there a safe smoking threshold?

A

No

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7
Q

What is How long does it take for an ex smokers risk factor to return to standard level?
And why?

A

A long time (15+ years)! Because the genetic damage that is caused by tobacco carcinogens takes a long time to be flushed out of the epithelial cell population.

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8
Q

What % of UK people smoke in the UK?

A

20-30%

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9
Q

Is tobacco and smoking in China/S, SE Asia/South America increasing or decreasing ?

A

Increasing!! Amount of lung cancer is shooting up.

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10
Q

How many recognised carcinogens in a cig?

A

60+

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11
Q

What are the main 2 families of carcinogens present?

A

Polycyclic aromatic hydrocarbons and N-Nitrosamines

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12
Q

What type of cancers are most likely to appear after polycyclic aromatic hydrocarbons ?

A

Central part of lung - in the bronchi - squamous/small cell carcinoma

From unfiltered toacco products - more common 50/60 years ago.

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13
Q

What type of cancers are most likely to appear after N-nitrosamines?

A

More prone to cause adenocarcinomes (especially more in women than men)

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14
Q

How do the carcinogens affect the epithelia? How many genomic alterations?

A

3-12 key genomic alterations in the stem cell epithelia ( 2 populations of epithelia) , usually in a particular sequence to keep the cells alive with the mutations.

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15
Q

What are pro-carcinogens?

A

They are substances that aren’t carcinogens when we inhale/digest them, but then they are processed by our bodies to become carcinogens

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16
Q

What varies so we develop different risk of developing carcinogens?

A

Genetics! We inherit different isoenzymes of metabolising enzyme families

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17
Q

Where are the 2 stem cells populations?

A

In the larger areas of the bronchi and in the peripheral lung epithelium (small bronchioles and alveoli)

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18
Q

What are the pathways for aleveolar/bronchi cancers

A

Alveoli - Adenocarcinoma:
Bronchioloalveolar epithelial stem cells transform - Atypical Adenomatous Hyperplasia - develop into adenocarcinomas - Adenocarcinoma in Situ - Invasive adenocarcinoma

Bronchi - Squamous cell carcinoma:
Bronchial epithelial stem cells transform - Bronchial basal cell
Hyperplasia - Squamous dysplasia and carcinoma in situ - Invasive
squamous cell carcinoma

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19
Q

What can be other causes for masses in the lung?

A

Consolidation/fibrosis from pneumonia,

20
Q

What are the 4 main types of primary lung cancer?

A

Squamous cell carcinoma (40% decreasing)
Adenocarcinoma (41% increasing)
Small cell carcinoma (15%)
Large cell carcinoma (4%)

21
Q

Which are the most prevalent? And in which genders, due to rise in N-nitrosamines?

A

Adenocarcinomas and squamous cell carcinomas are most prevelant.

Adenocarcinomas are on the rise, especially in women (as they have increased in smoking and potentially have a higher susceptibility) and due to the increasing amount N-nitrosamines in tobacco.

22
Q

Small cell carcinoma is related to which carcinogen group?

A

Polycyclic aromatic hydrocarbons

23
Q

Is non small cell carcinoma a biological entity?

A

Nope, its a group of lng cancers that aren’t small cell carcinomas

24
Q

If presenting as lung cancer has it spread?

A

Yes, there are rarely any symptoms in early stage lung cancer, so if someone presents as lung cancer the chances are that it is quite late and it has already spread.

25
Q

Is surgery the best option ?

A

Depends on the tumour. Usually only adenocarcinomas/ carcinomas on the periphery of the lungs against the chest wall can be surgically removed. Cancers on the mediastinum boarder/diaphragmatic border are usually not surgically removed.

26
Q

Which tumours are more likely to bleed?

A

Central tumours involving the large bronchi

27
Q

What else can a lung cancer cause?

A 
Bronchial collapse (due to obstruction) 
endogenous lipoid pneumonia/infection/abcess
Bronchiectasis

Can affect the pleura, nerves, lympth nodes, invasion of other tissues

28
Q

When can pleural disease occur?

A

Malignant Invasion of cancer or just pleural effusion etc due to infection as a result of the cancer, eg. pneumonia causing inflammation and thickening of pleura. Can also cause pleural fibrosis.

29
Q

Which nerves can become affected and what can these present as clinically?

A

Phrenic - change of cough, increase in breathlessness (diaphragmatic paralysis)
Left Recurrent Laryngeal - causes Hoarse voice, Bovine cough
Brachial plexus - hand numbness - pancost T1 dmaage
cervical Sympathetic - Horner’s syndrome - paralysed eyelid one side, no face sweating, fixed pupil, droopy skin

30
Q

What happens if the SVC becomes obstructed?

A

Fat face (plethoric infused face). Upper limb veins = engorged even when raised above heart height. Risk of deveolping cerebral odeama.

31
Q

What is lymphangitis carcinomatosa

A

tumour spread through the lymphatics of the lung

32
Q

Where are distant metastases common?

A

Liver, Adrenals (adrenal gland at the top of the kidneys), bone, brain, skin

33
Q

Some key Non-metastatic effects?

A

Clubbing, hypertrophic pulmonary Osteoarthopathy (HPOA) Sore v sore periosteal swelling around wrists (swollen wrists)

34
Q

Will Non-metastatic effects disappear if tumour is removed?

A

Yes!

35
Q

What are small cell carcinomas characterised by?

A

Neuroendocrine differentiation

36
Q

In which type of carcinoma can a hormone similar to ACHT/ADH be secreted and how may this present clinically?

A

In small cell carcinoma. Presents similar to hyper ACTH secretion like in Cushing’s syndrome.

37
Q

Which carcinoma produces a hormone similar to parathyroid hormone (PTH) and what would this present as?

A

Squamous cell carcinoma, and present as Hypercalcemia

38
Q

What are the cure (5 years+) rate for stage 1 and stage 2 lung cancers?

A

Stage 1 = more than 60%

Stage 2 = 35%

39
Q

Which is worse – non small cell carcinoma or small cell?

A

Small Cell carcinoma!

40
Q

What is the median survival for all small cell carcinoma

A

9 months

41
Q

Where are squamous and small cell carcinomas generally found and what is usually the origin?

A

Tobacco, found in the larger bronchi

42
Q

Never smoked generally what type of carcinoma?

A

Adenocarcinoma

43
Q

What is the standard treatment that we have to use in squamous cell carcinoma? Why?

A

Chemotherapy or immunotherapy, because usually caused by tobacco, complicated molecular changes have occurred and so there are no specific treatments available.

44
Q

What is the standard treatment that we have to use in small cell carcinoma? Why?

A

Chemotherapy (but a different type to what is used in squamous cell carcinoma), because usually caused by tobacco, complicated molecular changes have occurred and so there are no specific treatments available, no molecular targets to go after.

45
Q

If complex molecular background of adenocarcinoma (from tobacco smoke) how do we have to treat?

A

Chemotherapy/immunotherapy

46
Q

If an adencarcinoma has a simple molecular change background, can these be targeted? If so give examples.

A 
Yes! 
EGFR
BRAF/HER2
ALK rearrangements
ROS1 gene rearrangements
47
Q

What does immunotherapy target?

A

PD1 and PDL1

Resp week 4 (8 decks)

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