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Core teaching week A > Lung tumours > Flashcards

Lung tumours Flashcards

1
Q

what is Bronchogenic carcinoma

A

malignant and epithelial

aka lung cancer
95% of all primary lung tumours
2nd most common cancer
Incidence still rising in women
Most common fatal malignancy
Peak incidence in 50-70 age group
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2
Q

what is carcinoid

A

borderline malignant and epithelial

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3
Q

what is bronchial adenoma

A

benign epithelial

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4
Q

what are leiomyosarcoma and liposarcoma

A

malignant and connective tissues

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5
Q

what are leiomyoma and lipoma

A

benign and connective tissue

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6
Q

what is a Pulmonary hamartoma

A

A developmental disorder of cell growth in which there is
excessive growth of cells and tissues normally present at
that site.

Well- defined peripheral lesion

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7
Q

risk of smoking in lung cancer

A

Compared with non-smokers – average smokers have 10 x increased risk and heavy smokers (>40/day) have 60 x increased risk.

Directly related to amount of daily smoking, tendency to inhale and duration of habit
Women apparently more susceptible to the carcinogens.

Cessation of smoking for 10years reduces risk but never to control levels.

Also assocd with ca of the mouth, pharynx, larynx, oesophagus, pancreas, cervix, kidney, bladder
Cigar and pipe smoking also related but not as bad.

Statistically related to ‘pack years’:
(packs/day x years of smoking)

80% of cancers occur in smokers

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8
Q

6 stages of normal tissue to invasive cancer

A 
1 - normal epithelium
2 - hyperplasia
3 - squamous metaplasia
4 = dysplasia
5 - carcinoma in situ 
6 - invasive carcinoma

Estimated 10 to 20 genetic mutations have occurred by the time tumour is clinically apparent
Multiple hits

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9
Q

8 complications of lung cancer

A

1 - Hoarseness – Left laryngeal nerve palsy

2 - Haemoptysis – Vascular destruction

3 - Pneumonia, bronchiectasis, abscess – Obstruction

4 - Dysphagia – Oesophageal invasion

5 - Diaphragm paralysis – Phrenic nerve invasion

6 - SVC syndrome – SVC obstruction (Superior vena cava syndrome (SVCS) is obstruction of blood flow through the superior vena cava (SVC). It is a medical emergency and most often manifests in patients with a malignant disease process within the thorax.)

7 - Pleural effusion – Tumour invasion

8 - Pericarditis – Tumour invasion

9- horner’s syndrome due to sympathetic ganglia invasion. (constricted pupil, sunken eye, ptosis, ipsilateral loss of sweating.

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10
Q

whats a Pancoast’s tumour and what are the possible complications

A

Apical tumour invades sympathetic ganglia&raquo_space;
Horner’s syndrome = constricted pupil, sunken eye, ptosis and ipsilateral loss of sweating

Shoulder and arm pain from brachial plexus involvement

Hoarseness from laryngeal
nerve palsy

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11
Q

what are Paraneoplastic syndromes

A

A syndrome associated with tumour but not due to either local or metastatic spread

Often associated with ectopic hormone production

May precede a macroscopically identifiable lesion

Common in lung cancer
Related to histological type

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12
Q

5 lung cancer endocrinopathies

A

Endocrinopathies
Hyponatraemia - Syndrome of inappropriate anti-diuretic hormone secretion (SIADH)

Cushing’s syndrome – ACTH or ACTH-like production

Hypercalcaemia – Parathyroid hormone, parathyroid hormone related peptide or prostaglandin E secretion

Hypocalcaemia – Calcitonin secretion

Gynaecomastia – Gonadotrophin secretion

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13
Q

what happens in SIADH

A

Syndrome of inappropriate anti-diuretic hormone secretion (SIADH) - – hyponatraemia, cerebral oedema and neurologic manifestations

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14
Q

what happens in cushing’s

A

Hypertension, weight gain, truncal obesity, moon facies, buffalo hump, proximal limb weakness, secondary diabetes, fragile skin with easy bruising, osteoporosis

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15
Q

5 non endocrine syndromes that can be caused by lung cancer systemic effects

A

Non-endocrine syndromes

1 - Myasthenia (Lambert-Eaton syndrome) – autoantibodies against pre-synaptic calcium channel

2 - Hypertrophic osteoarthropathy (clubbing, periosteal new bone formation in small long bones and arthritis of adjacent joints) – Unknown mechanism

3 - Trousseau’s syndrome (migratory thrombophlebitis) – tumour mucins that activate clotting

4 - Dermatomyositis – auto-antibody production

5 = Acanthosis nigricans – secretion of epidermal growth factor

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16
Q

what is Squamous cell carcinoma

A

30% tumours (from 40% previously)
M>F
Strongest link to smoking – 98% are in smokers

Hypercalcaemia is the commonest paraneoplastic syndrome

Central in position
Locally advanced before metastatic spread
Arise from stem cell population (reserve cells)
Following squamous metaplasia of respiratory epithelium
After undergoing increasing dysplasia and carcinoma-in-situ formation

Large poorly-circumscribed mass with direct origin
from main bronchus

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17
Q

what is squamous metaplasia

A 
Squamous metaplasia – 
a change from 1 epithelial 
cell type to another in 
response to environmental 
insult
18
Q

what is dysplasia

A

Dysplasia – cytological and architectural atypia without breach of the basement membrane

19
Q

what is adenocarcinoma

A 
30% of tumours (from 25% previously)
F>M, but increase is in males
Least association with smoking
But 75% still in smokers
Paraneoplastic syndromes rare

Can be peripheral as well as central
Peripheral tumours occasionally associated with scarring (scar cancers)
Arise from stem cell population
Via dysplasia without metaplasia

A poorly-circumscribed mass whether central or
peripheral. Bronchial origin only identifiable if central.

20
Q

what is Bronchioloalveolar carcinoma

A

A rare specific subtype of adenocarcinoma
<1% lung cancers
Usually peripheral
Arise from distal bronchi/bronchioles
Extend into alveolar spaces
All well-differentiated histologically so not graded further
Better prognosis than other adenocarcinomata
Mimics consolidation clinically and radiologically

An ill-defined parenchymal
mass that mimics the
consolidation of pneumonia

Tumour cells extend along alveolar walls

21
Q

what is Large cell carcinoma

A 
aka anaplastic carcinoma
10% of tumours
Not a specific entity 
Represents unrecognisable squamous and adenocarcinomas
Lack of differentiation prevents further typing 
All by definition high grade
Poor prognosis
Paraneoplastic phenomena rare

Poorly-circumscribed large
mass arising centrally and
with cavitation due to
tumour necrosis

Large cells with marked cytological atypia including
nuclear pleomorphism and high mitotic activity. No
obvious differentiation.

22
Q

what is Small Cell Carcinoma

A 
Arise from neuroendocrine cells
25% of tumours
Strongly associated with smoking
99% in smokers, M>F
Cushing’s and SIADH common

Central in position

Metastasise early

All high grade so not graded further

Poorly-circumscribed
relatively small mass arising
centrally from bronchial wall

23
Q

overview of lung cancer treatment and prognosis

A

Mostly dependent on histological type:

Small cell carcinoma 		
vs 		
Non-small cell 		
Squamous cell carcinoma 	
Adeno
Large cell

Stage also affects prognosis and management

Grade (where present) alters prognosis but not management

24
Q

treatment and prognosis of small cell lung cancer

A

Metastases usual at time of presentation

70% have extensive metastatic disease
2-4 months survival untreated
Chemotherapy as highly sensitive initially
Radiotherapy if SVC obstruction
Surgery contra-indicated in most cases
10-20 months survival with treatment
25
Q

treatment and prognosis of Non-Small Cell Lung Cancer (NSCLC)

A 
5 year survival dependent on stage
Wide range (3-60%) but overall only 20%

About 25% have resectable local disease
Surgery if resectable and no metastasis
Radiotherapy if non-resectable
Chemotherapy if metastatic, but response poor

26
Q

staging of lung cancer

A

A measure of how far tumour has spread

T (tumour) N (nodes) M (distant metastases) commonly used

Information derived from:
Clinical – Bronchoscopy, Surgery

	Radiology – CT, MRI, Bone scan, PET scan

	Pathology – Cytology, Histology, PM

Common distant sites include adrenal, brain, liver and bone

27
Q

Staging NSCLC

A

TNM used to produce stage grouping
Useful prognostic tool:

	Stage I – 60% 5 year survival

	Stage II – 40% 5 year survival

	Stage IIIa – 20% 5 year survival

	Stage IIIb – 5% 5 year survival

	Stage IV – 3% 5 year survival
28
Q

Staging SCLC

A

TNM not used as most tumours metastatic

Instead use limited vs extensive disease:

Limited – 1-2 year median survival. Disease confined to ipsilateral thorax, Including supraclavicular fossa and pleural effusion

Extensive – 6-12 month median survival
All other patients

29
Q

what are carcinoid tumours

A

Low grade malignant tumour
CF from their intraluminal growth, capacity to metastasise, ability of some lesions to emanate vasoactive amines.

Multiple Endocrine Neoplasia type 1 (MEN1) is a rare hereditary endocrine cancer syndrome - tumors of the parathyroid glands (95% of cases), endocrine gastroenteropancreatic (GEP) tract (30-80% of cases), and anterior pituitary (15-90% of cases).

Other endocrine and non-endocrine neoplasms including adrenocortical and thyroid tumors, visceral and cutaneous lipomas, meningiomas, facial angiofibromas and collagenomas, and thymic, gastric, and bronchial carcinoids also occur.
MEN 2 – thyroid, pth and adrenal usually

5% of all lung tumours

Arise from neuroendocrine cells

M=F, <40 years
No known relationship with smoking. Carcinoid tumours – younger patients, not usually smoking related

Can occur as part of Multiple Endocrine Neoplasia (MEN) syndromes

Can cause local and paraneoplastic symptoms
Carcinoid syndrome most common
90% benign and 10% malignant

Usually small and well-circumscribed yellow mass.
Peripheral or central position.

30
Q

what is carcinoid syndrome

A 
Due to Serotonin (5HT) production
Enters systemic circulation
Flushing
Nausea and vomiting
Abdominal pain
Coughing and wheezing
Carcinoid heart disease:
Endocardial, Tricuspid & pulmonary valve scarring
Rarely Aortic & Mitral stenosis

Cardiac problems in 50% of people with carcinoid syndrome
Serotonin and bradykinin have direct effect on right side of heart

These are inactivated as travel through the pulmonary circulation due to high monoamine oxidase levels

31
Q

details on lung metastases

A

Most common lung tumour
Common in both carcinoma and sarcoma

Breast, GI tract and kidney most common sites

Therefore adenocarcinoma most common histological type
Can’t usually be distinguished histologically from a primary tumour

Use immunohistochemistry to give a “clue” as to the primary

Haematogenous spread – discrete nodules

Lymphatic spread – diffuse dissemination with macroscopic nodularity (lymphangitis carcinomatosa) or microscopic only

32
Q

what is Lymphangitis carcinomatosa

A

tumour dispersed

within lymphatic vessels

33
Q

what is malignant mesothelioma

A

Primary pleural tumour

Arise from mesothelial cells

Often extensive and bilateral

Aggressive - direct invasion to lung and mediastinum

Metastatic spread less common

34
Q

Aetiology and Pathogenesis of malignant mesothelioma

A

Rare overall, about 1000 cases yearly in UK

Asbestos exposure
Mining, fabrication and working with insulation
10% lifetime risk if heavy exposure
Up to 40 year latency period
Smoking does not increase risk of mesothelioma

But magnifies risk of lung cancer in smokers

35
Q

Clinical Presentation of malignant mesothelioma

A

Chest pain
Dyspnoea
Pleural effusion
Weight loss

Diagnosis can be difficult but IMPORTANT!

Diffuse and widespread thickening of pleura with extension into underlying lung

Variable histology - spindle cell ‘sarcoma-like’
areas & acinar ‘adenocarcinoma-like’ areas.

Diagnosis between mesothelioma and adenocarcinoma requires immunohistochemistry

36
Q

Treatment and Prognosis of malignant mesothelioma

A

Surgery rarely possible

Poor response to radio and chemotherapy

50% dead within 1 year, most within 2 years

If known occupational exposure then an ‘unnatural’ cause of death

Requires referral to Coroner, post mortem (if diagnosis not confirmed in life) and inquest

37
Q

diagnostic method of lung and pleural tumours

A

History and examination

Chest X-ray
Low specificity / positive predictive value
Many mimics of tumour
Tumour type not identifiable
20% of tumours not visible

CT / MRI
High specificity but expensive
Tumour type still not identifiable

Bronchoscopy

38
Q

Pathological Diagnosis of lung and pleural tumours

A

Sputum Cytology
Can be induced
Samples large volume of lung

Pleural Fluid
Drained for symptomatic relief
Diagnosis is an extra “bonus”

Bronchoscopic specimens
Best for central lesions
Bronchial washings and brushings
Bronchial or transbronchial biopsy
Transbronchial fine needle aspiration

Transthoracic Fine Needle Aspiration or biopsy
Peripheral lesions
CT guided

so usually:
Central:
Bronchoscopic diagnosis - Washings / Brushings / Biopsy

Peripheral:
CT guided transthoracic FNA / biopsy

Pleural:
Pleural fluid
CT guided transthoracic FNA / biopsy

39
Q

what are benign lung tumours often like?

A

Well-circumscribed usually single masses of one cell type

that are well-differentiated and show little cytological atypia

40
Q

clinical features of lung cancer

A

Usually presents at late stage:

Local tumour growth:			
Cough – mucosal irritation
Dyspnoea – atelectasis, obstruction 
Weight loss – tumour cachexia
Chest pain – invasion of chest wall

Metastatic tumour spread

Paraneoplastic phenomena

41
Q

how are lung cancers graded

A

by degree of differentiation.

Core teaching week A (17 decks)

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