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Y5 Path > Histopath - Respiratory disease > Flashcards

Histopath - Respiratory disease Flashcards

1
Q

3 types of cancer in order from most to least common

A

Squamous cell
Adenocarcinoma
Small cell carcinoma

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2
Q

How common is lung cancer in women? most common cancers in women?

A

Breast,
Bowel
Lung

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3
Q

Smoking has the strongest association with which types of lung cancer?

A

Squamous cell carcinoma

Small cell carcinoma

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4
Q

Smoke contains..??

A

. Tumor initiators - polycyclic aromatic hydrocarbons
. Tumour promoters - Phenols, nicotine
. Carcinogens - Nickel, Arsenic

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5
Q

Risk factors for smoking

A 
Smoking
Asbestos exposure
Radiation 
Head metals - arsenic, nickel
Genetics
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6
Q

Susceptibility genes for lung cancer

A
  • Nicotine addiction
  • Polymorphisms of cyp450 enzymes which metabolise carcinogens
  • Susceptibility to chromosomal breaks + DNA damage.
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7
Q

How can a pathologist look at cytology to determine type of lung cancer

A
  • Sputum
  • Bronchial washings
  • Pleural fluid
  • Endoscopic FNA of tumour/lymph nodes
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8
Q

How can a pathologist look at histology to determine type of lung cancer

A
  • Biopsy at bronchoscopy
  • Percutaneous CT-guided biopsy
  • Mediastinoscopy
  • Frozen section from a biopsy at time of surgery
  • Resection specimen from final excision
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9
Q

Describe the general changes in cells during development of SCC

A

Normal epithelium –> hyperplasia –> squamous metaplasia –> dysplasia –> carcinoma in situ –> invasive carcinoma

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10
Q

Special type of dysplasia seen in smoker with or without SqCC? what is seen on histology??

A

Angiosquamous dysplasia

  • Intramucosal CAPILLARY LOOPS
  • BM thickening + vascular budding
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11
Q

SqCC

  • Site?
  • Behaviour?
  • Histology?
  • Subtypes?
A
  • Tend to be central. Incidence of peripheral SCCs is rising
  • Local spread. late metastasis
  • Keratinisation and intracellular ‘prickles’
  • Papillary, Basaloid
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12
Q

Preceding histology to adenocarcinoma? describe it?

A

Atypical adenomatous hyperplasia

= proliferation of atypical larger cells lining the alveolar walls.

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13
Q

Progression of AAh

A

Atypical adenomatous hyperplasia –> non-mucionous –> mixed pattern adenocarcinoma

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14
Q

Risk factors for adenocarcionma

A

Far east, female, non-smoker

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15
Q

Adenocarcinomas

  • Site?
  • Behaviour
  • Histology
A
  • peripheral and more often MULTIPLE sites
  • Extrathoracic mets are common and early - 80% present with mets
  • Glandular differentiation and mucin vacuoles
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16
Q

2 main molecular pathways in adenocarcinoma?

A

. Smokers - K-ras + p53 mutation, DNA methylation

. Non-smokers - EGFR mutation/amplification

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17
Q

Large cell carcinomas - what are they?

A

Large cells which are poorly differentiated

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18
Q

Small cell carcinomas

  • RF?
  • Site?
  • Behaviour?
  • Histology and mutations?
A
  • Smoking is an RF
  • Central near bronchi
  • Presents with advanced disease + paraneoplastic syndromes
  • Small, poorly differentiated cells. p53 + RB1 mutations.
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19
Q

General prognosis and treatment of small cell lung carcinoma

A

2-4months if untreated. 10-20 months if treated.

- CHEMO + RADIO as most are too spread for surgery

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20
Q

NSCLC - general management?

A

20-30% suitable for surgery

LESS chemosensitive than SCLC

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21
Q

What drug do some adenocarcinomas respond well to?

A

anti-EGFR = tarceva

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22
Q

Which stains are useful for sub typing NSCLCs?

A
  • TTF1 = adenocarcinoma

- CK5/6 + P63 = SqCC

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23
Q

3 key molecular markers in lung cancer?

A
  1. ERCC1
  2. EGFR
  3. EML4-ALK1
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24
Q

ERCC1 - what is it? how is measuring its levels prove useful?

A

A protein which removes drug-DNA adducts.

High levels - cisplatin based chemo will be ineffective at treating the advanced NSCLC

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25
Q

EGFR - what does it do?

In whom is it upregulated?

A

Promotes angiogenesis, proliferation, cell migration

- asians, non-smokers, females

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26
Q

Drugs used in NSCLC which is EGFR positive

A

Cetuximab

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27
Q

Indication for use of TKI

A

Young/female/nonsmoker
Responder mutation!!
EGFR amplification
Recurrent adenocarcinoma

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28
Q

Contraindication for use of TKI

A 
Kras mutation
Resistance mutation(to TKI) = 790M
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29
Q

Significance of K-ras mutation

A

Predicts non-response to anti-EGFR therapy

Often seen in smokers

30
Q

Translocation that is a useful molecular marker in lung cancer?

31
Q

EML4-ALK lung cancers

  • what does this translocation result in?
  • who is affected? common histology?
A
  • Translocation –> increased Alk function
  • Seen in young/nonsmokers/adenocarcinoma
  • signet ring pattern or solid pattern
32
Q

Staging of lung cancer

A

TNM
Tumour (T1-4)
- the SIZE and invasion of pleura/pericardium

Nodes (N0-2)
- N1 vs 2 depends on extent of LN involvement

Metastasis (M0-1)

33
Q

Local effects of lung tumour - 3 main categories

A
  1. Bronchial obstruction
  2. Invasion of local structures
  3. Invasion of pleura/pericardium
34
Q

Effects of bronchial obstruction

A
  1. collapse of distal lung - SOB

2. impaired drainage of bronchus - cheese infection

35
Q

5 effects of invasion of local structures

A
  1. Oesophagus affected - dysphagia
  2. Large vessels - SVC syndrome w dusky skin
  3. Local airways and vessels - haemoptysis
  4. Chest wall - pain
  5. Nerves - Horners syndrome
36
Q

Effects of invasion of pleura/pericardium

A

Pleuritis/pericarditis - Cardiac compromise, SOB

37
Q

Physical effects of mets

A

Seizures
Skin lumps
Liver pain/deranged LFTs
Bone pain/fractures

38
Q

Paraneoplastic syndromes

A
  • Cushing from ACTH secretion
  • SIADH
  • PTH related peptides causing hypercalcemia
39
Q

Small cell carcinoma is associated with which paraneoplastic syndromes?

A

ACTH secretion –> Cushings

SIADH –> hyponatremia

40
Q

3 rare lung tumours

A

Rare epithelial tumours
Sarcomas
MALT type lymphoma

41
Q

Mesothelioma - what is it?

  • Epidem and time course?
  • Cause
  • Behaviour + prognosis
  • Sx?
A
  • Tumour of the pleura
  • presents 4/50 years post-asbestos exposure. Peaking now. MALES.
  • Fatal diagnosis
  • SOB, chest pain
42
Q

3 common congenital lung disorders

A
  1. Lung genesis + hypoplasia
  2. Tracheal/bronchial stenosis
  3. Congenital cysts
43
Q

3 main causes of pulmonary oedema

A
  1. Alveolar injury
  2. Left Heart Failure
  3. Neurogenic
44
Q

Cells seen on histology in pulmonary oedema?

A

Heart failure cells = iron laden macrophages

45
Q

What is diffuse alveolar damage in adults called? what can cause it?

A

ARDS

Infection, aspiration, trauma, irritant gas inhalation, shock, DIC, drug OD,

46
Q

Macroscopic appearance in diffuse alveolar damage?

A

Heavy, airless lung.

PLUM coloured

47
Q

pathophysiology of diffuse alveolar damage

A
  1. Diffuse alveolar damage leads to blood cells in alveoli
  2. Protein rich fluid in alveoli
  3. Hyaline membrane formation in alveoli
  4. Organising phase
48
Q

Complications of diffuse alveolar damage?

A

Superimposed infection

Fibrous scarring of lung –> bronchopulmonary dysplasia in RDS children

49
Q

Associations with hyaline membrane disease

A 
Prematurity
GDM
2nd twin
C-section
Birth asphyxia
50
Q

Complications of RDS

A
  • Infection
  • Resp failure
  • Interstitial emphysema (from over ventilation)
  • Bronchopulmonary dysplasia
51
Q

Causes and associations of asthma

A

allergens and atopy
NSAIDS
occupational
physical exertion (cold)

52
Q

macroscopic features in asthma

A

mucus plug

Overinflated lung

53
Q

Microscopic features of asthma (2 v important ones)

A

SM cell hyperplasia, eosinophils, excess mucus

  • Curshmann spirals
  • Charcot-Leyden crystals
54
Q

Definition of chronic bronchitis

A

Chronic productive cough

On most days for at least 3 months in 2 consecutive years

55
Q

Histology of chronic bronchitis

A

Goblet cell hyperplasia and dilatation of airways

56
Q

4 complications of chronic bronchitis

A
  1. Recurrent infections
  2. chronic hypoxia
  3. Pulm HT (RHF)
  4. Lung Ca
57
Q

Causes of emphysema

A

Smoking
a1 antitrypsin deficiency
IVDU, Marfans

58
Q

Pathogenesis of emphysema

A

Cigarette smoke –> neutrophil and macrophage activation –> elastase activity –> emphysema

59
Q

Difference in location affected in smoking vs a1 antitrypsin deficiency associated emphysema

A

Smoking - alveolar loss is centred on the bronchioles (centrilobular)

a1- diffuse loss of alveoli (panacinar)

60
Q

3 Complications of emphysema

A

Large bullae
Resp failure
Pulmonary HT

61
Q

Causes and associations of bronchiectasis

A
  • Post-infectious
  • Post-inflammatory
  • Abnormal host defence(1 ciliary dyskinesia)
  • Obstruction from tumour/stenosis
  • Secondary to fibrotic lung disease
62
Q

3 complications of bronchiectasis

A

recurrent infections
Haemoptysis
Amyloidosis

63
Q

CF - manifestations?

A 
Lung - infections, airway obstruction
GIT - meconium ileus, malabsorption
Liver - cirrhosis
Pancreas - pancreatitis
Infertility
64
Q

Bronchopneumonia vs lobar pneumonia

A

Broncho:

  • patchy, peribronchial distribution
  • elderly its
  • low virulence organisms

Lobar:
- v acute presentation
- Strep pneumonia
Widespread fibrinosuppurative consolidation

65
Q

Histopathology of lobar pneumonia

A
  1. congestion
  2. red hepatisation (neutrophils)
  3. grey hepatisation (fibrosis)
  4. Resolution
66
Q

5 Complications of pneumonia

A 
Abscess
Pleuritis
Empyema
Fibrous scarring
Septicaemia
67
Q

Atypical pneumonia

A

interstitial inflammation without accumulation of inflamm cells in alveoli

68
Q

What is a granuloma

A

Collection of histiocytes and macrophages +/- multinucleate giant cells

69
Q

Causes of granulomatous infections

A

TB!!!!

FUNGAL - cryptococcus, coccidioides, aspergillus

70
Q

Non-infectious granulomatous conditions

A
  • Sarcoid
  • aspiration
  • IVDU
  • OCCUPATIONAL lung disease
71
Q

Presumed pathogenesis of sarcoidosis

A

Abnormal host response to commonly encountered antigens

72
Q

lung involvement in sarcoid?

Diagnosis?

A

epithelioid and giant cell granulomas

  • in upper zones
  • fibrotic and cystic changes

-biopsy (non-caseating granulomas), elevated ACE

Y5 Path (64 decks)

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