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a path 3 > HISTO: Lung pathology > Flashcards

HISTO: Lung pathology Flashcards

1
Q

List 4 common airway diseases.

A

(1) Asthma
(2) COPD – Chronic Bronchitis
(3) Bronchiectasis
(4) Infections

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2
Q

Define asthma. List some causes.

A

Widespread reversible narrowing of the airways that changes in severity over short periods of time.

Causes:

  • Allergens/atopy
  • Pollution
  • Drugs (NSAIDs)
  • Occupational (gases)
  • Diet
  • Physical exertion
  • Intrinsic
  • Genetics
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3
Q

Describe the pathophysiology of asthma.

A
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4
Q

Whata are the macroscopic features of asthma?

A
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5
Q

What are the histological features of asthma?

A
  • Hyperaemia
  • Eosinophilic inflammation and goblet cell hyperplasia - mucus
  • Hypertrophic constricted muscle
  • Mucus plugging and inflammation
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6
Q

Define COPD/chronic bronchitis. What are the causes?

A

COPD is chronic injury to airways elicits local inflammation and reactive changes

Definition = chronic cough productive of sputum; most days for ≥3 months over ≥2 consecutive years

Causes = smoking, air pollution, occupational exposures

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7
Q

What are the histopathological features of CODP?

A
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8
Q

What are the complications of CODP/chronic bronchitis?

A
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9
Q

Define bronchiectasis. What are the most common causes?

A

Bronchiectasis – permanent abnormal dilatation of the terminal bronchi

Causes:

  1. Congenital (CF, ciliary dyskinesia [i.e. Kartagener’s syndrome])
  2. Inflammatory (post-infectious, obstruction, 2nd to bronchiolar disease and interstitial fibrosis, asthma)
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10
Q

What are the complications of bronchiectasis?

A

RHF - cor pulmonale

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11
Q

How common is CF?

A

1 in 2,500 but 1 in 20 are carriers (heterozygous carriers as it is recessive)

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12
Q

What is the aetiology of CF?

A

Chr 7q3 = CFTR gene (ion transporter protein)–> defective Cl- ion transfer so less water transfer to secretions

Affects all organs (from abnormally thick secretions):

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13
Q

What are the complications of CF? What are the most common infections?

A
  • Lung –> obstruction, respiratory failure, recurrent infection**, **bronchiectasis (90%), etc.
    • S. aureus H. influenzae
    • P. aeruginosa B. cepacia
  • GI tract - meconium ileus, malabsorption
  • Pancreas - pancreatitis, 2nd malabsorption
  • Liver - cirrhosis
  • Male infertility - blockage of sperm ducts
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14
Q

What is the management of CF? What is the prognosis?

A

Imrpoved treatment with PT, antibiotics, enzyme supplements, parenteral nutrition

Survival to 4th decade

Increased with lung transplantation

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15
Q

List 5 common parenchymal diseases.

A

(1) Pulmonary oedema and diffuse alveolar damage (include acute resp. distress syndrome and HMD)
(2) Infections
(3) COPD – emphysema
(4) Granulomatous diseases
(5) Fibrosing interstitial lung disease and occupational lung disease

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16
Q

Define pulmonary oedema. What are the causes?

A

= fluid accumulation in alveolar spaces

  • Causes – LHF, alveolar injury, neurogenic, high altitude
  • Pathology:
    • Intra-alveolar fluid on histology (left)
    • “Heart failure cells” = iron-laden macrophages (right)
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17
Q

What is seen on histopathology of pulmonary oedema?

A
  • Intra-alveolar fluid on histology (left)
  • “Heart failure cells” = iron-laden macrophages (right)
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18
Q

Define alveolar damage. What is the pathogenesis?

A

Pattern of acute diffuse lung injury in which patient present with rapid onset respiratory failure, requiring ventilation on ITU. CXR shown “white out” of all lung fields.

Pathogenesis: Acute damage to endothelium ± alveolar epithelium leading to an exudative inflammatory reaction

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19
Q

What are the causes of alveolar damage such as ARS and hyaline membrane disease?

A
  • Adults = acute respiratory distress syndrome / ARDS
    • Infection
    • Aspiration
    • Trauma
    • Inhaled irritant
    • Shock
    • Blood transfusion
    • DIC
    • Drug overdose
    • Pancreatitis
  • Neonates = hyaline membrane disease of the newborn / RDS (HMD of newborn = RDS)
    • Insufficient surfactant
    • Premature babies
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20
Q

What is the prognosis of diffuse alveolar damage?

A
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21
Q

What is the gross pathology of diffuse alveolar damage (DAD)?

A
  • Fluffy white infiltrates in all lung fields
  • Lungs expanded/firm
  • Plum-coloured lungs, airless
  • >1kg mass
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22
Q

What is the micropathology of DAD?

A
    1. Capillary congestion
    1. Exudative phase
    1. Hyaline membranes
    1. Organising phase
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23
Q

What are the patterns of baterial pneumonia?

A
  • Bronchopneumonia
  • Lobar pneumonia - aggressive phase, not seen as much
  • Abscess formation
  • Granulomatous inflammation
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24
Q

Describe the difference between bronchopneumonia and lobar pneumonia.

A
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25
Q

Who is usually affected by bronchopneumonia? What organisms are implicated?

A

Elderly

Low virulence organisms such as staph, H influenzae, strep and pneumococcus

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26
Q

What is the pathology of bronchopneumonia?

A

Patchy bronchial and peribronchial distribution, lower lobes, inflammation surrounding the airways themselves and is within the alveoli

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27
Q

What is the micro pathology of bronchopneumonia?

A
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28
Q

What is the pathology of lobar penumonia? What organism is the most likely culprit?

A

Affects entire lobe

Infrequently due to antibiotics

90-95% due to pneumococci (i.e. strep)

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29
Q

What is the micropathology/staging of lobar pneumonia?

A
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30
Q

What are the complications of lung infection?

A
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31
Q

What are the atypical causes of pneumonia? What is the pathology?

A
  • Mycoplasma, viruses (CMV if immunosuppressed, influenza), Coxiella, chlamydia, etc.
  • Interstitial inflammation without accumulation of intra-alveolar inflammatory cells and chronic inflammatory cells within alveolar septa with oedema ± viral infections
32
Q

Define emphysema. What are the causes?

33
Q

What is the pathogenesis of emphysema?

A

Alpha 1 antitrypsin usually protects but there is less in smokers or those with deficiencies.

34
Q

What is the gross histopathology of emphysema in smoking/a1 deficiency?

35
Q

What are the complications of emphysema?

36
Q

Define granulomatous disease/granuloma. What are the causes?

A

Granuloma = collection of histiocytes, macrophages ± giant multinucleate cells

Causes:

  • infection,
  • sarcoidosis,
  • foreign body aspiration / IVDU,
  • drugs,
  • occupational

TB must first be excluded before looking for other causes of granulomatous lung disease

37
Q

What parts of the body does sarcoid most commonly affect? What is the aetiology?

A
  • Affects: lungs, skin, lymph nodes and eyes
  • Pathogenesis: abnormal host immunological response to variety of commonly encountered antigens, probably environmental in origin
38
Q

What are the micro and macroscopic features of sarcoid? How is it diagnosed?

A
  • MICRO/MACRO - discrete epithelioid and giant cell granulomas, usually in upper zones of lung with a tendency to peri-lymphatic and peri-bronchial; in advanced disease becomes fibrocystic
  • DIAGNOSIS - non-caseating granuloma, elevated serum ACE, hypercalcaemia (1a-hydroxylase)
39
Q

Define idiopathic pulmonary fibrosis and give examples. What is it also known as? Describe the micro/macropathology.

40
Q

List some causes of fibrosing interstitial/occupational lung disease.

A
  1. Idiopathic pulmonary fibrosis/cryptogenic fibrosing alveolitis
  2. Extrinsic allergic alveolitis/”Farmer’s” lung (better over weekend away from work)
  3. Industrial lung disease/”Pneumoconiosis” (asbestosis, silicosis, coal-miner’s lung)
41
Q

What is the prognosis of idiopathic pulmonary fibrosis? How is it diagnosed?

A

Over 50% die in 2-3 years

High resolution CT and biopsy diagnosis

42
Q

What are the macro/microscopit features of idiopathic pulmonary fibrosis?

A
  • Macro = basal and peripheral fibrosis and cyst formation
  • Micro = interstitial fibrosis (varying stages)
43
Q

What is seen on histology in asbestosis?

A
  • Fine sub-pleural basal fibrosis with asbestos bodies in tissue
  • May also see pleural disease e.g. fibrosis, pleural plaques
44
Q

List 3 common pulmonary vascular disease.

A
  • (1) Pulmonary hypertension
  • (2) Pulmonary thromboembolism
  • (3) Pulmonary vasculitis
45
Q

What are the causes of pulmonary hypertension? What is the definition in mm/Hg?

46
Q

What are the morphological feaures of pulmonary HTN?

A
  • Morphological changes:
    • Eccentric intimal fibrosis
    • Thickening muscle wall
47
Q

What is the most common site for clot formation in PE?

A

DVT is the cause in 95%

48
Q

What are the symptoms of PE in small emboli? What are the consequences?

49
Q

What are the symptoms of PE in large emboli? What are the complications?

50
Q

Give 5 examples of non-thrombotic emboli which can cause PE.

A
  • Bone marrow
  • Amniotic fluid
  • Trophoblast
  • Tumour
  • Foreign body
  • Air
51
Q

Give some examples of pulmonary vasculitis.

A

Small-medium vessel disease e.g. EGPA

Leukocytoclastic vasculitis involving capillaries e.g. RhA

52
Q

What is the epidemiology of lung cancer?

A
  • Incidence in men dropping
  • Incidence in women rising (women took longer to quit smoking)
53
Q

What sites can lung tumours arise in?

A
  • Airways (SCC)
  • Peripheral alveolar spaces (Adenocarcinoma)
  • SCLC can arise either centrally or peripherally
  • Mesothelioma is a tumour of the pleura
54
Q

Give examples of benign and malignant lung tumours. What are the most common types in smokers and non-smokers?

A
  • Benign Tumours – no metastasis, local complications (i.e. obstruction)
    • Chondroma
  • Malignant Tumours – metastasise, most commonly epithelial (90-95%):
    • Squamous cell carcinoma (30%) = smokers, central, spread locally, late metastasis, PTHrP
    • Adenocarcinoma (30%) = non-smokers, peripheral, early metastasis
    • Large cell carcinoma (20%)
    • Small Cell Lung Carcinoma (20%)= smokers, central, SIADH, ACTH, Lambert-Eaton Myasthenic Syndrome (LEMS)
55
Q

What % of lung cancer in smokers is due to passive smoking? What substances in smoke are carcinogenic?

A

25% of lung cancer in non-smokers is attributed to passive smoking

Smoke contains:

  • Tumour initiators (polycyclic aromatic hydrocarbons)
  • Tumour promoters (nicotine)
  • Complete carcinogens (nickel, arsenic)
56
Q

What % of lung cancer is in non-smokers? What are the risk factors?

A

10-20%

  • Asbestos
  • Radiation (radon exposure)
  • Air pollution
  • Heavy metals
  • Genetics (familial lung cancers are rare)
  • Susceptibility genes:
    • Chemical modification of carcinogens
    • Susceptibility to chromosomal damage
    • Nicotine addiction
57
Q

What are the steps leading to development of carcinoma?

A
  • Metaplasia –> Dysplasia –> Carcinoma in situ –> Invasive carcinoma
  • Due to an accumulation of gene mutations
58
Q

Describe the progression of the phenotype of SCC.

A

Squamous cells do not have cilia so mucus production can build up and carcinogens may be trapped within this and accumulate.

59
Q

What % of lung cancer consists of SCC? What is its pattern of distribution? What hormone may be produced?

A

~30% of all lung cancers

Central around bronchial epithelium, spreads locally with late metastasis. But there is increasing incidence of peripheral SCC

PTHrP

60
Q

Describe the macro/microscopic features of invasive adenocarcinoma of the lung.

A
  • Gland formation
  • Papillae formation
  • Mucin
  • Histology shows evidence of glandular differentiation
  • Affect terminal airways with a multi-centric pattern (many tumours at different stages of differentiation)
61
Q

Which molecular pathways are implicated in the development of adenocarcinoma?

A

In smokers- K-ras issues with DNA methylation and p53

In non-smokers - EGFR mutations (important to identify as they are a drug target)

62
Q

Which populations is invasive adnocarcioma more common in?

A
  • Incidence increasing
  • Far east
  • Females
  • Non-smokers
63
Q

Is metastasis common in adenocarcinoma?

A

Yes, extrathoracic metastases common and early

64
Q

Describe the progression of atypical adenomatous hyperplasia (AAH) of the lung.

A

Precursor lesion –> proliferation of atypical cells lining the alveolar wall –> increase in size and eventually becomes invasive

  1. AAH
  2. Non-mucinous adenocarcinoma in-situ
  3. Mixed pattern invasive adenocarcinoma
65
Q

Describe the macro/microscopic features of large cell carcinoma.

A

Peripheral or central

No histological evidence of glandular/squamous cells BUT ON EM may show evidence of glandular, squamous or neuroendocrine differentiation i.e. poorly differentiated

Composed of large cells

66
Q

What % of lung cancer is made up by large cell carcinoma? What is the prognosis?

A

10%

Poor prognosis

67
Q

What % of lung cancer is made up by small cell carcinoma? What are risk factors for this?

A

20%

Smoking is closely associated

68
Q

Where are small cell lung carcinomas usually located? Describe their micro/macroscopic features.

A

Central near the bronchi

Small poorly differentiated cells

69
Q

Why is prognosis in small cell lung cancer poor? What are the complications?

A

80% present with advanced disease/ chemosensitive but come back very quickly

Complications:

  • Can cause paraneoplastic syndromes
  • Necrotic core because they quickly outgrow their blood supply
70
Q

Which mutations are commonly found in small cell carcinoma?

A

p53 and RB1

71
Q

Compare the prognosis of small cell and non-small cell lung carcinomas.

A

Small cell:

  • 2-4 month survival untreated, 10-20 months on treatment usually by chemotherapy (surgery uncommon as usually spread by time of diagnosis)

Non-small cell:

  • More chemosensitive and early stage 1 tumours have 60% 5-year survval BUT late stage 4 have 5% 5-year survival
72
Q

What are the molecular targets for treating adenocarcinoma and SCC? What is the consequence of treating SCC as adenocarcinoma?

A

Adenocarcinoma molecular targets:

  • EGFR mutation (responder or resistance) - tyrosine kinase therapy
  • ALK translocation (responds to Crizotinib)
  • Ros1 translocation
  • PD-L1 expression

Squamous cell carcinoma targets:

  • PDL1 expression

​If SCC is treated with biologics used for adenocarcinoma e.g. bebevacizumab, it can cause fatal haemorrhage.

73
Q

What types of cytology and histology are used in lung cancer diagnosis?

A
  • Cytology – looking at cells:
    • Sputum
    • Bronchial washings and brushings
    • Pleural fluid
    • Endoscopic fine needle aspiration of tumour/enlarged lymph nodes
  • Histology – looking at tissue:
    • 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 not accessible otherwise - frozen section
    • Resection specimen - confirm excision and staging
74
Q

What are the complications of high levels of PD1/PDL1 expression in SCC?

A

High levels of PD1/PDL1 can inhibit the immune response

75
Q

What is mesothelioma and what is the most common cause?

A

Malignant tumour of the PLEURA

Associated with exposire to asbestos - there is a long lag between exposure and disease development

76
Q

What % of cancer deaths are made up by mesothelioma? Who is it more common in? What is the prognosis?

A

<1% of cancer deaths but peaked around 2010-2020

M:F ratio 3:1 (50-70years)

Essentially fatal

77
Q

What are the endocrine/non-endocrine features of paraneoplastic syndrome?

A

Endocrine:

  • (1) Antidiuretic hormone (ADH) –> hyponatremia (SCC)
  • (2) Adrenocorticotropic hormone (ACTH) –> Cushing’s syndrome (SCC)
  • (3) Parathyroid hormone-related peptide –> hypercalcaemia (SCC)
  • (4) Other:
    • Calcitonin –> hypocalcaemia
    • Gonadotropins –> gynecomastia
    • Serotonin –> “carcinoid syndrome” (especially carcinoid tumours; rarely SCC)

Non-endocrine:

  • Haematological/coagulation defects, skin, muscular, miscellaenous

a path 3 (89 decks)

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