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YEAR 5: Histopathology - PK Edited > Histo: Lung Pathology > Flashcards

Histo: Lung Pathology Flashcards

1
Q

What type of epithelium lines the airways?

A

Ciliated respiratory epithelium

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2
Q

Which types of cells line the alveoli?

A

Type 1 pneumocytes

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3
Q

What is pulmonary oedema?

A

Accumulation of fluid in the alverolar spaces either due to leaky capillaries or back pressure from a failing left ventricle

This leads to poor gas exchange

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4
Q

List some causes of pulmonary oedema.

A
  • Left heart failure
  • Alveolar injury (e.g. drugs, smoke from a fire)
  • Neurogenic following head trauma
  • High altitude at a rapid pace (physiological response)
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5
Q

What is the main histological feature of pulmonary oedema?

A

Intra-alveolar fluid

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6
Q

List some causes of acute respiratory distress syndrome in adults.

A
  • Infection
  • Aspiration
  • Trauma
  • Inhaled irritant gases
  • Shock
  • DIC
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7
Q

What causes hyaline membrane disease in newborns?

A

Lack of surfactant (mainly in premature babies)

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8
Q

On a cellular level, what insult results in ARDS?

A

Acute damage to the endothelium and/or alveolar epithelium

The basic pathology is the same regardless of cause: diffuse alveolar damage

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9
Q

Describe the appearance of the lungs on post-mortem examination in a patient who died from ARDS.

A
  • Plum-coloured
  • Heavy (>1kg)
  • Airless
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10
Q

Outline the pathophysiology of ARDS.

A
  • Exudative phase - the lungs become congested and leaky
  • Hyaline membranes - form when serum protein that is leaked out of vessels end up lining the alveoli
  • Organising phase - organisation of the exudates to form granulation tissue sitting within the alveolar spaces
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11
Q

What are the outcomes of ARDS?

A
  • Death
  • Superimposed infection
  • Resolution (restoration of normal lung function)
  • Residual fibrosis (leads to chronic respiratory impairment)
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12
Q

Define asthma.

A

Chronic inflammatory airway disorder with recurrent reversible episodes of widespread narrowing of the airways

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13
Q

What is the term used to describe a severe attack of asthma where attacks occur one after the other?

A

Status asthmaticus

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14
Q

List some non-atopic triggers of asthma.

A
  • Air pollution
  • Occupational
  • Exercise
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15
Q

List some acute changes seen in asthma.

A
  • Bronchospasm
  • Oedema
  • Hyperaemia
  • Inflammation
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16
Q

List some chronic changes seen in asthma.

A
  • Muscular hypertrophy
  • Airway narrowing
  • Mucus plugging
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17
Q

Describe the main histological features of asthma.

A
  • Lots of eosinophils and mast cells
  • Goblet cell hyperplasia
  • Mucus plugs within airways
  • Thickening of bronchial smooth muscle and dilatation of blood vessels (hyperaemia)
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18
Q

Define chronic bronchitis.

A

Chronic cough productive of sputum presents for most days for at least 3 months over 2 consecutive years

causes dilatation of the airways and excess mucus production

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19
Q

List some histological features of chronic bronchitis.

A
  • Diluted airways
  • Mucus gland hyperplasia
  • Goblet cell hyperplasia
  • Mild inflammation
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20
Q

List some complications of chronic bronchitis.

A
  • Recurrent infections (this is what they present with, and die with!)
  • Chronic respiratory failure
  • Chronic hypoxia resulting in pulmonary hypertension and right heart failure (cor pulmonale)
  • Increased risk of lung cancer (independent of smoking)
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21
Q

Define emphysema.

A

Permanent loss of alveolar parenchyma distal to the terminal bronchiole

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22
Q

List some causes of alveolar damage that can lead to emphysema.

A
  • Smoking (damage to alveolar epithelium)
  • Alpha-1 antitrypsin deficiency
  • Rare: cadmium exposure, IVDU, connective tissue disorder
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23
Q

Describe how the pattern of alveolar damage is different with smoking compared to alpha-1 antitrypsin deficiency. And what is the pathophysiology of damage in smoking and A1AT

A
  • Smoking - centrilobular damage (where the smoke goes)
  • Alpha-1 antritrypsin deficiency - panacinar (throughout the lungs)

Smoking and alpha q antitrypsin means that proteases are no longer inhibited and this causes tissue damage

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24
Q

List some complications of emphysema.

A
  • Bullae (can rupture to cause pneumothorax)
  • Respiratory failue
  • Chronic hypoxia —> Pulmonary hypertension and right heart failure
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25
Q

Define bronchiectasis.

A
  • Permanent abnormal dilatation of the bronchi with inflammation and fibrosis extending into adjacent parenchyma

(chronic bronchitis is basically less severe)

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26
Q

Which part of the lungs tends to be affected most frequently in idiopathic bronchiectasis?

A

Lower lobe

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27
Q

List some causes of bronchiectasis.

A
  • Infection (MOST COMMON)
    • Post-infectious (e.g. CF)
    • Abnormal host defence (e.g. chemotherapy, immunodeficiency)
    • Ciliary dyskinesia
  • Obstruction
  • Post-inflammatory (aspiration)
  • Interstitial disease (e.g. sarcoidosis)
  • Asthma
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28
Q

List some complications of bronchiectasis.

A
  • Recurrent infections
  • Haemoptysis
  • Pulmonary hypertension and right heart failue
  • Amyloidosis
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29
Q

Where is the CFTR gene found?

A

7q3

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30
Q

What is the most common mutation associated with CF?

A

Delat F508

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31
Q

List some clinical manifestations of CF.

A
  • GI - meconium ileus, malabsorption
  • Pancreas - pancreatitis
  • Liver - cirrhosis
  • Male reproductive system - infertility
  • Recurrent chest infections
32
Q

List some causes of community-acquired bacterial pneumonia.

A
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Mycoplasma
33
Q

List some causes of hospital-acquired bacterial pneumonia.

A

Gram negatives (Klebsiella, Pseudomonas)

34
Q

Which types of bacteria tend to be implicated in aspiration pneumonia?

A

Mixture of aerobic and anaerobic

35
Q

What is bronchopneumonia?

A
  • Infection is centred around the airways
  • Tends to be associated with compromised host defence (mainly the elderly) and is caused by low virulence organisms (e.g. Staphylococcus, Haemophilus, Pneumococcus)
  • It will show patchy bronchial and peribronchial distribution often involving the lower lobes
36
Q

What is lobar pneumonia?

A
  • Infection is focused in a lobe of the lung
  • 90-95% caused by S. pneumoniae
  • Widespread fibrinosuppurative consolidation
37
Q

What are the histopathological stages of lobar pneumonia?

A
  • Stage 1: congestion (hyperaemia and intra-alveolar fluid)
  • Stage 2: red hepatisation (hyperaemia, intra-alveolar neutrophils)
  • Stage 3: grey hepatisation (intra-alveolar connective tissue)
  • Stage 4: resolution (restoration of normal tissue architecture)
38
Q

List some complications of pneumonia.

A
  • Abscess formation
  • Pleural effusion
  • Empyema
  • Fibrous scarring
  • Septicaemia
39
Q

What is a granuloma?

A

Collection of macrophages and multi-nucleate giant cells

40
Q

Describe the histological appearance of atypical pneumonia.

A
  • Interstitial inflammation (pneumonitis) without accumulation of intra-alveolar inflammatory cells

NOTE: causes include Mycoplasma, viruses, Coxiella and Chlamydia

41
Q

What is a long term consequence of repeated small pulmonary emboli?

A

Pulmonary hypertension

42
Q

List some types of non-thrombotic emboli.

A
  • Bone marrow
  • Amniotic fluid
  • Trophoblast
  • Tumour
  • Foreign body
  • Air Fat
43
Q

What are the main types of lung cancer?

A
  • Non-small cell carcinoma
    • Squamous cell carcinoma (30%)
    • Adenocarcinoma (30%)
    • Large cll carcinoma (20%)
  • Small cell carcinoma (20%)
44
Q

What components of cigarette smoke are responsible for its carcinogenicity?

A
  • Tumour initiators (polycyclic aromatic hydrocarbons)
  • Tumour promoters (nicotine)
  • Complete carcinogens (nickel, arsenic)
45
Q

Which types of lung cancer are most strongly associated with smoking?

A
  • Squamous cell carcinoma
  • Small cell carcinoma

S, S, S!

46
Q

Which type of lung cancer tends to occur in non-smokers?

A

Adenocarcinoma

47
Q

List some risk factors for lung cancer.

A
  • Smoking
  • Abestos
  • Radiation
  • Air pollution
  • Heavy metals
  • Susceptibility genes (e.g. nicotine addiction)
48
Q

Describe the sequence of histological changes that results in lung cancer.

A

Metaplasia → Dysplasia → Carcinoma in situ → invasive carcinoma

49
Q

What feautre of squamous epithelium makes it vulnerable to undergoing malignant changes?

A
  • It does not have ciliar leading to a build-up of mucus
  • Within the mucus carcinogens accumulate
50
Q

Where do squamous cell carcinomas tend to arise?

A

Centrally - arising from the bronchial epithelium (which undergoes metaplasia to turn into a more resilient squamous cell to protect itself from the smoke)

NOTE: there is an increasing incidence of peripheral squmous cell carcinomas (possibly due to deeper inhalation of modern cigarette smoke)

51
Q

Where does adenocarcinoma of the lung tend to arise?

A

Peripherally - around the terminal airways

NOTE: it tends to be multi-centric and extra-thoracic metastases are common and occur early

52
Q

What is the precursor lesion for adenocarcinoma of the lung?

A

Atypical adenomatous hyperplasia (proliferation of atypical cells lining the alveolar walls)

53
Q

Which mutations are associated with adenocarcinoma in smokers?

A
  • Kras
  • Issues with DNA methylation
  • P53
54
Q

Which mutation is associated with adenocarcinoma in non-smokers?

A

EGFR

55
Q

What is large cell carcinoma of the lung?

A
  • Poorly differentiated tumour composed of large cells
  • There is no evidence of squamous or glandular differentiation
  • It has a poor prognosis
56
Q

Where does small cell lung cancer tend to arise?

A
  • Central - around the bronchi

NOTE: 80% present with advanced disease (i.e. brain mets or bone) and it carries a poor prognosis

57
Q

List some common mutations seen in small cell lung cancer.

A

P53

RB1

58
Q

What is the difference in the chemosensistivity of small cell lung cancer and non-small cell lung cancer?

A
  • Small cell - sensitive (but recur so often even after chemotherapy)
  • Non-small cell - not very chemosensitive
59
Q

Which molecular changes are important to test for in adenocarcinoma?

A
  • EGFR (responder or resistance)
  • ALK translocation
  • Ros1 translocation
  • PDL1 expression
60
Q

Why is it important to know the tumour type precisely?

A

Some treatments can be fatal if the cancer is misdiagnosed

E.g. bevacizumab can cause fatal haemorrhage if used for squamous cell carcinoma

61
Q

What is cancer of the pleura?

A

Mesothelioma

62
Q

what lung pathology do vapers get?

A

acute lung injury –> ITU admission

63
Q

right and left lung lobes?

A

right has 3 left has 2

64
Q

causes of chronic bronchitis?

A

chronic injury which elicits local inflammation - i.e. smoking, air pollution or occupational exposures

65
Q

Inheritance pattern of CF

A

Autosomal recessive

66
Q

what is a MAJOR risk factor for bronchiectasis

A

cystic fibrosis

67
Q

what lung disorder are you at a large risk factor for in CF

A

bronchiectasis

68
Q

CXR - white out of all lung fields - diagnosis?

A

diffuse alveolar damage (DAD) = acute respiratory distress syndrome = hyaline membrane disease of the newborn

lungs are filled with fluid and exudate

69
Q

Causes of granulomatous lung disease

A

infection
sarcoid
foreign body
IVDU

70
Q

Three important types of fibrosing lung disease?

A

Idiopathic pulmonary fibrosis (cryptogenic fibrosing alveolitis)
- 50% dead in 2-3y

Extrinsic allergic alveolitis (farmers’ lung)

Industrial lung diseases (pneumoconiosis)

71
Q

What is included in virchow’s triad

A

Vessel damage
increased coagulation
Promotion of stasis

72
Q

what is the pulmonary HTN bp

A

> 25mmHg at rest - pulmonary circulation usually reasonably low pressure

73
Q

survival for small cell lung cancer?

A

1 year - 18m
Chemo works but it recurs so often

74
Q

what treatment for EGFR mutation positive lung cancers?

A

TKI therapy (tyrosine kinase inhibitors)

75
Q

What does the tumour having high levels of PDL1 mean?

A

It means you can give immunotherapy and help their own immune system make t cells against this marker

76
Q

Which molecular changes are important to test for in squamous cell carcinoma?

A

PDL1

77
Q

what % of lung cancers in the UK develop in non-smokers

A

10-20%

YEAR 5: Histopathology - PK Edited (29 decks)

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