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Histopathology > Histopathology 12 - Respiratory pathology > Flashcards

Histopathology 12 - Respiratory pathology Flashcards

1
Q

What are the causes of pulmonary hypertension?

A
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2
Q

What causes diffuse alveolar damage? How does diffuse alveolar damage appear on CXR?

A

Caused by: a) ARDS in adults and b) hyaline membrane disease of the newborn in neonates

Firm and expanded lungs

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3
Q

What are the acute features of the airway in asthma?

A

Acute bronchospasm
Acute mucosal oedema
Inflammation

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4
Q

What are the chronic features of the airway in asthma?

A

Muscular hypertrophy
Airway narrowing
Mucus plugging

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5
Q

What are the features of COPD?

A

Chronic bronchitis and emphysema

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6
Q

Describe the features of chronic bronchitis

A

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

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7
Q

How does chronic hypoxia affect the heart?

A

Pulmonary hypertension —> right heart failure

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8
Q

What is emphysema?

A

Permanent loss of the alveolar parenchyma distal to the terminal bronchiole

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9
Q

What is the genetic association of emphysema?

A

Alpha 1 anti-trypsin

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10
Q

Recall the pathophysiology of emphysema

A

Smoking causes inflammation
Neutrophil and macrophage involvement
Proteases recruited
Breakdown of epithelium

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11
Q

What does lung bullous rupture cause?

A

Pneumothorax

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12
Q

What is bronchiectasis?

A

Permanent abnormal dilatation of bronchi with inflammation and fibrosis into adjacent parenchyma

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13
Q

Recall the complications of bronchiectasis

A

Haemoptysis
Pulmonary HTN
RHF
Amyloidosis secondary to chronic inflammation

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14
Q

Which condition has the strongest association with bronchiectasis?

A

Cystic fibrosis

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15
Q

What is bronchopneumonia?

A

Inflammation centred around airway

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16
Q

Where does bronchopneumonia often affect?

A

Lower lobes

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17
Q

Which type of pneumonia has become much rarer since ABx have been in use?

A

Lobar pneumonia

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18
Q

What is empyema?

A

Infected pleural effusion

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19
Q

Which type of pneumonia is most likely to cause interstitial inflammation?

A

Atypical pneumonias

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20
Q

What are the most common lung tumours?

A

Epithelial tumours - non small cell and small cell

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21
Q

What are the 3 subtypes of non-small cell lung cancer?

A

Adenocarcinoma
Squamous cell carcinoma
Large cell carcinoma

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22
Q

Which 2 types of lung cancer are most associated with smoking?

A

Squamous cell
Small cell

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23
Q

Where is squamous cell carcinoma most likely to develop in the lung?

A

Centrally

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24
Q

Where do adenocarcinomas typically develop?

A

Peripherally

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25
Q

Which mutations are smokers most likely to develop in adenocarcinomas?

A

K ras
p53

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26
Q

Which mutations are non-smokers most likely to develop in adenocarcinomas?

A

EGFR

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27
Q

Which type of lung cancer is assoiated with the most paraneoplastic syndromes?

A

Small cell

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28
Q

Which mutations are most likely to develop in squamous cell carcinomas?

A

They’re not - it’s the adenocarcinomas that tend to get the mutations

29
Q

What type of lung cancer is the most common in the UK?

A

Squamous cell carcinoma

30
Q

List the obstructive lung diseases

A
  1. chornic bronchitis
  2. bronchiectasis
  3. asthma
  4. emphysema
  5. small airway disease/ bronchiolitis
31
Q

What are the causes of bronchiectasis?

A

Inflammatory
o Post-infectious (e.g. pertussis) o Abnormal host defense 1º (hypogammaglobulinaemia) and 2º (chemotherapy, NG)
o Obstruction (extrinsic/intrinsic/middle lobe syn.)

o Post-inflammatory (aspiration)

o Secondary to bronchiolar disease (bronchiolitis obliterans) and interstitial fibrosis (CFA, sarcoidosis)

o Systemic disease (connective tissue disorders)

o Asthma
● Congenital
o Cystic fibrosis o Primary ciliary dyskinesia o Hypogammaglobulinema o Young’s syndrome = rhinosinusitis, azoospermia and bronchiectasis

32
Q

Which infectious pathogen is most likely to cause bronchiectasis?

A

Staph aureus

33
Q
A
34
Q

Which obstructive resp disease causes haemptysis?

A

Bronchiectasis

35
Q

WHat are the features of restrictive lung disease?

A
  • decreased CO diffusion capacity
  • decreased lung volume
  • decreased lung compliance
36
Q

Typical presentation of interstitial lung disease

A
  • fine end inspiratory crackles
  • chronic shortness of breath
  • cyanosis, pulmonary HTN and cor pulmonale
37
Q

What is the CT appearance of interstitial lung disease?

A

Honeycombing

38
Q

What can you split up the causes of interstitial lung disease into?

A

1. fibrosing

a. Cryptogenic Fibrosing Alveolitis/ Idiopathic pulmonary fibrosis
b. Pneumoconiosis
c. Cryptogenic organizing pneumonia
d. Associated with connective tissue disease
e. Drug-induced
f. Radiation pneumonitis
2. granulomatous
- sarcoid
- extrinsic allergic alveolitis
- associated with vasculitides - wegener’s, churg strauss, microscopic polyangiitis

39
Q
A
40
Q

Histology of idiopathic pulmonary fibrosis

A

Usual Interstitial Pneumonia
o Progressive patchy interstitial fibrosis with loss of normal lung architecture and
honeycomb change, beginning at periphery of the lobule, usually sub-pleural

o Hyperplasia of type II pneumocytes causing cyst formation – honeycomb fibrosis

41
Q

Tx of idiopathic pulmonary fibrosis

A

steroids, cyclophosphamide, azathioprine, pirfenidone (not especially effective)

42
Q

Where does pneumoconiosis affect the lungs vs. asbestosis?

A

Pneumocniosis- upper lobes

Asbestosis- lower lobes

43
Q

Pathophsyiology of extrinsic allergic alevolitis

A

Group of immune-mediated lung disorders caused by intense/prolonged exposure to inhaled ORGANIC antigens → widespread ALVEOLAR inflammation (cf asthma = airway inflammation).

Extrinsic allergic alveolitis is typically an occupational lung disease and can be acute or chronic.

44
Q

Presetation of EAA

A

inhalation of antigenic dust in SENSITISED individual -→ systemic symptoms (fever, chills, chest pain, SOB, cough) within hours of exposure, usually settle by following day.

Progresses to chronic EAA.

45
Q

Types of EAA

A

e.g. Farmers lung (mouldy hay/grain/silage – Saccharopolyspora rectivirgula)

Pigeon fancier’s lung (proteins in excreta/feathers)

Humidifier’s lung (heated water reservoirs – thermactinomyces spp.),

Malt-workers lung (germinating barley – Aspergillus clavatus/fumigatus)

Cheese washer’s lung (mouldy cheese – Aspergillus clavatus/penicillium casei).

46
Q

Type of antigen in pneumoconiosis vs EAA

A

pneumoconiosis- inorganic antigen (mineral dust or coal)

eaa- organic antigens

47
Q

What are the 3 patterns of pneumonia?

A
  1. bronchopneumonia- inflammation around the airways
  2. lobar pneumonia - entire lobe is affected. basc a more severe version; incidence is lower now
  3. atypical - affects the INTERSTITIUM. interstitial pneumonitis; without any intra-alevolar cells
48
Q

Histology and Stages of lobar pneumonia

A

Fibrinosuppurative consolidation.

Stages:

  1. Consolidation;
  2. RedHepatisation (neutrophilia);
  3. Grey Hepatisation (Fibrosis);
  4. Resolution
49
Q

Male female preponderance of squamous cell carcinoma vs adenocarcinoma

A

squamous cell carcinoma- more common in males

adenocarcinoma- more common in females

50
Q

Where in the lungs do small cell carcinomas occur?

A

Centrally, proximal bronchi (similar to squamous)

51
Q

Which cells du small cell caricnomas arise from?

A

neuroendocrine cells

52
Q

paraneoplastic syndromes of small cell carcinoma

A
  1. etcopic acth secretion
  2. lambert-eaton- immune system attacks the neuromuscular junctions
  3. cerebellar degeneration
53
Q

between squamous cell carcinoma and adenocarcinoma which one is more aggressive?

A

squamous: metastasises late. less responsive to chemo.
adeno: metastasises early. more responsive to chemo.

*one positive, one negative for each one*

54
Q

Mutations in small cell carcinoma

A

p53 and rb1

55
Q

how quickly does small cell carcinoma metastasise?

A

quite quickly

poor prognosis despite being chemosensitive

56
Q

where does small cell carcinoma metastaisse to?

A

bone

adrenal

liver

brain

57
Q

histology of large cell carcinoma

A

Poorly differentiated malignant epithelial tumour – large cells, large nuclei, prominent nucleoli.

Histology – no evidence of glandular or squamous differentiation. Poor prognosis.

**basic poorly differentiated**

58
Q

what paraneoplastic syndrome is this: flushing, diarrhoea, bronchoconstriction?

A

carcinoid syndrome - serotonin release

59
Q

which mutation, if present, allows targeted treatment?

A

EGFR mutation- present usually in adenocarcinoma

target with tyrosine kinase inhibitor

60
Q

What % of pulmonry bed needs to be occluded to cause shock and death from pulmonary emboli?

A

60%

61
Q

What is a saddle embolus?

A

Blocks pulmonary trunk

62
Q
A
63
Q

what are heart failure cells?

A

iron laden macrophages found in pulmonary oedema

64
Q
A
65
Q

What enzyme does alpha 1 antitrypsin deficiency affect?

A

neutrophil elastase

66
Q

Signet ring sign positive?

A

Bronchiectasis

67
Q

Which cancer is associated with oat shaped cells on biopsy?

A

Small cell lung cancer

68
Q

Diagnostic investigation for pulmonary fibrosis?

A

High resolution chest CT

**changes not seen on x-ray or standard CT**

69
Q

Intracellular desmosomes/ bridges (prickles) - classic

A

squamous cell carcinoma

Histopathology (18 decks)

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