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Pathology by week > W9 - Respiratory pathology > Flashcards

W9 - Respiratory pathology Flashcards

1
Q

Name the 3 classifications adult non-neoplastic lung diseases are divided into?

A

1. Airway diseases i.e. asthma, COPD, bronchiectasis

2. Parenchymal disease i.e. pulmonary oedema & diffuse alveolar damaage (ARDS, HMD), COPD-emphysema, granulomatosis diseases, fibrosing intersititial lung disease

3. Pulmonary vascular disease

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2
Q

What are some causes (7) of asthma

A
  1. Allergens and atopy (house dust mite)
  2. Pollution
  3. Drugs - NSAIDs
  4. Occupational - inhaled gases/fumes
  5. Diet
  6. Physical exertion - “cold”
  7. Intrinsic/Underlying genetic factors
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3
Q

Explain the pathogenesis behind asthma, from sensitisation to allergen to later re-exposure.

A

Sensitisation to allergen = allrgen picked up by DC => TH2 primed => B cell primed => B cell class switch to IgE secreting => mast cell + eosinophils recruited and activated.

Re-exposure to allergen = allergen-specific IgE bind to alletgen => mast cells degranulate on contact with antigen => mediators released cause vascular permeability, eosinophil and mast cell recruitment => bronchospasm

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4
Q

What physiological changes (3) take place in the lung in the late phases of asthma?

A

Late phases:

1) tissue damage
2) increased mucus production
3) muscle hypertrophy

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5
Q

Name 3 mascropcopic features of asthma in asthma-related deaths

A
  1. Mucus plug
  2. Hyperinflated lung
  3. Mucus plug in-situ
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6
Q

Name 4 histological features of asthma

A
  1. Hyperaemia (increased blood flow to lung tissue)
  2. Eosinophilic inflammation + goblet cell hyperplasia (mucus)
  3. Hypertrophic contricted muscle
  4. Mucus plugging
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7
Q

What are common causes (3) of COPD?

A
  1. Smoking
  2. Air pollution
  3. Occupational exposures
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8
Q

The 2 main types of COPD are…

A

Chronic bronchitis

Emphysema

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9
Q

3 histological features of COPD Chronic bronchitis

A
  1. Dilatation of airways
  2. Hypertrophy mucous glands
  3. Goblet cell hyperplasia
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10
Q

4 possible complications of chronic bronchitis COPD

A
  1. Repeated infections
  2. Chronic hypoxia
  3. Pulmonary hypertension and cor pulmonale (due to chronic hypoxia)
  4. Increased risk of lung cancer
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11
Q

What are the common causes of bronchiectasis?

A

1. Congenital

2. Inflammatory:

A) Post-infectious (esp in children or CF patients)

B) CIliary dyskinesia - primary and 2ndary

C) Obstruction (extrinsic/intrinsic)

D) Post-inflammatory (aspiration)

E) Secondary to bronchiolar disease & interstitial fibrosis (sarcoidosis)

F) systemic disease (connective tissue disorders)

G) asthma

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12
Q

Name 4 complications of bronchiectasis

A
  1. Recurrent infections
  2. Haemoptysis
  3. Pulmonary hypertension and cor pulmonale
  4. 2ndary amyloidosis
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13
Q

What are the main causes (4) of pulonary oedema?

A
  1. Left heart failure (typically acute-on-chronic LHF)
  2. Alveolar injury
  3. Neurogenic (i.e. post-severe head injury)
  4. High altitude (poor compensation of lungs => flooding of lungs)
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14
Q

Which is more severe - pulmonary oedema or diffuse alveolar damage? and why?

A

Diffuse alveolar damage - ACUTE diffuse lung injury with rapid onset of respiratory failure, often requiring ventilation on ITU.

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15
Q

What is a typical CXR finding of diffuse alveolar damage?

A

White-out on all lung fields

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16
Q

What is the pathogenesis behind diffuse alveolar damage?

A

Acute damage to endothelium +/- alveolar epithelium => exudative inflammatory reaction

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17
Q

What does diffuse alveolar damage cause in 1) neonates and 2) adults

A

1) Neonates => Hyaline membrane disease of newborn
2) Adults => Acute respiratory distress syndrome (ARDS) aka “Shock lung”

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18
Q

What is the cause of hyaline membrane disease of newborn? Which group of neonates is it more common in?

A

insufficient surfactant production => sitff lungs => 2ndary alveolar epithelial damage

premature babies

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19
Q

What are the causes of ARDS (7) in adults?

A

Numerous causes:

  1. Infection (local (COVID) or generalised sepsis)
  2. Massive aspiration
  3. Trauma
  4. Inhaled irritant gases (smoke)
  5. Shock (hypovolaemic)
  6. Blood tranfusion
  7. DIC
  8. Idiopathic
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20
Q

What are the stages (4) that lungs go through in diffuse alveolar damage?

A

Capillary congestion => Exudative phase => Hyaline membranes (dead debris) => Organising phase (fibrotic changes)

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21
Q

What are the outcomes of DAD?

A

40% mortality

superimposed infection

residual fibrous scarring of lung => chronic respiratory impairment

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22
Q

Name 4 patterns of lung involvement in BACTERIAL pneumonia

A
  1. Bronchopneumonia (most common pattern)
  2. Lobar pneumonia
  3. Abscess formation
  4. Granulomatous inflammation
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23
Q

Bronchopneumonia and lobar pneumonia - what pattern do you see in each?

A

Bronchopneumonia = Patchy/spotty bronchial and peribronchial distribution, often lower lobes

Lobar pneumonia = massive consolidated pattern

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25
Q

What organisms (4) cause bronchopneumonia?

A

Often low virulence organisms:

Staphylococcus

Haemophilius

Streptococcus

Pneumococcus

26
Q

Why don’t we see lobar pneumonia as frequently?

A

b/c we usually begin treating with abx before the infections spreads throughout entire lobe.

27
Q

Which organisms (1) cause lobar pneumonia?

A

More fatal pathogens than those causing bronchopneumonia

i.e. 90-95% pneumococci (S. pneumoniae)

28
Q

What histopathological features (4) do you see in lobar pneumonia?

A
  1. Congestion - hyperaemia, inter-alveolar fluid
  2. Red hepatisation - hyperamia, intra-alveolar neutrophils
  3. Grey hepatisation - intra-alveolar connective tissue
  4. Resolution - restoration of normal architecture with some fibrosis
29
Q

What are some complications (5) of pneumonias?

A
  1. Abscess formation
  2. Pleuritis and PE
  3. Infected PE = EMPYEMA
  4. Fibrous scarring
  5. Septicaemia
30
Q

COPD has two components - name them.

A

Airway component = chronic bronchitis

Alveolar parenchymal component = Emphysema

31
Q

What is COPD Emphysema?

A

Permanent loss of the alveolar parenchyma distal to the terminal bronchiole

32
Q

In terms of histopathology, how can you differentiate emphysema caused by cigarette smoke vs emphysema xaused by alpha-1 antitrypsin deficiency?

A

Smoking => comes in via airways => loss centred on bronchioles => CENTRILOBULAR

Alpha-1 antitrypsin deficiency => affects all lung tissue => diffuse loss of alveolae => PANACINAR

33
Q

Name risk factors (3) for developing COPD emphysema?

A
  1. SMOKING
  2. Pollution
  3. Alpha-1 anti-trypsin deficiency
35
Q

Complications (4) of emphysema

A
  1. Bullae => may lead to pneumothorax
  2. Respiratory failure => due to loss of alveolar wall for gas exchange
  3. Pulmonary hypertension => due to the vascular changes in response to hypoxia
  4. Cor pulmonale => as a result of 3
36
Q

What is a granuloma in terms of histopathology?

A

Collection of 1) histiocyte/macrophages +/- 2) multinucleate giant cells

3) necrotising OR non-necrotising

37
Q

Describe idiopathic pulmonary fibrosis: macro & micro changes

A

macro: basal and peripheral fibrosis and cyst formation
micro: interstitial fibrosis at varying stages

38
Q

What are the causes (3) of granulomatous lung disease?

A
  1. Infection (TB, fungal infection)
  2. Sarcoidosis
  3. Foreign body - aspiration or IVDU
39
Q

What is fibrosing lung disease? Name 3 types

A

Parenchymal diseases that are chronic and progressive fibrosing diseases of lung

  1. Idiopathic pulmonary fibrosis (cryptogenic fibrosing alveolitis)
  2. Extrinsic allergic alveolitis (Farmer’s lung)
  3. Industrial lung diseases (pneumoconiosis)
41
Q

Name 3 types of pulmonary vascular disease

A
  1. Pulmonary thromboembolism
  2. Pulmonary hypertension
  3. Pulmonary vasculitis
42
Q

Compare and contrast small vs large pulmnary embolus in terms of:

  • area occluded
  • presentation
  • type of infarct
A

Small:

  1. peripheral pulmonary arterial occlusion (small)
  2. Presents with: pleuritic chest pain, acute SOB, chronic progressive SOB
  3. Haemorrhagic infarct

Large:

  1. occludes main pulmonary trunk = saddle embolus
  2. Presents with: sudden death, acute RHF, CVS shock
  3. non-haemorrhagic infarct
43
Q

What is a complication of repeated small pulmonary emboli?

A

Increasing occlusion of pulmonary vascular bed => pulmonary hypertension

44
Q

What defines pulmonary hypertension?

A

mean pulmonary arterial pressure >25 mmHg at rest

45
Q

What cell type do the commonest malignant lung tumours originate from?

A

Epithelial tumours (90-95%) of all malignant tumours

46
Q

Name the types of non-small cell and small cell carcinomas

A

Non-small cell carcinoma (80%):

  • Squamous cell carcinoma (30%)
  • Adenocarcinoma (30%)
  • Large cell carcinoma (20%)

Small cell carcinoma (20%):

  • small cell carcinoma
47
Q

Describe the pathway of development of squamous cell carcinoma with exposure to cigarette smoke

A

normal epithelium => hyperplasia => squamous metaplasia => dysplasia => carcinoma in situ => invasive carcinoma (k-ras mutation)

48
Q

Which is more aggressive - small cell or non-small cell carcinomas?

A

small cell carcinomas

49
Q

Which part of the lung do adenocarcinomas typically affect? What is the name of that initial area? How does it spread?

A

Proliferation of atypical cells lining the alveolar walls => increase in size then finally become invasvie

Precursor lesion (red) = atypical adenomatous hyperplasia (AAH)

AAH => grows in area = non-mucinous adenocarcinoma in-situ => invades into blood vessels = mixed pattern invasive adenoCa

50
Q

Which 2 types of lung cancer is smoking most commonly associated with?

A
  1. NSCLC squamous cell carcinoma
  2. SCLC
51
Q

Name causes (5) of lung cancer in non-smokers?

A
  1. Asbestos
  2. Radiation (radon exposure, therapeutic radiation)
  3. Air pollution
  4. Heavy metals (arsenic, nickel)
  5. Genetic susceptbility (familial cases are rare)
53
Q

Where does lung squamous cell carcinoma usually take place?

How does it behave in terms of spread?

A

traditionally centrally located arising from bronchial epithelium (centrally around large bronchi)

local spread, metastasise later.

55
Q

Describe risk factor of adenocarcinoma lung cancer

A
  • Smoking + others

BUT commoner in FAR EAST, FEMALES, and NON-SMOKERS

56
Q

Which part of lung does large cell carcinoma affect?

What is its’ histological features?

Prognosis?

A

peripheral or central tumours

Poorly differentiated tumours composed of large cells = no histological evidence of glandular or squmamous differentiation

57
Q

Rank NSCLC from best to worst prognosis

A

Squamous cell carcinoma (best) > adenocarcinoma > large cell carcinoma

58
Q

NSCLC vs SCLC - which has a poorer prognosis?

A

SCLC - very aggressive tumour!

59
Q

Where in the lung do small cell carcinomas usually occur?

How do they spread?

A

often central near bronchi

small poorly differentiated cells that divide rapidly (lots of mitoses)

60
Q

Name the risk factors (1) for SCLC and the genetic mutations associated with it

A
  • smoking
  • genetic mutations: p53 and RB1 mutations
61
Q

Which lung cancers are more chemosensitive?

A

SCLC - however 80% present with metastases so it doesn’t prolong life by too much

62
Q

All lung cancers are now sent for molecular testing - name 3 important test and its implications in terms of treatment for lung cancers

A
  1. checking for certain EGFR mutations => EGFR is a receptor and some targeted therapies with tyrosine kinase inhibitors (TKIs, such as gefitinib) can block these pathways and BLOCK/SLOW tumour growth
  2. Checking for ALK translocation
  3. Checking for Ros1 translocation
    - both 2 + 3 respond to Crizotinib (TK receptor inhibitor)
63
Q

what marker do lung tumour cells usually express to modulate immune response? What is the direct effect?

A

Tumour cell expresses PDL-1 => interacts with PD-1 on cytotoxic CD8 T cells to suppress them = turns off entire immune cascase (DCs, Tregs, TH2, macrophages, etc).

64
Q

Which molecular/immuno testing are adenocarcinoma and squamous cell carcinoma now sent for?

A

Adenocarcinoma:

  • EGFR mutations - responder mutation or resistance mutation
  • Alk translocation
  • Ros1 translocation
  • PDL-1 expression

Squamous cell carcinoma:

  • PDL-1 expression

Pathology by week (70 decks)

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