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Histopathology > Lung pathology > Flashcards

Lung pathology Flashcards

1
Q

Types of obstructive lung disease

A 
Chronic bronchitis
Bronchiectasis
Asthma
Emphysema
Small airway disease / Bronchiolitis
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2
Q

Site, pathology, aetiology, clinical & histological features, complications of chronic bronchitis

A

S - Bronchus
P - Dilatation of the airways and excess mucus production
A - Tobacco smoke, air pollution
CF - Cough & sputum on most days for 3 months over 2 years
HF - Dilatation of the airways, goblet cell hyperplasia and hypertrophy of mucous glands
C - Recurrent infections, chronic hypoxia, pulm HTN

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3
Q

Site, pathology, clinical & histological features, complications of bronchiectasis

A 
S - Bronchus
P - Airway dilatation and scarring
CF - Cough, purulent sputum, fever
HF - Permanent dilatation of the bronchi
C - Recurrent infections, haemoptysis, pulm HTN, amyloidosis
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4
Q

Site, pathology, aetiology, clinical & histological features, complications of Asthma

A

S - Bronchus
P - SM cell hyperplasia, excess mucus, inflammation
A - Immunologic: allergens, drugs, cold air, exercise
CF - Episodic cough, wheezing, dyspnoea
HF - Whorls of shed epithelium (Curschmann spirals), eosinophils, Charcot-Leyden crystals
C - Chronic asthma, death

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5
Q

Site, pathology, aetiology, clinical & histological features, complications of emphysema

A

S - Acinus
P - Airspace enlargement, wall destruction
A - Tobacco smoke, a1-AT deficiency
CF - Dyspnoea, cough
HF - Loss of the alveolar parenchyma distal to the terminal bronchiole
C - Pneumothorax, resp failure, pulm HTN

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6
Q

Site, pathology, aetiology, clinical features, of small airway disease / bronchiolitis

A

S - Bronchiole
P - Inflammatory scarring / obliteration
A - Tobacco smoke, air pollutants
CF - Dyspnoea, cough

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7
Q

Aeitiology of bronchiectasis

A

● Inflammatory
Post-infectious (e.g. pertussis)
Abnormal host defense 1º (hypogammaglobulinaemia) and 2º (chemotherapy, NG)
Obstruction (extrinsic/intrinsic/middle lobe syn.)
Post-inflammatory (aspiration)
Secondary to bronchiolar disease (OB) and interstitial fibrosis (CFA, sarcoidosis)
Systemic disease (connective tissue disorders)
Asthma
● Congenital
Cystic fibrosis
Primary ciliary dyskinesia
Hypogammaglobulinema
Young’s syndrome = rhinosinusitis, azoospermia and bronchiectasis

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8
Q

Define interstitial lung disease

A

Group of >200 diseases characterized by inflammation and fibrosis of the pulmonary connective
tissue, accounting for 15% of respiratory disease burden.

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9
Q

Features of interstitial lung disease

A

Typical presentation
● Chronic shortness of breath
● End-inspiratory crackles
● Cyanosis, pulmonary HTN and cor pulmonale

Show features of RESTRICTIVE lung disease on spirometry:
● Decreased CO diffusion capacity
● Decreased lung volume
● Decreased compliance

In advanced disease, interstitial lung disease will have a honeycomb appearance on CT CAP.

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10
Q

Categories of interstitial lung disease

A

Fibrosing
Granulomatous
Eosinophilic
Smoking related

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11
Q

Types of fibrosing lung disease

A

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

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12
Q

Types of granulomatous lung diseases

A

a. Sarcoid
b. Extrinsic allergic alveolitis
c. Associated with vasculitides e.g. Wegener’s, Churg-Strauss, microscopic polyangiitis

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13
Q

Features of Cryptogenic Fibrosing Alveolitis / Idiopathic Pulmonary Fibrosis

A

● M>F
● Causative agents unknown
● Histological pattern of fibrosis = Usual Interstitial Pneumonia, required for diagnosis (also
seen in connective tissue disease, asbestosis and EAA)
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.
● Can have inflammatory cause e.g. RA, SLE, systemic sclerosis
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● Clinical presentation: increasing exertional dyspnoea and non-productive cough. 40-70y at
presentation, with hypoxaemia à cyanosis and pulmonary HTN +/- cor pulmonale, and
clubbing.
● Rx: steroids, cyclophosphamide, azathioprine, pirfenidone (not especially effective)

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14
Q

Features of pneumoconiosis

A

Occupational lung disease caused by inhlation of mineral dusts or inorganic particles. Classically
seen in coal miners. The disease has a predilection for the upper lobes.
NB: asbestosis can cause benign pleural lesions (plaques, fibrosis) but can also cause malignant
lesions (adenocarcinoma, mesothelioma). Asbestosis (fibrosis resulting from asbestos exposure)
tends to affect the lower lobe.

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15
Q

Features of granulomas

A

Granuloma = collection of histiocytes, macrophages +/- multi-nucleate giant cells.
Granulomatous infections include TB, fungal (histoplasma, Cryptococcus, coccidioides, aspergillus,
mucor) and others (pneumocystis, parasites). Non-infectious granulomatous conditions include
sarcoid, foreign body (aspiration or IVDU), drugs or occupational lung disease.

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16
Q

Features of Extrinsic Allergic alveolitis / Hypersensitivity Pneumonitis/ Cryptogenic Organising
Pneumonia / Bronchiolitis Obliterans Organising Pneumonia (BOOP)

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.
Histologically there is the presence of polypoid plugs of loose connective tissue within
alveoli/bronchioles – granuloma formation and organising pneumonia.
Acute presentation: 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.
Chronic presentation: progressive persistent productive cough and SOB, finger clubbing and
severe weight loss
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).
Recognise early as progression to fibrosis can be prevented by early removal of antigen.

17
Q

Types of pneumonia and their features

A

• Bronchopneumonia – patchy bronchial/peri-bronchial distribution. Low virulence
organisms. Typically seen in the elderly and frail.
• Lobar pneumonia – Fibrinosuppurative consolidation. Stages: 1.Consolidation; 2. Red
Hepatisation (neutrophilia); 3. Grey Hepatisation (Fibrosis); 4. Resolution
• Atypical – interstitial pneumonitis. No intra-alveolar inflammation.

18
Q

Features of squamous cell carcinoma

A

30-50%
● Risk factors: M>F, closely correlated with smoking
● Highest rate of p53/c-myc mutations.
● Usually proximal bronchi, local spread with late metastasis. Less responsive to chemo.
● Histology: Keratinisation, intercellular prickles (desmosomes).
● Cytology: squamous cells.
167
● There are a variety of subtypes e.g. papillary, basaloid. It is associated with cavitation and
hypercalcaemia.
● Progression: Epithelium → hyperplasia →squamous metaplasia→angiosquamous
dysplasia→carcinoma in situ→invasive carcinoma

19
Q

Features of adenocarcinoma

A

20-30%
● Most common in women and non-smokers.
● Malignant epithelial tumour with glandular differentiation or mucin production.
● Tumour occurs peripherally and metastasizes early.
● Histology: glandular differentiation (gland formation and mucin production). Cytology –
cells containing mucin vacuoles. Molecular – EGFR mutations. Progression;
● Atypical adenomatous hyperplasia→non-mucinous BAC→mixed pattern adenocarcinoma

20
Q

Features of small cell carcinoma

A

20-25%
Usually occurs centrally, proximal bronchi.
● Arising from neuroendocrine cells.
Associated with ectopic ACTH secretion, Lambert-Eaton, cerebellar degeneration.
● Highly malignant, metastasize early, usually by diagnosis commonly to bone, adrenal, liver
and brain. It has a poor prognosis due to rapid metastases despite being very
chemosensitive. It has a strong relationship to smoking. p53 and RB1 mutations are
common.

21
Q

Features of large cell carcinoma

A

10-15%
● Poorly differentiated malignant epithelial tumour – large cells, large nuclei, prominent
nucleoli. Histology – no evidence of glandular or squamous differentiation. Poor prognosis.

22
Q

Paraneoplastic syndromes

A

ADH → SIADH
ACTH → Cushing’s syndrome
PTH/ PTHrP → primary hyperparathyroidism, hypercalcaemia and bone pain
Calcitonin → hypercalcaemia
Serotonin → carcinoid syndrome (flushing + diarrhoea + bronchoconstriction)
Bradykinin → cough

23
Q

Molecular features of lung cancers

A
  • ERCC1 – NSCLC = poorer response to cisplatin
  • EGFR – adeno (usually) = target for Anti-EGFR (usually tyrosine kinase inhibitor (TKI)) therapy
  • Kras – adeno/squamous = poor prognosis, non-response to TKI
  • EML4-ALK – adeno (usually) = no benefit from TKI
24
Q

Staging of lung cancers

A
  • Tumour (T1-4) – based on size and invasion of pleura, pericardium
  • Lymph node metastasis (N0-2) - N0 – lymph node not involved by tumour, N1 or N2 - lymph nodes involved. 1 vs 2 depends on extent of involvement
  • Distant metastasis (M0 or 1) - M1 – tumour has spread to distant sites.
25
Q

Features of mesothelioma

A

Arise from either parietal or visceral pleura. It spreads widely within the pleural
space and usually associated with extensive pleural effusion, chest pain and dyspnoea. There
is a long latent period of 25-45 years for development of asbestos-related mesothelioma.

26
Q

Features of pulmonary embolus

A

95% originate from DVTs. Risk factors include female, immobility, cardiac disease, cancer,
primary and secondary hypercoagulable states (Virchow’s triad = stasis + vessel wall injury
+ hypercoagulability)

● Large emboli impact in the main pulmonary arteries leading to acute cor pulmonale,
cardiogenic shock and death if >60% of pulmonary bed occluded. (N.B. occluding
pulmonary trunk = saddle embolus).
● Small emboli may can be silent or cause peripheral wedge infarctions. Repeated
infarctions can result in pulmonary HTN.
● Non-thrombotic emboli – bone marrow, amniotic fluid, tumour, air, foreign bod

27
Q

Features of pulmonary hypertension

A

Mean pulmonary arterial pressure of >25mmHg at rest.
Classified according to aetiology
● Class 1:
○ Pulmonary arterial hypertension (idiopathic, hereditary, drug/toxins, associated
with congenital heart disease) - primary PAH most common in women aged
20-40yrs
● Class 2:
○ Pulmonary hypertension associated with left heart disease (systolic/diastolic
dysfunction, valve disease)
● Class 3:
○ Pulmonary hypertension due to lung disease
● Class 4:
○ Chronic Thromboembolic Pulmonary Hypertension
● Class 5:
○ Pulmonary Hypertension with unclear multifactorial mechanisms (metabolic
disorders, systemic disorders, haematological disorders)

28
Q

Pathophysiology and complications of pulmonary hypertension

A

Pathophysiology:
● Pre-capillary (chronic hypoxia/embolus)
● Capillary (Pulmonary Fibrosis)
● Post-capillary (left heart disease/ veno-occlusive disease)
● Pulmonary vasoconstriction of arterioles – intimal fibrosis, thickened walls
Complications: RHF – venous congestion of organs (nutmeg liver), peripheral oedema.

29
Q

Features of pulmonary oedema

A

Intra alveolar fluid accumulation leads to poor gas exchange. Main aetiology:
left heart failure. Histology: intra-alveolar fluid, iron laden macrophages (“heart failure cells”).

30
Q

Features of diffuse alveolar damage

A

ARDS in adults (e.g. infection, aspiration, trauma etc); HMD (hyaline
membrane disease) in neonates (e.g. insufficient surfactant production in prems).
Rapid onset respiratory failure. Histo: lung expanded, firm, plum-coloured, airless

Histopathology (7 decks)

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