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Clinical pathology > Resp Lectures 15+16 lung pathology > Flashcards

Resp Lectures 15+16 lung pathology Flashcards

1
Q

What makes up the conducting airways?

A

Trachea
Left & right main bronchi
Segmental & smaller bronchi
Bronchioles, terminal bronchioles

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2
Q

What constitutes gas exchange

A

Respiratory bronchioles
Alveolar ducts
Alveolar sacs
Alveoli

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3
Q

Histology of conducting airways

A

Pseudostratified cilliated columnar mucus secreting epithelium

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4
Q

Histology of Alveoli

A

Mostly flat Type I pneumocytes (gas exchange) & some rounded Type II pneumocytes (surfactant production)

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5
Q

Respiratory failure caused by defective….what

A

Ventilation
Perfusion
Gas exchange

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6
Q

Type 1 resp failure

A

(paCO2

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7
Q

Type 2 resp failure

A

(paCO2>6.3kPa)

Hypercapnic respiratory drive

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8
Q

Sputum Resp Signs and symptoms

A

Mucoid, purulent, haemoptysis

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9
Q

Cough Resp Signs and symptoms

A

Reflex response to irritation

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10
Q

Stridor Resp Signs and symptoms

A

Proximal airway obstruction

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11
Q

Wheeze Resp Signs and symptoms

A

Distal airway obstruction

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12
Q

Pleuritic pain Resp Signs and symptoms

A

Pleural irritation

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13
Q

Auscultation resp exam: Crackles, Wheeze, bronchial breathing, pleural rub

A

Crackles – Resisted opening of small airways
Wheeze – narrowed small airways
Bronchial breathing – Sound conduction through solid lung
Pleural rub – Relative movement of inflamed visceral & parietal pleura

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14
Q

Percussion resp exam: Dull, hyper resonant

A

Dull – Lung consolidation or pleural effusion

Hyperesonant – Pneumothorax or emphysema

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15
Q

Primary tumours: Benign and malignant Lung Neoplasm

A

Benign: Adenochondroma (glandular/cartilage involvement)
Malignant: Carcinoma (epithelial)

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16
Q

Lung carcinoma risk factors

A

Asbestosis and silicosis

cigarette smoking

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17
Q

Asbestos

A 
Amphiboles - blue asbestos (crocidolite) – the most dangerous  
brown asbestos (amosite)  
Serpentines  - white asbestos  (chrysotile)- the least dangerous
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18
Q

Asbestosis

A

High level exposure produces pulmonary interstitial fibrosis

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19
Q

How can asbestosis bodies be seen?

A

By light microscopy, their Fibres are coated with mucopolysacharide & ferric iron salts

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20
Q

Asbestosis and lung carcinomas

A

Higher incidence of all types of lung carcinoma associated with high level exposure to asbestos

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21
Q

Lung carcinoma with asbestosis, asbestos related diffuse pleural fibrosis or silicosis

A

Prescribed occupational disease (Not with mixed dust pneumoconiosis (coal workers pneumoconiosis) )

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22
Q

Lung carcinoma in the absence of asbestosis

A

Prescribed industrial disease

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23
Q 
Malignant primary lung tumours:
Non small cell
small-cell 
Carcinoid
(Others: lymphomas, sarcomas, carcinosarcomas)
A

-Non-Small cell carcinoma: (squamous carcinoma, adenocarcinoma, large cell neuroendocrine carcinoma,
undifferentiated large cell carcinoma)

  • Small-cell carcinoma: All are Neuroendocrine
  • Carcinoid: Low grade neuroendocrine epithelial tumours
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24
Q

Secondary lung tumours

A

Secondary tumours - commonest tumours in the lung usually from a known primary but may be the presenting feature of a distant primary tumour
Typically multiple bilateral nodules but can be solitary
May be difficult to determine whether primary or secondary

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25
Q

How to know if primary or secondary

A 
History
Morphology 
 some adenocarcinomas, but not squamous
Antigen expression
Immunocytochemistry is useful but not 100% reliable
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26
Q

Lung non-mucinous adenocarcinoma & small cell

Immunocytochemistry

A

cytokeratin & thyroid transcription factor positive

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27
Q

Colorectal Immunocytochemistry

A

cytokeratin 7 negative & cytokeratin 20 positive

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28
Q

Upper G.I Tract Immunocytochemistry

A

cytokeratin 7 positive & cytokeratin 20 positive

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29
Q

Breast Immunocytochemistry

A

may be oestrogen receptor positive

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30
Q

Melanoma Immunocytochemistry

A

S100, HMB45, MelanA positive & cytokeratin negative

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31
Q

Lung Carcinoma usual sites

A

Most central, main or upper lobe bronchus (bronchogenic)

Adenocarcinoma more peripheral

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32
Q

Squamous carcinoma

A

desmosomes link cells like epidermis (‘epidermoid’)
+/- keratinization
~90% in smokers
central > peripheral
hypercalcaemia due to parathyroid hormone related peptide

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33
Q

what epithelium lines the bronchus

A

Pseudostratified columnar epithelium with ciliated and mucus-secreting cells

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34
Q

Squamous metaplasia

A

Irritants such as smoke cause the epithelium to undergo a reversible metaplastic change from pseudostratified columnar to stratified squamous type which may keratinize (like skin)

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35
Q

Dysplasia

A

One metaplastic cell undergoes irreversible genetic changes (a series of sequential somatic mutations of oncogenes & anti-oncogenes) producing the first neoplastic cell

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36
Q

Developing dysplasia

A

The neoplastic cell proliferates more sucessfully than the metaplastic cells
The neoplastic clone relaces the metaplastic cells producing dysplasia ( intraepithelial neoplasia or carcinoma-in-situ)

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37
Q

Squamous carcinoma

A

Neoplastic cells breach the basement membrane producing invasive squamous carcinoma
Invading neoplastic cells infiltrate lymphatic & blood vessels –> produce metastases in lymph nodes & distant sites

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38
Q

Adenocarcinoma

A

glandular cells, serous or +/- mucus vacuoles, in acinar, tubular, solid or papillary structures
central = peripheral
~80% in smokers
Thyroid transcription factor (TTF) is expressed in many non-mucinous lung adenocarcinomas

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39
Q

Bronchioloalveolar carcinoma

A

Spread of well differentiated mucinous or non-mucinous neoplastic cells on alveolar walls
Not invasive - “adenocarcinoma in situ”
Mimics pneumonia
Uncommon nodal & distant metastases

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40
Q

Neuroendocrine differentiation in lung & lung tumours

A

Look for neuroendocrine cell proteins by immunocytochemistry:
Neural cell adhesion molecule (CD56)
Neural secretory granule proteins (chromogranin, synaptophysin)
Neural secretory granule by electron microscopy

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41
Q

spectrum of malignancy of neuroendocrine tumours

A

carcinoid, atypical carcinoid, large cell neuroendocrine carcinoma and small cell carcinoma

42
Q

Typical carcinoid tumours

A

Often grow and occlude a bronchus

Organoid, bland cells, no necrosis,

43
Q

Atypical carcinoid tumours

A

11% of lung carcinoids
Less organoid, more atypia, nucleoli - may be focal atypia in an otherwise typical carcinoid
Necrosis, 2-10 mitotic figure per 2sqmm
More aggressive than typical carcinoids

44
Q

Large cell neuroendocrine carcinomas

A

Neuroendocrine morphology
-organoid architecture, eosinophilic granular cytoplasm
-antigen expression
Severe atypia, nucleoli, necrosis, >11 mitotic figures per 2sqmm
Prognosis similar to or worse than other non-small cell lung carcinomas
Associated with smoking

45
Q

Small Cell Carcinoma

A

Rapidly progressive malignant tumours
Neurosecretory granules with peptide hormones such as ACTH
May have small primary with metastases before presentation
~99% in smokers
No “small cell carcinoma in situ” identified

46
Q

Carcinomas with multiple differentiation

A 
Mixed NSCLC (contains 2 different types of cells)
-Adenosquamous

Combined small cell carcinoma
-Any proportions of small cell carcinoma & NSCLC
~3% of small cell carcinoma, depends on extent of sampling

47
Q

Large cell carcinomas

A

No specific squamous or glandular morphology
~50% express thyroid transcription factor
Can be neuroendocrine
-Express CD56 &/or neurosecretory granule proteins (synaptophysin, chromogranin)

48
Q

Effects of Lung carcinomas

A

Cachexia

Clubbing

49
Q

Effects of Lung carcinomas of skin

A

Acanthosis nigricans, tylosis

50
Q

Effects of Lung carcinomas on blood

A

Coagulopathies - thrombophebitis migrans

51
Q

Effects of Lung carcinomas Neurology

A

Encephalomyelitis, neuropathies & myopathies

Lambert Eaton myasthenic syndrome due to anti-neuromuscular junction autoantibodies in small cell carcinoma

52
Q

Effects of Lung carcinomas Endocrinologically

A
  • Parathyroid hormone-related peptide from squamous cell carcinoma causing hypercalcaemia
  • ACTH and antidiuretic hormone from small cell carcinoma
  • 5-hydroxytryptamine - carcinoid (uncommon)
53
Q

EGFR-TK inhibitors

A

Gefitinib (Iressa) and erlotinib (Tarceva) are ATP analogues that inhibit EGFR-TK if activating mutations are present

(Sensitising mutations present in 10% of non-small cell lung cancers and are commoner in adenocarcinomas in non-smoking Asian women?????)

54
Q

ALK (Anaplastic lymphoma kinase) gene re-arrangements

A

Variable break point inversion on short arm of chromosome 2 fuses ALK and EML (echinoderm microtubule like protein) genes activating ALK tyrosine kinase.
Present in about 10% of lung adenocarcinomas
Non-smoking, Asian, women again
Independent of EGFR or RAS mutations

Crizotinib

  • ATP analog inhibits ALK, ROS1, c-Met (Hepatocyte Growth Factor receptor /HGFR) tyrosine kinases.
  • Temporary control – no progress or regress
55
Q

Pleural diseases

A 
Pneumothorax- air
-Tension pneumothorax
Pleural effusion
-transudate or exudate
Haemothorax- blood
Chylothorax- lymph
Empyema- Pus
56
Q

Causes of Pleural effusion

A 
Inflammatory:
-Serous/fibrinous –exudate
-Due to inflammation/infection in adjacent lung
Non inflammatory: 
-Congestive Cardiac Failure – transudate
57
Q

Non-neoplastic Pleura diseases

A

inflammation (pleurisy, pleuritis)

  • collagen vascular diseases
  • pneumonia, tuberculosis
  • lung infarct, usually secondary to pulmonary embolus
  • lung tumour

asbestos
-effusion, fibrous plaques, diffuse fibrosis

58
Q

Pleural Tumours Benign and malignant

A

Benign - rare
-fibroma

Malignant - common

  • Usually secondary adenocarcinoma - lung, breast
  • Primary malignant mesothelioma is rarer
59
Q

Malignant Mesothelioma

A

Occupational, paraoccupational or environmental contamination
Initial nodule and effusion. Later obliterates pleural cavity growing around the lung
Invades chest wall (pain) & lung
Nodal and distant and metastases less common than with carcinomas
Mixed spindle cell and epithelioid cells. May be very fibrous (desmoplastic)

60
Q

Early malignant Mesothelioma

A

Small plaques on the parietal pleura
Difficult to image & biopsy
May produce a significant pleural effusion

61
Q

Fibrous pleural plaques

A

On the lower thoracic wall & diaphragmatic parietal pleura
Associated with low level asbestos exposure
No physiological effect
Not premalignant
Seen on radiographs, a marker of possible asbestos exposure

62
Q

What does a Weak fluorodeoxyglucose uptake in mediastinal lymph nodes mean?

A

probably reactive rather than neoplastic

63
Q

Why secondary infections can occur more often?

A

Mucocilliary escalator

  • Physical obstruction – tumour, foreign body
  • Cough reflex
  • Cilliary dysmotility – Kartagener’s syndrome
  • Mucus viscosity – cystic fibrosis

Immunity

  • Hypogammaglobulinaemia , lymphomas, -immunosuppressive drugs, AIDS
  • Macrophage function – smoking, hypoxia

Pulmonary oedema

64
Q

Cause of Acute Bronchitis

A

Viral (RSV), H. influenzae, Strep. pneumoniae
Croup
Exacerbations of COAD

65
Q

Causes of Bronchiolitis

A

Primary acute in infants, RSV, rare, resolve or develop bronchopneumonia
Follicular bronchiolitis
Bronchiolitis obliterans

66
Q

Pneumonia

A

Inflammatory exudate in alveoli & distal small airways - consolidation

67
Q

Classifying Pneumonia (Clinical, aetiological, anatomical, reaction)

A 
Classifications:
Clinical - primary or secondary
Aetiological - Bacterial, viral, fungal 
Anatomical - lobar pneumonia or bronchopneumonia
Reaction - purulent, fibrinous
68
Q

Bronchopneumonia

A 
Secondary - compromised defences
Often low virulence bacteria or occasionally fungi
Common
Patchy
Bronchocentric
Resolve or heal with scarring
69
Q

Lobar Pneumonia

A

Primary - typically male 20 to 50 years
90% - virulent Strep pneumoniae
Uncommon
Confluent segments, whole lobe or lobes with overlying pleuritis
Congestion, red then grey hepatisation, resolution without scarring
Klebsiella pneumoniae - elderly, diabetic, alcoholic

70
Q

Atypical pneumonias (not immunosuppressed)

A

Non-immunosuppressed

  • Viral - flu, varicella, RSV, rhino, adeno, measles
  • Mycoplasma pneumoniae - Mild, chronic, fibrosis
  • Chlamydia (psittacosis), Coxiella burnetti (Q-fever)
  • Legionella pneumophilla - Systemic, 10- 20% fatal

Severity mild to fatal
Intersitial lymphocytes, plasma cells, macrophges
Intra-alveolar fibrinous cell-poor exudate
Diffuse alveolar damage (DAD)

71
Q

Atypical pneumonias (immunosuppressed)

A

Lymphomas, medication, AIDS
Opportunistic infections by low virulence or non-virulent organisms
-Fungi - candida, aspergillus, Pnumocystis carinii
-Viruses - CMV, HSV, measles

72
Q

Non-infective pneumonias (Aspiration, lipid, cryptogenic)

A

Aspiration pneumonia
-Secondary infection often with mixed anaerobes produces abscesses

Lipid pneumonia

  • Endogenous – retention pneumonitis
  • Exogenous – aspiration

Cryptogenic organising pneumonia & bronchiolitis obliterans organising pneumonia (COP & BOOP)

73
Q

Pulmonary tuberculosis

A 
Mycobacterium tuberculosis
Lung is the commonest site of infection
Associations
Socioeconomic deprivation
Immunosuppression  -  including  AIDS
74
Q

Pulmonary Tuberculosis

A

Granulomas with multinucleated Langhans’ giant cells & caseous necrosis
Usually few bacilli but intense immune reaction causes tissue damage
Type IV hypersensitivity to tuberculin - Heaf & Mantoux tests
Atypical mycobacteria –tend to infect lungs with preexisting pathology such as COPD & are more resistant to treatment than M tuberculosis.
Can lead to empyema, pneumonia, miliary

75
Q

Pulmonary Vasculitis features

A

Necrotising granulomatous vasculitis - Wegener’s granulomatosis (kidneys & nose, elevated serum ANCA)

Churg-Strauss syndrome (eosinophilia & asthma)

Goodpasture’s syndrome - Anti-glomerular basement membrane antibody, Intra-alveolar haemorrhage & glomerulonephritis

Microvascular damage - ARDS & DAD, SLE

76
Q

Obstruction- types of Emboli

A

Thromboemboli

  • Common
  • Deep leg vein thrombosis - risk factors & prevention
  • Size determines symptoms - sudden death, SOB, chest pain, pulmonary hypertension, right ventricular failure
Fat emboli - fat & marrow from bone fractures
Air
Amniotic fluid
Tumour
Foreign bodies
77
Q

Obstructive pulmonary diseases (Localised)

A
  • Tumour or foreign body
  • Distal alveolar collapse (total) or over expansion (valvular obstruction)
  • Distal retention pneumonitis (endogenous lipid pneumonia) and bronchopneumonia
  • Distal bronchiectasis (bronchial dilatation)

Can be resected

78
Q

Bronchiectasis

A

Site: Bronchus/bronchioles
Cause: Infections (…)
Signs/ symptoms: Cough, fever, copious amounts of foul smelling sputum

  • Permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue
  • Results from chronic necrotizing infection
79
Q

Predisposing conditions for Bronchiectasis

A
  • Cystic fibrosis
  • Primary ciliary dyskinesia, Kartagener syndrome
  • Bronchial obstruction: tumour, foreign body
  • Lupus, rheumatoid arthritis, inflammatory bowel disease, —GVHD
80
Q

Obstructive pulmonary diseases (Diffuse)

A

Diffuse

  • Chronic obstructive pulmonary disease (COPD) aka chronic obstructive airways disease.
  • Asthma
81
Q

What is COPD

A

A combination of chronic bronchitis & emphysema

82
Q

What is chronic bronchitis

A

Cough & sputum for 3 months in each of 2 consecutive years
Site: Bronchus
Cause : Chronic irritation, Smoking & air pollution, Middle aged & old

Pathology: Mucus gland hyperplasia and hypersecretion, secondary infection by low virulence bacteria, chronic inflammation

Chronic inflammation of small airways of the lung causes wall weakness & destruction thus centrilobular emphysema

83
Q

What is Emphysema

A

Emphysema: Abnormal permanent dilation of airspaces distal to the terminal bronchiole, with destruction of airspace wall, without obvious fibrosis

84
Q

Emphysema classification:
Centrilobar
Panlobar
Paraseptal

A

Centrilobular (centiacinar) Coal dust, smoking

Panlobular (panacinar) - >80% a1 antitrypsin deficient (rare, autosomal dominant) , severest in lower lobe bases

Paraseptal (distal acinar) - Upper lobe subpleural bullae adjacent to fibrosis. Pneumothorax if rupture

85
Q

Blue bloater

A

Chronic Bronchitis

  • Excessive mucus production with airway obstruction resulting from hyperplasia of mucus-producing glands, goblet cell metaplasia, and chronic inflammation around bronchi.
  • body responds to the increased obstruction by decreasing ventilation and increasing cardiac output. There is a dreadful ventilation to perfusion mismatch leading to hypoxemia and polycythemia.
  • Hypercapnia
  • Cyanotic appearance
86
Q

Pink Puffer

A

Emphysema

  • Gradual destruction of the pulmonary capillary bed and thus decreased inability to oxygenate the blood.
  • body then has to compensate by hyperventilation
  • develop muscle wasting and weight loss
87
Q

Prescribed Occupational disease

A

Chronic bronchitis &/ Emphysema

88
Q

Asthma

A

Chronic inflammatory disorder of the airways
Mucosal inflammation & oedema
Hypertrophic mucous glands & mucus plugs in bronchi
Hyperinflated lungs
Clinicopathological classification
-Atopic , non-atopic, aspirin-induced, allergic bronchopulmonary aspergillosis (ABPA)

89
Q

Atopic Asthma Pathology

A

Type I hypersensitivity reaction

  • Allergen - dust, pollen, animal products
  • Degranulation of IgE bearing mast cells
    - histamine initiated bronchoconstriction & mucus production obstructing air flow
    - eosinophil chemotaxis

Persistent or irreversible changes

  • bronchiolar wall smooth muscle hypertrophy
  • mucus gland hyperplasia
  • respiratory bronchiolitis leading to centrilobular emphysema
90
Q

Interstitial Lung disease

A 
Usually diffuse and chronic
Diseases of pulmonary connective tissue
(Mainly alveolar walls)
Restrictive rather than obstructive  lung disease
Causes often unknown

Increased tissue in alveolar-capillary wall
Inflammation & fibrosis
Limited morpholgical patterns that differ with site and with time in any individual but with many causes & clinical associations
Decreased lung compliance

Increased gas diffusion distance

91
Q

Acute interstitial disease

A

Diffuse alveolar damage – exudate & death of type I pneumocytes form hyaline membranes lining alveoli followed by type II pneumocyte hyperplasia. Histologically acute interstitial pneumonia
-Adult respiratory distress syndrome (shock lung) - shock, trauma, infections, smoke, toxic gases, oxygen, paraquat, narcotics, radiation, aspiration, DIC

92
Q

Chronic Interstitial Disease

A

Dyspnoea increasing for months to years
Clubbing, fine crackles, dry cough
Common end-stage fibrosed “honeycomb lung”

Examples:

  • idiopathic pulmonary fibrosis,
  • many pneumoconioses (dust diseases)
  • sarcoidosis,
  • collagen vascular diseases-associated lung diseases
93
Q

Idiopathic pulmonary fibrosis (cobblestone look)

A

cryptogenic fibrosing alveolitis
Sub-pleural, lower lobes affected first & most severely
Histology - usual interstitial pneumonia (UIP)
-Interstitial chronic inflammation & variably mature fibrous tissue
-Adjacent normal alveolar walls
-Similar pattern of fibrosis in collagen vascular disease associated interstitial lung disease and in asbestosis

94
Q

Sarcoidosis

A

Non-caseating perilymphatic pulmonary granulomas, then fibrosis
Hilar nodes usually involved
Other organs may be affected- skin,heart, brain
Hypercalcaemia & elevated serum ACE
Typically young adult females, aetiology unknown

95
Q

Pneumoconioses“The dust diseases”

A 
Inhaled dusts 
-inert
-fibrogenic
-allergenic
-oncogenic 
    lung carcinoma & pleural mesothelioma
96
Q

Coal workers’ pneumoconiosis (CWP)
Anthracosis
Silicosis
Asbestosis

A 
Anthracosis:
Simple (macular) CWP
Nodular CWP
Progressive massive fibrosis 
COPD (‘chronic bronchitis & emphysema’) if  >20yrs underground mining

Silica - sand & stone dust
Kills phagocytosing macrophages
Fibrosis & fibrous silicotic nodules, also in nodes
Possible reactivation of tuberculosis
Increased risk of lung carcinoma - lung carcinoma with silicosis is a UK “prescribed occupational disease”
Mixed dust pneumoconiosis – silica with other dusts

High level exposure produces interstitial fibrosis, in a usual interstitial pneumonia pattern
Histologically like idiopathic pulmonary fibrosis or collagen vascular disease associated pulmonary fibrosis but asbestos bodies are identifiable in tissue sections
Increased risk of lung cancer with asbestosis and with high asbestos exposure but no fibrosis

97
Q

Hypersensitivity pnumonitis

aka extrinsic allergic alveolitis

A

Type III hypersensitivity reaction organic dusts

  • farmers’ lung - actinomycetes in hay
  • pigeon fanciers’ lung - pigeon antigens

Peribronchiolar inflammation with poorly formed non-caseating granulomas extends alveolar walls

Repeated episodes lead to interstitial fibrosis

98
Q

Cystic Fibrosis

A

Mutation in CFTR gene
Autosomal recessive inheritance
affects fluid secretion in exocrine glands and the epithelial lining of the respiratory, gastrointestinal and reproductive organs

99
Q

Cystic fibrosis Lung

A

Bronchioles distended with mucus
Hyperplasia mucus secreting glands
Multiple repeated infections
Severe chronic bronchitis and bronchiectasis

100
Q

Cystic fibrosis Pancreas

A

Exocrine gland ducts plugged by mucus
Atrophy and fibrosis of gland
Impaired fat absorption, enzyme secretion, vitamin deficiencies ( pancreatic insufficiency)

101
Q

Cystic fibrosis: Other organs

A

Small bowel: mucus plugging - meconium ileus
Liver: plugging of bile cannaliculi – cirrhosis
Salivary glands: Similar to pancreas: artophy and fibrosis
95% of males are infertile

Clinical pathology (5 decks)

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