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Y5 Histopathology > Lung Histo Qs > Flashcards

Lung Histo Qs Flashcards

1
Q

What are the 5 main obstructive lung dseases?

A

Chronic Bronchitis, Bronchiectasis, Asthma, Emphysema, Small aiway disease/Bronchiolitis

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2
Q

Describe the pathology of Chonic Bronchitis

A

Dilatation of the airways nd excess mucus production

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3
Q

Describe the pathology of Bronchiectasis

A

Airway dilatation and scarring

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4
Q

Describe the pathology of Asthma

A

SM cell hyperpplasia, excess mucus, inflammatioon

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5
Q

Describe the pathology of Emphysema

A

Airspace nelargement, wall destruction

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6
Q

Describe the pathology of Bronchiolitis

A

Inflammatory scarring/obliteration

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7
Q

What is the aetiology of Chronic Bronchitis?

A

Tobacco smoke, air pollution

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8
Q

What is the aetiology of Asthma?

A

Immunologic: allergens, drugs, cold air, exercise

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9
Q

What is the aetiology of Emphysema?

A

Tobacco smoke, alpha1-AT deficiency

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10
Q

What is the aetiology of Bronchiolitis?

A

Tobacco smoke, air pollutants

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11
Q

What are the clinical features of Chronic Bronchitis?

A

Cough, sputum on most days for 3 months over 2 years

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12
Q

What are the clinical features of Bronchiectasis

A

Cough, purulent sputum, fever

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13
Q

What are the clinical features of Asthma

A

Episodic cough, wheezing, dyspnoea

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14
Q

What are the clinical features of Emphysema?

A

Dyspnoea, cough

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15
Q

What are the clinical features of Bronchiolitis?

A

Dyspnoea, cough

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16
Q

What are the histological features of Chronic Bronchitis?

A

Dilatation of the airways, goblet cell hyperplasia, and hypertrophy of mucous glands

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17
Q

What are the histological features of Bronchiectasis?

A

Permenent dilatation of the bronchi

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18
Q

What are the histological features of Asthma?

A

Whorls of shed epithelium (Curschmann spirals), eosinophils, Charcot-Leyden crystals

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19
Q

What are the histological features of Emphysema?

A

Loss of alveolar parrenchyma distal to the terminal bronchiole

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20
Q

Complications of Chronic Bronchitis

A

Recurrent infections, chronic hypoxia, pulmonary hypertension

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21
Q

Complications of Bronchiectasis

A

Recurrent infections, haemoptysis, pulmonary hypertension, amyloidosis

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22
Q

complications of Asthma

A

Chronic asthma, death

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23
Q

Complications of Emphysema

A

Pneumothorax, Respiratory falure, pulmonary hypertension

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24
Q

What are the inflammatory causes of bronchiectasis?

A

Post-infectious, abnormal host defense (primary and secondary), ciliary dyskinesia (primary and secondary), post-inflammatory, secondary to bronchiolar disease and interstitial fibrosis, systemic disease, asthma

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25
Q

What are the congenital causes of bronchiectasis?

A

Cystic Fibrosis, Primary ciliary dyskinesia, Hypogammaglobulinema

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26
Q

What are interstitial lung diseases? (general characteristics)

A

Group of over 200 disease, characterised by inflammation and fibrosis of the pulmonary connective tissue, particularly the most peripheral and delicate interstitium of the alveolar wall

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27
Q

What are the 4 categories of interstitial lung disease?

A

Fibrosinf, Granulomatous, Eosinophilic, Smoking Related

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28
Q

How do Interstitial lung diseases present on spirometry?

A

Show features of RESTRICTIVE lung disease: decreased CO diffusion capacity, decreased lung volume, decreased compliance

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29
Q

How do interstitial lung diseases usually present?

A

SOB, end-inspiratory crackles, cyanosis, pulmonary hypertension, and cor pulmonale

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30
Q

What do all interstitial lung diseases have at end-stage?

A

Honey-comb lung

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31
Q

Main 6 types of Fibrosing Interstitial Lung Disease

A

Idiopathic pulmonary fibrosis, pneumoconiosis, cryptogenic organizing pneumonia, associated with CTD, drug-induced, radiation pneumonitis

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32
Q

3 subgroups of Granulomatous Interstitial Lung Disease

A

Sarcoid, Extrinsic Allergic Alveoplitis, Associated with vasculitides e.g. Wegener’s, Churg-Strauss, microscopic polyangitis

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33
Q

Epidemiology and Aetiology of Cryptogenic Fibrosing Alveolitis/Idiopathic Pulmonary Fibrosis

A

M>F, 60years +, causative agent unknown

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34
Q

Histological Pattern of Diffuse Interstitial Fibrosis

A

Progressive patchy interstitial fibrosis with loss of normal lung architecture and honeycomb change, beginning at periphery of the lobule, usually sub-pleural. Hyperplasia of type II pneumocyts causing cyst formation - honeycomb fibrosis

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35
Q

Clinical presentation of Cryptogenic Fibrosing Alveolitis/Idiopathic Pulmonary Fibrosis

A

Increasing exertional dyspnoea and non productive cough. 40=70yo at presentation, with hypoxaemia leading to cyanosis and pulmonary HTN +/- cor pulmonale, and clubbing

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36
Q

Treatment of Cryptogenic Fibrosing Alveolitis/Idiopathic Pulmonary Fibrosis

A

Steroids, Cyclophosphomide, Azathioprine - but these have little impact on survival

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37
Q

What CTDs are associated with lung fibrosis? (3 main)

A

RA, systemic sclerosis, SLE

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38
Q

What is pneumoconiosis?

A

A non-neoplastic lung reaction to inhalation of mineral dusts or inorganic compounds - typically an occupational lung disease

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39
Q

What part of the lung do pneumoconioses typically affect? What is the exception?

A

Upper zones. Asbestosis = lower sone

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40
Q

Give 3 examples of pneumoconioses

A

Coal worker’s pneumoconiosis, silicosis, asbestosis

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41
Q

What two types of lesions can be caused by Asbestosis?

A

Benign pleural lesions (plaques, fibrosis); Malignant ledions (adenocarcinoma, mesothelioma)

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42
Q

What is a granuloma?

A

Collection of histiocytes, macrophages +/- multi nucleate giant cells

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43
Q

Name some Fungal granulomatous infections

A

histoplasma, cryptococcus, coccidiodes, aspergillus, mucor

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44
Q

What are the causes of non-infectious granulomatous conditions?

A

Sarcoid, foreign body, drugs, occupational lung disease

45
Q

What are the infectious causes of Granulomatous Lung Disease

A

TB, Parasites, Pneumocystis, fungal

46
Q

What is seen on histology of Extrinsic Allergic Alveolitis and Cryptogenic organising pneumonia/BOOP?

A

prescence of polyploid plugs of loose connective tissue within alveoli/bronchioled - granuloma formation and organising pneumonia

47
Q

Acute presentation of Extrinsic allergic alveolitis and Cryptogenic organising pneumonia (Immune-mediated granulomatous lung diseases)

A

inhalation of antigenicdust in sensitised indivisual –> systemic symptoms (fever, chills, chest pain, SOB, cough) within hours of exposure, usually settle by following day,

48
Q

Chronic presentation of Extrinsic allergic alveolitis and Cryptogenic organising pneumonia (Immune-mediated granulomatous lung diseases)?

A

progressive persistent cough, SOB, finger clubbing, severe weight loss

49
Q

What causes Farmer’s lung?

A

Saccharopolyspora rectivirgula (mouldy hay, grain, silage)

50
Q

What causes Pigeon’s fancier’s Lung?

A

proteins in excreta/feathers

51
Q

What causes Malt-workers lung?

A

Aspergillus clavatus/fumigatus (Germinating barley)

52
Q

What causes Humidifiers lung?

A

thermactinomyces spp. (heated water reservoirs)

53
Q

What causes cheese washer’s lung?

A

Aspergillus clavatus/penicillium casei (mouldy cheese)

54
Q

What are Extrinsic allergic alveolitis and Cryptogenic organising pneumonia?

A

Immune mediated lung disorders cause by intense/prolonged exposure to inhaled organic antigens –> widespread alveolar inflammation

55
Q

What is Extrinsic allergic alveolitis typically associated with?

A

Occupational lung disease (person will probably have a weird hobby or job on Q)

56
Q

What is another name for extrinsic allergic alveolitis?

A

Hypersensitivity pneumonitis

57
Q

What is another name for Cryptogenic organising pneumonia?

A

Bronchiolitis obliterans organising pneumonia (BOOP)

58
Q

Give 5 examples of an Extrinsic Allergic Alveolitis

A

farmer’s lung, Pigeon fancier’s lung, Humidifier’s Lung, Malt-workers Lung, Cheese washer’s lung

59
Q

What are the 4 stages of Lobar pneumonia?

A
  1. Consolidation 2. Red Hepatisation (neutrophilia) 3. Grey Hepatisation (Fibrosis) 4. Resolution
60
Q

What kind of consolidation is seen in Lobar pneumonia?

A

Fibrinosupparative consolidation

61
Q

What is the most common cause of Lobar pneumonia?

A

Strep. Pneumonia

62
Q

What kind of consolidation is seen in Bronchopneumonia?

A

Patchy bronchial/peri-bronchial distribution

63
Q

What kind of organisms cause bronchopneumonia?

A

Low virulence organisms

64
Q

What kind of consolidation/inflammation do you get in Atypical pneumonias?

A

Interstitial pneumonitis. No intra-alveolar inflammation.

65
Q

What are your atypical causes of pneumonia? (there are 6)

A

Legionella pneumophilia; Mycoplasma pneumonia; Chlamydia pneumonia; Chlamydia psittaci; Boratella pertussis; TB

66
Q

What is the most common tumour of the lung?

A

Squamous cell carcinoma

67
Q

What lung tumour is most common in women and non-smokers?

A

Adenocarcinoma

68
Q

Which lung cancer is associated with ectopic ACTH secretion and Lambert-Eaton?

A

Small Cel carcinoma

69
Q

Which lung cancer has the highest rate of p53/c-myc mutations?

A

Squamous cell carcinoma

70
Q

Where do squamous cell carcinomas typically occur? And how quickly do they metastasize?

A

Proximal bronchi - local spread with late metastasis

71
Q

Where do adenocarcinomas typically occur? And how quickly do they metastasize?

A

Peripherally (alveoli). Metastasizes early

72
Q

Where do small cell carcinomas typically occur? And how quickly do they metastasize?

A

Occur centrally, proximal bronchi. Highly malignant, metastasize early, usually by diagnosis they have spread to bone, adrenal, liver and brain.

73
Q

Which lung cancer is the most chemosensitive? Which is the least chemosensitive?

A

Most sensitive = Small Cell carcinoma, but still has bad prognosis due to early metastasis. Least sensitive = Squamous Cell Carcinoma

74
Q

What is seen on histology of a squamous cell carcinoma?

A

Keratinisation, intracellular prickles (desmosomes)

75
Q

What is seen on cytology of Squamous Cell Carcinoma?

A

Squamous cells!!

76
Q

How does Squamous Cell Carcinoma progress?

A

Epithelium –> Hyperplasia –> squamous metaplasia –> angiosquamous dysplasia –> carcinoma in situ –> invasive carcinoma

77
Q

Which lung cancer is associate with cavitation and hypercalcaemia?

A

Squamous cell carcinoma

78
Q

What is seen on histology of an Adenocarcinoma?

A

glandular differentiation (gland formation and mucin production)

79
Q

What is seen on cytology of Lung Adenocarcinoma

A

Cells containing mucin vacoules

80
Q

What mutations are seen in Adenocarcinoma?

A

EGFR mutations

81
Q

What is the progression of Adenocarcinoma?

A

Atypical adenomatous hyperplasia –> non mucinous BAC –> mixed pattern adenocarcinoma

82
Q

From what type of cell does Adenocarcinoma originate? What differentiation is seen?

A

Epithelial cell, glandular differentiation or mucin production

83
Q

Where do Small Cell Carcinomas arise from?

A

Neuroendocrine cells

84
Q

What mutations are commonly seen in Small cell carcinoma?

A

p53 and RB1

85
Q

Which lung cancers have a strong correlation with Smoking?

A

Squamous cell carcinoma, Small cell carcinoma

86
Q

What type of cell does a Large cell carcinoma evolve from?

A

Epithelial cell –> it is a poorly differentiated epithelial tumor

87
Q

What is seen on histology of Large Cell Carcinoma?

A

No evidence of glandular or squamous differentiation. Large cells, large nuclei, prominent nucleoli.

88
Q

Staging of lung cancer

A

TNM staging: T1-4 based on size and invasion of pleura, pericardium; N0-2 lymph node involvement; M0-1 whether there is distant metastasis

89
Q

Which gene is associated with poorer response to Cisplatin?

A

ERCC1-NSCLC

90
Q

Which gene provides a taregt for Anti-EGFR therapy, and what type of lung cancer is it normally seen in?

A

EGFR, usually in adenocarcinomas

91
Q

Which genes have no response to TK inhibitors, and so a poor prognosis? What form of lung cancer are they each associated with?

A

Kras = Adenocarcinoma + Squamous; EML4-ALK = usually Adeno

92
Q

Risk factors for PE?

A

Female, immobility, cardiac disease, cancer, OCP, pregnancy, primary and secondary hypercoaguable states

93
Q

What is a saddle embolus?

A

An embolus occluding the pulmonary trunk

94
Q

What happens in a PE (Pathologically)?

A

Large emboli impact in the main pulmonary arteries leading to acute cor pulmonale, cardiogenic shock and death if >60% of pulmonary bed occluded

95
Q

How can small emboli present?

A

May be silent, or cause peripheral wedge infarction. Repeated infarctions can result in pulmonary HTN, and then RHF

96
Q

Give some examples of non-thrombotic emboli

A

bone marrow, amniotic fluid, tumour, air, foreign body

97
Q

What is the definition of Pulmonary HTN?

A

Mean pulmonary arterial pressure of over 25mmHg at rest

98
Q

What are the causes of Pulmonary HTN?

A

Primary or Secondary (more common), due to chronic lung diseases, heart disease, recurrent thrombo-emboli and autoimmune disorders

99
Q

Secondary causes of Pulmonary HTN can be split up by aetiology. List these, and give an example for each.

A

Pre-capillary: chronic hypoxia/embolus; Capillary: Pulmonary Fibrosis; Post-Capillary = Left Heart Disease/Veno-occlusive Disease

100
Q

Who is most likely to present with a primary pulmonary HTN?

A

Women aged 20-40yrs.

101
Q

What are the complications of Pulmonary HTN?

A

RHF - venous congestion of organs (nutmeg liver), peripheral oedema

102
Q

What is pulmonary oedema?

A

INTRA ALVEOLAR fluid accumulation leads to poor gas exchange

103
Q

What is the main cause of pulmonary oedema?

A

Left Heart Failure

104
Q

In pulmonary oedema, what is seen on histology?

A

Intra-alveolar fluid and iron laden macrophages (‘heart failure cells’)

105
Q

What is the name of Diffuse Alveolar damage in adults and neonates?

A

Adults = ARDS; Neonates = HMD (Hyaline Membrane Disease)

106
Q

What is the cause of diffuse alveolar damage in Neonates?

A

Insufficient surfactant production in prems

107
Q

What is the cause of diffuse alveolar damage in adults?

A

Infection, aspiration, trauma.

108
Q

What is seen on histology in diffuse alveolar damage?

A

Lung expanded, firm, plum-coloured, airless.

109
Q

How does Diffuse Alveolar damage present?

A

Rapid onset respiratory failure!

Y5 Histopathology (3 decks)

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