Respiratory Pathology Flashcards

1
Q

What type of epithelium does the conducting airways of the lung have?

A

Pseudostratified ciliated columnar epithelium.

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2
Q

What type of epithelium is present in the alveoli?

A

Type 1 and 2 Pneumocytes

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3
Q

What is the function of Type 1 Pneumocytes?

A

Mucus production.

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4
Q

What is the function of Type 2 Pneumocytes?

A

Surfactant production

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5
Q

Under what partial pressure of oxygen are you in respiratory failure?

A

8.0kPa

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6
Q

What is Type 1 respiratory failure?

A

PaCO2

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7
Q

What is Type 2 respiratory failure?

A

PaCO2 >6.3kPa

Hypercapnic resp drive

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8
Q

What is a stridor?

A

Proximal airway obstruction

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9
Q

What is a wheeze?

A

Distal airway obstruction

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10
Q

Why are crackles heard on resp auscultation?

A

Resisted small airways opening

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11
Q

Why are wheezes heard on resp auscultation?

A

Narrowed small airways

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12
Q

What is a pleural rub?

A

Relative movement of inflamed viscera and parietal pleura.

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13
Q

Why would a dull percussion be felt ?

A

Lung consolidation/pleural effusion.

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14
Q

Why would a hyper resonant percussion be felt?

A

Pneumothorax/emphysema.

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15
Q

What malignant lung tumours are common?

A

Carcinoma (90%)

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16
Q

What is the biggest risk factor for lung carcinoma?

A

Cigarettes

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17
Q

What type of material is asbestos?

A

Fibrous metal silicate

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18
Q

Which asbestos is the most dangerous?

A

Blue asbestos

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19
Q

Which asbestos is the least dangerous?

A

White asbestos

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20
Q

What disease can high level exposure to Asbestos cause?

A

Pulmonary interstitial fibrosis asbestosis

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21
Q

How can asbestos bodies be viewed?

A

Light microscopy

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22
Q

What are asbestos fibres coated with?

A

Mucopolysaccharide and ferric iron salts.

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23
Q

What type of carcinoma is in 85% of cases?

A

Non-small cell carcinoma

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24
Q

What type of carcinoma is in 15% of cases?

A

Small cell carcinoma

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25
Q

What is the most common type of non-small cell carcinoma?

A

Squamous carcinoma

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26
Q

What type of carcinomas are small cell carcinomas?

A

All neuroendocrine

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27
Q

In what type of carcinoma is multiple differentiation common?

A

Small cell carcinoma

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28
Q

What can be detected in lung non-mucinous adenocarcinomas and small cell carcinomas?

A

> Thyroid transcription factor

> Cytokeratin

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29
Q

Where is the most common lung carcinoma site?

A

Central, upper lobe, main bronchus.

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30
Q

Where is adenocarcinoma mostly?

A

More peripheral

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31
Q

What is present in squamous carcinoma?

A

> Keratin

> Desmosomes

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32
Q

Where is squamous carcinoma more present?

A

Central > peripheral

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33
Q

Why can squamous carcinoma cause hypercalcaemia?

A

Parathyroid hormone related peptide

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34
Q

What change occurs in a squamous metaplasia?

A

Pseudostratified columnar epithelium –> Stratified squamous.

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35
Q

How is a neoplastic cell made?

A

Irreversible genetic changes to a metaplastic cell

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36
Q

What occurs in dysplasia?

A

> Neoplastic cell made
Neoplastic cell proliferate more than metaplastic cell
Neoplastic clone replaces metaplastic cell.

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37
Q

What is an adenocarcinoma?

A

Malignant tumour of glandular structures of epithelial tissue.

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38
Q

Where are adenocarcinomas most likely found?

A

Central as much as peripheral.

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39
Q

In non-mucinous lung adenocarcinomas what may be expressed?

A

Thyroid transcription factor.

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40
Q

What is a bronchioalveolar carcinoma ?

A

When well-differentiated non/mucinous neoplastic cells spread to alveolar walls.

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41
Q

What does bronchioalveolar carcinoma mimic?

A

Pneumonia

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42
Q

Where do typical carcinoid tumours occlude?

A

Bronchi

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43
Q

What are typical carcinoid tumours associated with?

A

Multiple endocrine neoplasia syndrome type 1.

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44
Q

Where do approx. 10% of typical carcinoid tumours metastasize to?

A

Hilar nodes

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45
Q

How are atypical carcinoid tumours different from typical?

A

> Necrotic
Less organoid, more atypical
More aggressive

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46
Q

What are the features of large cell neuroendocrine carcinomas?

A

> Severe atypia

> Necrosis

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47
Q

What are large cell neuroendocrine tumours assc with?

A

Smoking

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48
Q

What are the features of small cell carcinoma?

A

> Rapidly progresses + malignant.
Have neurosecretory granules w/ peptide hormones.
~99% in smokers

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49
Q

What do 50% of Large cell carcinoma express?

A

Thyroid transcription factor

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50
Q

What do large cell carcinomas express that can make them neuroendocrine?

A

> Express CD56

> Neurosecretory granule proteins (synaptophysin, chromogranin)

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51
Q

What are some of the paraneoplastic effects of lung carcinoma?

A
> Cachexia
> Skin - tylosis, acanthosis,  nigricans
> Clubbing
> Thrombophlebitis migrans
> Lambert- Eaten syndrome 
> Hypercalcaemia
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52
Q

What are Getifinib and Erlotinib examples of?

A

Epidermal growth factor receptor tyrosine kinase inhibitors

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53
Q

How do EGFR-TR inhibitors work?

A

> Inhibit EGFR-TK mediated protein phosphorylation

> Activate mitotic cycle

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54
Q

EGFR-TK sensitising mutations are present in what cancer?

A

Non-small cell lung cancers

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55
Q

ALK gene rearrangements are found in what cancer?

A

Lung adenocarcinomas

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56
Q

What is Crizotinib?

A

An ATP analog that inhibits tyrosine kinases.

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57
Q

What is Crizotinib effective in?

A

90% of tumours w/ ALK-EML fusion gene.

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58
Q

What are the two causes (broad) of Pleural diseases?

A

Inflammatory and non-inflammatory.

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59
Q

What are the inflammatory causes of pleural diseases?

A

> Serous/fibrinous exudate

> Inflammation/ infection in adjacent lung.

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60
Q

What are the non-inflammatory causes of pleural disease?

A

Congestive heart failure forms a transudate.

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61
Q

How are pleural diseases diagnosed?

A

> Lactase dehydrogenase
pH
Glucose of fluid

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62
Q

What conditions can cause Pleuritis?

A
> Collagen vascular diseases
> TB
> Lung infarct, secondary to PE
> Lung Tumour
> Asbestos
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63
Q

Is malignant or benign pleurisy more common?

A

Malignant

64
Q

What is pleurisy usually secondary to?

A

Adenocarcinoma

65
Q

What exposure is malignant mesothelioma associated with?

A

Asbestos (low level)

66
Q

What is the latent period for malignant mesothelioma?

A

15-60 year latent period

67
Q

What is the pathway of malignant mesothelioma?

A

> Initial nodule and effusion
Obliterates pleural cavity
Invades chest wall and lung

68
Q

What is malignant mesothelioma hard to differentiate from?

A

Reactive mesothelial cells in inflamed pleura.

69
Q

How do you differentiate malignant mesothelioma from adenocarcinoma?

A

Cellular antigen expression

70
Q

What may early malignant mesothelioma present as?

A

Small plaques on the parietal pleura

71
Q

Where are fibrous pleural plaques found?

A

Lower thoracic wall and diaphragmatic parietal pleura.

72
Q

What are fibrous pleural plaques assc with?

A

Low level asbestos exposure

73
Q

Define: Pneumonia

A

An inflammatory exudate in the alveoli & distal small airways.

74
Q

What different classes does Pneumonia have?

A

> Clinical
Aetiological
Anatomical
Reaction

75
Q

What is bronchopneumonia secondary to?

A

Compromised defences

76
Q

What is the cause of bronchopneumonia?

A

Low virulence bacteria / occ fungi.

77
Q

What is the consolidation of bronchopneumonia like?

A

Patchy and common

78
Q

What is the cause of 90% of lobar pneumonia?

A

Streptococcus Pneumoniae

79
Q

Is consolidation common in Lobar Pneumonia?

A

No

80
Q

Which pneumoniae leaves scarring?

A

Lobar pneumonia

81
Q

What causes lobar pneumonia in the elderly, diabetic and alcoholic?

A

Klebsiella pneumoniae

82
Q

What virus can cause pneumonia in the non-immunosuppressed?

A
> Varicella
> Respiratory Syncytial Virus
> Adenovirus
> Measles 
> Flu
83
Q

What are the characteristics of pneumonia caused by Mycoplasma penumoniae?

A

Mild, chronic fibrosis.

84
Q

What is the severity of Legionella pneumophilia?

A

Mild to fatal

85
Q

What type of pneumonia is intra-alveolar fibrinous cell-poor exudate assc with?

A

Legionella pneumoniae

86
Q

What are aspiration, lipid, COP and BOOP examples of?

A

Non-infective pneumonias

87
Q

What does aspiration pneumonia result in?

A

Abscesses

88
Q

What are the two sources of lipid pneumonia?

A

> Exogenous

> Endogenous

89
Q

What is an example of endogenous lipid pneumonia?

A

Retention pneumonitis

90
Q

What does COP stand for?

A

Cryptogenic organising pneumonia

91
Q

What does BOOP stand for?

A

Bronchiolitis Obliterans Organising Pneumonia

92
Q

What is the cause of Pulmonary TB?

A

Mycobacterium Tuberculosis

93
Q

What is the most common site of Pulmonary TB?

A

The lungs

94
Q

What is the fatality rate of Pulm. TB?

A

50% if left untreated

95
Q

How is pulm. TB prevented?

A

BCG vaccine

96
Q

What is primary presentation of pulmonary TB?

A

Ghon complex (lesion) in peripheral lung and hilar nodes.

97
Q

Where does pulm. TB usually reactivate?

A

Apex

98
Q

What can pulm. TB progress into?

A

> Empeyma
Pneumonia
Miliary TB

99
Q

What is the scarring of pulm. TB?

A

FIBROUS CALCIFIED SCAR
> Granuloma with multi-nucleated Langhan’s giant cells
> Caseous necrosis

100
Q

The Heaf and Mantoux test what?

A

Type IV hypersensitivity to tuberculin.

101
Q

What are Wegner’s granulomatosis and Churg-Strauss syndrome examples of?

A

Necrotising granulomatous vasculitis

102
Q

What is the mechanism of Goodpasture’s syndrome?

A

Anti-glomerular basement membrane antibody attack basement membrane of lung/kidney.

103
Q

What is the result of Goodpasture’s syndrome?

A

> Intra-alveolar haemorrhage

> Glomerulonephritis

104
Q

What do Acute resp disress syndrome, diffuse alveolar damage and SLE do?

A

Microvascular pulmonary damage.

105
Q

How can fat emboli occur?

A

Fat and marrow from bone fractures

106
Q

What are examples of localised obstructive pulmonary diseases?

A

> Distal alveolar collapse (total)
Over expansion (valvular obstruction)
Distal retention pneumonitis
Distal bronchiecstasis

107
Q

What is bronchiectasis?

A

Elastic/tissue damage causing permanent dilation of bronchioles.

108
Q

What causes bronchiectasis?

A

Chronic necrotising infections.

109
Q

What are the signs/symptoms of bronchiectasis?

A

Cough, fever, lots of foul smelling sputum.

110
Q

What are the complications of bronchiectasis?

A

> Pneumonia
Septicaemia
Metastatic infection

111
Q

What are examples of diffuse obstructive pulmonary diseases?

A

> COPD

> Asthma

112
Q

Define: Chronic Bronchitis

A

Cough/sputum in 3 months of each of two consecutive years.

113
Q

What is the cause of chronic bronchitis? (Hint: long term)

A

Long term smoking/air pollution.

114
Q

What is the pathology of chronic bronchitis?

A

> Mucus gland hyper secretion/hyperplasia
Low virulence bacteria = secondary infection
Chronic inflammation of small airways
Wall weakness & destruction –> centrilobar emphysema.

115
Q

Define: Emphysema

A

Abnormal permanent dilation of areas distal to terminal bronchioles (alveoli).

116
Q

What are the different types of emphysema?

A

> Centrilobular
Panlobular
Paraseptal

117
Q

What causes centrilobular emphysema?

A

Coal dust and smoking

118
Q

What causes panlobular emphysema?

A

> 80% = a1 anti-trypsin deficient

119
Q

What causes paraseptal emphysema?

A

Upper lobe subplural bullae. If rupture –> pneumothorax

120
Q

What are the symptoms of Emphysema?

A

Dyspnoea - progressive and worsening.

121
Q

What is Asthma?

A

Chronic inflammatory disorder of the airways

122
Q

What are the symptoms of Asthma?

A

Wheeze, cough, variable bronchoconstriction

123
Q

What are the clinical features of asthma?

A
> Mucosal inflammation
> Mucosal oedema
> Mucosal plugs
> Hypertrophic mucous glands
> Hyperinflated lungs
124
Q

What are the classifications of Asthma?

A

> Atopic
Non-atopic
Aspirin-induced
Allergic bronchopulmonary aspergillosis (ABPA).

125
Q

What are the causes of Type 1 hypersensitivity reaction?

A

> Allergen, cold, exercise, resp infections

> Degranulation of IgE mast cells –> histamine mediated mucus production and bronchoconstriction –> obstruct airway.

126
Q

What are the irreversible changes of asthma?

A

> Bronchiole wall smooth muscle hypertrophy
Mucus gland hyperplasia
Respiratory bronchiolitis  centrilobular emphysema

127
Q

What are interstitial lung diseases?

A

Diseases affecting lung interstitium (tissue and space around lung air sacs)

128
Q

Are interstitial lung diseases restrictive or obstructive?

A

Restrictive

129
Q

Interstitial lung diseases have abnormal what tissue?

A

Pulmonary connective tissue

130
Q

What are the two phases of diffuse alveolar damage (DAD)?

A
  1. Exudative phase - Alveoli flooded with transudate

2. Hyaline membrane production, stop O2 being absorbed by damaged alveoli.

131
Q

What is the appearance of a chronically fibrosed lung?

A

Honeycomb

132
Q

What are the causes of Chronic interstitial lung disease?

A

> Interstitial fibrosis
Chronic inflammation
Pneumoconiosis (dust diseases)
Sarcoidosis

133
Q

What are the symptoms of chronic interstitial lung disease?

A

> Dyspnoea (for years)
Clubbing
Fine crackles
Dry cough

134
Q

What are affected first in idiopathic pulmonary fibrosis?

A

Lower lobes, and most severely.

135
Q

What histology characterizes idiopathic pulmonary fibrosis ?

A

Usual Interstitial Pneumonia

136
Q

What are the features of UIP?

A

> Normal alveolar walls
Interstitial chronic inflammation
Mature fibrous tissue

137
Q

Why is the pleura cobblestoned in idiopathic pulmonary fibrosis?

A

Contraction of fibrous tissue accentuates lobular architecture.

138
Q

What is Sarcoidosis? (HARD)

A

Non-caseating perilymphatic pulmonary granulomas, then fibrosis.

139
Q

What is involved usually in Sarcoidosis?

A

> Hilar nodes

> Skin, heart and brain ~affected.

140
Q

What do clinical tests for Sarcoidosis show?

A

> Hypercalcaemia

> Elevated serum angiotensin converting enzyme.

141
Q

What is Pneumoconiosis?

A

A non-neoplastic lung disease due to dust inhalation.

142
Q

What diameter do things need to be to reach the alveoli?

A
143
Q

What does coal worker’s pneumoconiosis begin as?

A

Anthracosis = milder, asymptomatic

144
Q

What forms does coal worker’s pneumoconiosis have?

A

Simple and nodular –> progress to massive fibrosis.

145
Q

What does >20 years of mining underground increase the risk of?

A

COPD

146
Q

What does Silicosis kill?

A

Kills phagocytosing macrophages.

147
Q

What does Silicosis reactivate?

A

TB

148
Q

What is the result of high level asbestos exposure?

A

Interstitial fibrosis

149
Q

What type of hypersensitivity reaction is Hypersensitivity pneumonitis?

A

Type 3

150
Q

What is CF?

A

A multiorgan epithelial disorder affecting exocrine gland secretion.

151
Q

On what chromosome is the CTFR gene?

A

Chromosome 7

152
Q

What is the presentation of CF in the lungs?

A

> Mucus secreting glands hyperplasia.
Bronchioles distended with mucus
Chronic bronchitis and bronchiectasis.

153
Q

What is the presentation of CF in the pancreas?

A

> Pancreatic insufficiency
Mucus plugged glands
Glands atrophy/fibrosis

154
Q

What is meconium ileus?

A

Mucus plug in small bowel.

155
Q

What are the other organ defects of CF (liver, salivary glands)

A

> Liver - plugging of bile cannaliculi

> Salivary glands - atrophy and fibrosis.