Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

3. CP - Diseases of the Respiratory System > (15+16) Respiratory pathology > Flashcards

(15+16) Respiratory pathology Flashcards

1
Q

What do the conducting airways consist of? (lung anatomy)

A
  • trachea
  • left and right main bronchi
  • segmental and smaller bronchi
  • bronchioles, terminal bronchioles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The respiratory bronchioles terminate in the lung acini where gas exchange occurs. What makes up the acini?

A
  • alveolar ducts
  • alveolar sacs
  • alveoli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How many lung acini make up a lobule?

A

3 to 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the histology of the conducting airways of the lungs?

A

Pseudostratified ciliated columnar mucus secreting epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the histology of the alveoli?

A

Mostly flat type I pneumocytes (gas exchange)

Some rounded type II penumocytes (surfactant production)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the function of the type I pneumocytes in the alveoli?

A

Gas exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the function of the type II pneumocytes in the alveoli?

A

Surfactant production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Respiratory failure is defined as having a PaO2 of what?

A

Less than 8.0kPa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Respiratory failure is due to defective what?

A
  • ventilation
  • perfusion
  • gas exchange
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What defines type I respiratory failure?

A

paO2 less than 8.0kPa
paCO2 less than 6.3kPa

Hypoxic respiratory drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What defines type II respiratory failure?

A

paO2 less than 8.0kPa
paCO2 more than 6.3kPa

Hypercapnic respiratory drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the general respiratory signs and symptoms?

A
  • sputum
  • cough
  • stridor
  • wheeze
  • pleuritic pain
  • dyspnoea
  • cyanosis
  • clubbing
  • weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the difference between stridor and wheeze?

A

Stridor = inspiratory sound, proximal airway obstruction

Wheeze = expiratory sound, distal airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How may sputum be described?

A
  • mucoid
  • purulent
  • haemoptysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a cough?

A

Reflex response to irritation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes pleuritic pain?

A

Pleural irritation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What causes dysponea?

A

Impaired alveolar gas exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What causes cyanosis?

A

Decreased oxygenation of haemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

When might you get weight loss?

A

Catabolic state with chronic inflammation or tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are you looking for on auscultation of the lungs?

A
  • crackles (fine or coarse)
  • wheeze
  • bronchial breathing
  • pleural rub
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When do you get fine crackles on auscultation of the lungs?

A

Resisted opening of small airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

When do you get coarse crackles on auscultation of the lungs?

A

Excessive fluid within the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is/when do you get bronchial breathing?

A

Sound conduction through solid lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When do you get pleural rub on auscultation of the lung?

A

Relative movement of inflamed visceral and parietal pleura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are you listening for on percussion of the lungs?

A
  • dull

- hyper-resonant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What might lungs that are dull on percussion suggest?

A

Lung consolidation or pleural effusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What might lungs that are hyper-resonant on percussion suggest?

A

Pneumothorax or emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Give some categories of lung diseases

A
  • neoplasms
  • infections
  • obstructive airways diseases
  • interstitial lung diseases
  • vascular diseases
  • pleural diseases
  • occupational lung diseases
  • paediatric lung pathology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Give some examples of infections affecting the lungs

A
  • pneumonia

- tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Give some examples of obstructive airways diseases

A
  • asthma

- COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Give some examples of interstitial lung diseases

A
  • adult respiratory distress syndrome
  • fibrosing alveolitis
  • sarcoidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Give some examples of vascular lung diseases

A
  • pulmonary embolism

- pulmonary hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Benign primary lung tumours are rare. Give one example

A

Adenochondroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What percentage of primary lung tumours are malignant carcinomas?

A

90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What percentage of lung carcinomas are due to smoking?

A

80%

secondary cigarette smoke - 10-30% increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How many deaths from malignant primary lung tumours are there in the UK every year?

A

35,000

8% of male deaths, 4% of female deaths

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What causes 10% of male lung carcinomas?

A

Asbestos

High level exposure, with or without asbestosis

About 2000 cases per year in UK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What 3 main lung diseases does asbestos cause?

A
  • mesothelioma
  • lung cancer
  • asbestosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the risk factors for lung carcinoma?

A
  • smoking
  • asbestos
  • lung fibrosis
  • radon
  • chromates, nickel, tar, hematite, arsenic, mustard gas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is squamous metaplasia?

A

Metaplastic change from pseudostratified columnar epithelium of the bronchus to stratified squamous type which may keratinise (like skin)

  • caused by irritants such as smoke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What percentage of primary lung tumours are malignant carcinomas?

A

90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What percentage of lung carcinomas are due to smoking?

A

80%

secondary cigarette smoke - 10-30% increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How many deaths from malignant primary lung tumours are there in the UK every year?

A

35,000

8% of male deaths, 4% of female deaths

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What causes 10% of male lung carcinomas?

A

Asbestos

High level exposure, with or without asbestosis

About 2000 cases per year in UK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What 3 main lung diseases does asbestos cause?

A
  • mesothelioma
  • lung cancer
  • asbestosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the risk factors for lung carcinoma?

A
  • smoking
  • asbestos
  • lung fibrosis
  • radon
  • chromates, nickel, tar, hematite, arsenic, mustard gas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is asbestos?

A

Fibrous metal silicates,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the different types of asbestos?

A

Amphiboles

  • blue asbestos (crocidolite)
  • brown asbestos (amosite)

Serpentines

  • white asbestos (chrysotile)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Which is the least dangerous type of asbestos?

A

White asbestos (chrysotile)

Serpentine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Which is the most dangerous type of asbestos?

A

Blue asbestos (crocidolite)

Amphibole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What does high level exposure of asbestos produce?

A

Pulmonary interstitial fibrosis

  • asbestosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What allows you to see asbestos bodies?

A

Light microscopy

  • fibres coated with mucopolysaccharide and ferric iron salts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

High level exposure to asbestos is associated with higher incidence of what?

A

All types of lung carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the hypotheses concerning asbestos?

A

fibrosis - no increased risk without asbestosis

fibre burden - dose-related, some risk at all exposure level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the problems concerning asbestos and lung carcinomas?

A

effects of smoking - multiplicative risk

diagnosing asbestosis

quantification of asbestos exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Give some epidemiological evidence FOR the connection between asbestos and lung carcinoma

A
  • increased risk in workers exposed to asbestos

- increased risk in the absence of “small opacities” on CXR in asbestos exposed workers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Give some epidemiological evidence AGAINST the connection between asbestos and lung carcinoma

A
  • no increased risk in low level exposed workers

- no increased risk in Canadian asbestos mining towns inhabitants with no occupational exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

When is lung carcinoma a ‘prescribed occupational disease’ in the UK?

A
  • lung carcinoma with asbestosis, asbestos related diffuse pleural fibrosis or silicosis
  • lung carcinoma without asbestosis but history of over 5 years work in a high exposure occupation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Give some examples of asbestos high exposure occupations

A
  • asbestos insulation work
  • ship building and repair
  • asbestos textile work
  • manufacture of gas masks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the different types of malignant primary lung tumours?

A

Carcinoma

  • non-small cell carcinoma
  • small cell carcinoma

Carcinoid tumours

Others (lymphomas, sarcomas, carcinosarcomas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Which is the most common lung carcinoma?

A

Non-small cell carcinoma = 85%

Small cell carcinoma = 15%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the different types of non-small cell carcinoma?

A
  • squamous carcinoma (52%)
  • adenocarcinoma (13%)
  • large cell neuroendocrine carcinoma
  • undifferentiated large cell carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

All small cell carcinomas are what?

A

Neuroendocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is a key feature of lung carcinomas?

A

Multiple differentiation is common

multiple different lines of differentiation, different characteristics, hard to classify

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are carcinoid tumours?

A

Low grade neuroendocrine epithelial tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

The comments tumours in the lung are what?

A

Secondary tumours - usually from a known primary but may be the presenting feature of a distant primary tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Secondary lung tumours are typically what?

A

Multiple bilateral nodules but can be solitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What do you look for to distinguish between a primary and secondary lung tumour?

A
  • history
  • morphology (some adenocarcinomas, but not squamous)
  • antigen expression (immunocytochemistry is useful but not 100% reliable)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What do lung non-mucinous adenocarcinoma and small cell express? (immunocytochemistry)

A
  • cytokeratin positive

- thyroid transcription factor positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What do colorectal tumours express? (immunocytochemistry)

A
  • cytokeratin 7 negative

- cytokeratin 20 positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What do upper gastrointestinal tract tumours express? (immunocytochemistry)

A
  • cytokeratin 7 positive

- cytokeratin 20 positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What do breast tumours express? (immunocytochemistry)

A
  • may be oestrogen receptor positive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What do melanomas express?

A
  • S100
  • HMB45
  • MelanA positive
  • cytokeratin negative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the sites of lung carcinomas?

A
  • mostly central, main or upper lobe bronchus (bronchogenic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Most lung carcinomas are central but which lung carcinomas are more peripheral?

A

Adenocarcinoma

  • scar cancers or cancer with a fibrous (desmoplastic) reaction?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Give some features of squamous carcinoma

A
  • desmosomes link cell like epidermis ‘epidermoid’
  • may or may not have keratinisation
  • more central than peripheral
  • 90% in smokers
  • cough and haemoptysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Which condition may you get in squamous carcinoma due to parathyroid hormone related peptide?

A

Hypercalcaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe the normal bronchial epithelium

A

The normal bronchus is lined by pseudostratified columnar epithelium with ciliated and mucus-secreting cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is squamous metaplasia?

A

Metaplastic change from pseudostratified columnar epithelium of the bronchus to stratified squamous type which may keratinise (like skin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

How does dysplasia initially begin?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What happens in developing dysplasia (after the first neoplastic cell has been produced)?

A

The neoplastic cell proliferates more successfully than the metaplastic cells

The neoplastic clone replaces the metaplastic cells producing dysplasia (intraepithelial neoplasia or carcinoma-in-situ)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

How does a developing dysplasia go on to form squamous carcinoma?

A

Neoplastic cells breach the basement membrane producing invasive squamous carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

How do neoplastic cells form metastases?

A

Invading neoplastic cells infiltrate the lymphatic and blood vessels to produce metastases in lymph nodes and distant sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

A carcinoma obstructing a bronchus may cause what?

A

Distal retention pneumonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Give the key features of adenocarcinoma

A

A malignant tumour formed from glandular structures in epithelial tissue

Forms in mucus-secreting glands throughout the body

  • serous +/- mucus vacuoles
  • in acinar, tubular, solid or papillary structures
  • 80% in smokers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is expressed in many non-mucinous lung adenocarcinomas?

A

Thyroid transcription factor (TTF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is adenocarcinoma in situ also called?

A

Bronchioloalveolar carcinoma - it is non-invasive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is adeoncarcinoma in situ/bronchioloalveolar carcinoma?

A

Term describing certain variants of lung cancer arising in the distal bronchioles or alveoli that initially exhibit a specific non-invasive growth pattern. BAC is a type of non-small-cell lung cancer (NSCLC)

Spread of well differentiated mutinous or non-mucinous neoplastic cells on alveolar walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What disease may bronchioloalveolar carcinoma mimic?

A

Pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What are the neuroendocrine cell proteins identified by immunocytochemistry?

A
  • neural cell adhesion molecule (CD56)

- neurosecretory granule proteins (chromogranin, snaptophysin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

How else can neurosecretory granules be identified?

A

Electron microscopy (not done in routine clinical practice)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are Kulchitsky cells?

A

Type of neuroendocrine cell occurring in the epithelia lining the respiratory tract (neuroendocrine cell in normal mucosa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Describe the spectrum of

malignancy of neuroendocrine tumours

A
  • large cell neuroendocrine carcinoma
  • small cell carcinoma
  • carcinoid
  • atypical carcinoid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What do neuroendocrine tumours develop from?

A

Intraepithelial neuroendocrine cell hyperplasia and carcinoid tumourlets (

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Give some features of carcinoid tumours

A
  • often grow into and occlude a bronchus
  • organoid
  • bland cells
  • no necrosis
  • low mitotic rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are typical carcinoid tumours associated with?

A

Multiple endocrine neoplasia syndrom type 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Which type of lung cancer is not associated with smoking?

A

Typical carcinoid tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Are carcinoid tumours benign or malignant?

A

Often thought of as being benign but they are not; they have low malignant potential

May invade lymphatic vessels and nodes but rare distant metastases

6-9% to hilar nodes, less to distant sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the general prognosis for typical carcinoid tumours?

A

95% 5 year survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What percentage of lung carcinoids are atypical?

A

11%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Describe the features of atypical carcinoid tumours compared to typical carcinoid tumours

A
  • less organoid
  • more atypia
  • nucleoli - may be focal atypia in an otherwise typical carcinoid
  • necrosis
  • slightly higher mitotic rate (2-10 mitotic figures per 2sqmm compared to
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is the prognosis for atypical carcinoid tumours compared to typical carcinoid tumours?

A

More aggressive than typical carcinoids

  • 70% metastasise
  • 60% 5 year survival
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Describe the morphology of large cell neuroendocrine carcinomas

A

Neuroendocrine morphology

  • organoid architecture
  • eosinophilic granular cytoplasm
  • antigen expression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Describe the features of large cell neuroendocrine carcinoma

A
  • severe atypia
  • nucleoli
  • necrosis
  • > 11 mitotic figures per 2sqmm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What is the prognosis for large cell neuroendocrine carcinomas?

A

Similar to or worse than other non-small cell lung carcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Is large cell neuroendocrine carcinoma associated with smoking?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Describe the main features of 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Has there been a “small cell carcinoma in situ” identified?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Small cell carcinoma usually presents at which stage?

A

At a late advanced stage with lots of metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

How common are carcinomas with multiple differentiation?

A

Common

Around 50%, depends on extent of sampling

  • mixed NSCLC
  • combined small cell carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is a combined small cell carcinoma?

A

When a tumour contains a component of small cell carcinoma mixed with NSCLC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is an adenosquamous carcinoma?

A

Mixed NSCLC

(need 10% of a component for classification)

Contains two types of cells: squamous cells and gland-like cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Describe the features of large cell carcinomas

A
  • no specific squamous or glandular morphology

- can be neuroendocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What do 50% of large cell carcinomas express?

A

Thyroid transcription factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

If a large cell carcinoma is neuroendocrine, what will it express?

A
  • CD56

- neurosecretory granule proteins (synaptophysin, chromogranin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What is lymphangitis carcinomatosa?

A

Inflammation of the lymph vessels caused by a malignancy

Caused by the dissemination of a tumor with its cells along the lymphatics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What are the paraneoplastic effects of lung carcinomas?

A
  • cachexia
  • skin - acanthoses nigricans, tylosis
  • clubbing
  • coagulopathies
  • encephalomyelitis, neuropathies and myopathies
  • endocrine effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Acanthoses nigricans is a paraneoplastic effect of lung carcinomas. What is it?

A

Darkened, thickened patches of skin that usually develop in the armpit and around the groin and neck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is the name of the condition that includes clubbing called when related to lung carcinoma?

A

Hypertrophic pulmonary osteoarthropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Coagulopathies are a neoplastic effect of lung carcinomas. Give and example

A

Thrombophebitis migrans

Phlebitis (vein inflammation) related to a thrombus

Thrombophlebitis migrans = occurs repeatedly in different locations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is encephalomyelitis?

A

Inflammation of the brain and spinal cord, typically due to acute viral infection

122
Q

Which syndrome may you get as a paraneoplastic effect of small cell carcinoma? (neuropathy/myopathy)

A

Lambert Eaton myasthenic syndrome

  • autoimmune disorder
  • antibodies against presynaptic voltage-gated calcium channels in the neuromuscular junction
  • muscle weakness
123
Q

Give a specific endocrine effect of squamous cell carcinoma

A

Parathyroid hormone-related peptide caused hypercalcaemia

124
Q

Give a specific endocrine effect of small cell carcinoma

A
  • ACTH
  • antidiuretic hormone
    from small cell carcinoma
125
Q

Give a specific endocrine effect of carcinoid

A
  • 5-hydroxytryptamine (uncommon)
126
Q

What are the different stages of lung malignancy according to TNM 7th edition?

A
  • T1
  • T2
  • T3
  • T4
127
Q

What are the different factors that are considered in TNM lung malignancy staging?

A
  • diam
  • scopy
  • atelectasis
  • invasion
  • nodules
128
Q

What would be the features of a T1 stage lung tumour?

A

Diam - T1a =

129
Q

What would the features of a T2 stage lung tumour be?

A

Diam - T2a = 3-5cm, T2b = 5-7cm

Scopy - >2cm to carina

Atelectasis - lobar atelectasis or obstructive pneumonia to hilus

130
Q

What would the features of a stage T3 lung tumour be?

A

Diam - >7cm

Scopy =

131
Q

What would the features of a stage T4 lung tumours be?

A

Scopy = tumour in carina

Invasion = Heart, great vessels, trachea, oesophagus, spine

Nodules = nodules in other ipsilateral lobes

132
Q

Give 2 examples of EGFR-TK inhibitors? (Epidermal growth factor receptor tyrosine kinase inhibitors)

A
  • gefitinib (Iressa)
  • erlotinib (Tarceva)

They are ATP analogues that inhibit EGFR-TK if activating mutations are present

133
Q

What type of medication is less toxic than standard cytotoxic chemotherapy?

A

Oral medication

134
Q

What do EGFR-TK inhibitors do?

A

Inhibition of EGFR-TK mediated protein phosphorylation and activation of the mitotic cycle

135
Q

EGFR-TK sensitising mutations are present in how many cancers and are most common in who?

A
  • 10% of NSCLC
  • more common in adenocarcinomas
  • more common in non-smoking Asian women
136
Q

Are EGFR-TK inhibitors curative?

A

Not curative but stabilises progression until resistance mutations develop

137
Q

What does ALK stand for?

A

Anaplastic lymphoma kinase

138
Q

What happens in ALK gene rearrangements?

A

inv(2)(p21;p23)

Variable break point inversion on short arm of chromosome 2 fuses ALK and EML genes activating ALK tyrosine kinase

139
Q

An ALK gene rearrangement causes ALK and EML genes to fuse. What does EML stand for?

A

Echinoderm microtubule like protein

140
Q

How would you detect an ALK gene rearrangement?

A

Detect mRNA by FISH, CISH of RT-PCR

Low expression so ICC is difficult

141
Q

What cancers are ALK gene rearrangements common in?

A

Present in about 10% of lung adenocarcinomas

142
Q

Who are ALK gene rearrangements common in?

A

Non-smoking, Asian women

independent of EGFR or RAS mutations

143
Q

What does the drug Crizotinib do?

A

ATP analogue inhibits ALK, ROS1, c-MET (hepatocyte growth factor receptor/HGFR) tyrosine kinases

144
Q

What does use of Crizotinib offer?

A

Temporary control - no progress or regress

145
Q

How many tumours is Crizotinib effective in?

A

Effective in about 90% of tumours with ALK-EML fusion gene

FDA approval Aug 2011 for late stage (local advanced or metastatic) NSCLC

UK approval expected

146
Q

What is the condition of air in the pleural cavity?

A

Pneumothorax

147
Q

What is the condition of transudate or exudate in the pleural cavity?

A

Pleural effusion (hydrothorax)

148
Q

What is the condition of blood in the pleural cavity?

A

Haemothorax

149
Q

What is the condition of lymph in the pleural cavity?

A

Chylothorax (caused by central line in the wrong place, needles through thoracic duct, thoracic duct disrupted by tumour etc)

150
Q

What is the condition of pus in the pleural cavity?

A

Empyema (pyothorax)

151
Q

What are the inflammatory causes of pleural effusion?

A
  • serous/fibrinous - exudate

- due to inflammation/infection in adjacent lung

152
Q

What are the non-inflammatory causes of pleural effusion?

A

Congestive cardiac failure - transudate

153
Q

How can you come up with a diagnosis for pleural effusion?

A

LDH, pH, glucose of fluid can be measured to suggest a diagnosis

Cytology used to assess the presence of malignant or inflammatory cells

154
Q

What are the non-neoplastic diseases of the pleura?

A

Inflammation (pleurisy, pleuritis)

  • collagen vascular diseases
  • pneumonia, TB
  • lung infarct, usually secondary to PE
  • lung tumour

Asbestos

  • effusion
  • fibrous plaques
  • diffuse fibrosis
155
Q

Benign tumours of the pleura are rare. Give an example

A

Fibroma

156
Q

Malignant pleural tumours are common. What types of cancer are they usually?

A
  • usually secondary adenocarcinoma (from lung, breast)

- some rarer primary malignant mesotheliomas

157
Q

How common is malignant mesothelioma?

A

2401 cases in 2007 in UK

Expected to increase to 3000 by 2020

158
Q

What is malignant mesothelioma associated with?

A

More than 90% associated with asbestos exposure, blue (especially) or brown (most hazardous)

Exposure may be low level

159
Q

What is the latent period of malignant mesothelioma?

A

Long latent period of 15 to 60+ years form exposure before the mesothelioma develops

160
Q

What are the stages in the development of malignant mesothelioma?

A
  • initial nodule and effusion
  • later obliterates pleural cavity growing around the lung
  • invades chest wall (pain) and lung
  • nodal and distant metastases less common than carcinomas
161
Q

What kinds of cells are in a malignant mesothelioma?

A

Mixed spindle and epithelioid cells - may be very fibrous (desmoplastic)

162
Q

How would you do a differential diagnosis of malignant mesothelioma from reactive mesothelial cells?

A

Differential diagnosis from reactive mesothelial cells in inflamed pleura can be very difficult

163
Q

How you do a differential diagnosis of malignant mesothelioma form adenocarcinoma?

A

Cellular antigen expression (immunocytochemistry on cytology or biopsy)

164
Q

How would you treat malignant mesothelioma?

A

Symptomatic treatment

165
Q

What is the prognosis for malignant mesothelioma?

A

Uniformly fatal in less than 1 to 3 years

166
Q

What would you see in early malignant mesothelioma?

A
  • small plaques on the parietal pleura
  • difficult to image and biopsy
  • may produce a significant pleural effusion
167
Q

What are fibrous pleural plaques associated with?

A

Low level asbestos exposure

168
Q

Where do you get fibrous pleural plaques?

A

On the lower thoracic wall and diaphragmatic pleural pleura

169
Q

Do fibrous pleural plaques have a physiological effect?

A
  • no physiological effect
  • not premalignant
  • seen on radiographs, a marker of possible asbestos exposure
170
Q

Should you complete a death certificate in the case of a death from an asbestos-related lung carcinoma?

A

No - the death should be refried to the coroner as a possible death due to an occupational disease and no death certificate should be completed

171
Q

When do you get a primary respiratory infection?

A

When you are previously healthy

172
Q

When do you get a secondary respiratory infection?

A

In the case of weakened defence

173
Q

Those with weakened defence may get a secondary respiratory infection. How might you have weakened defence?

A
  • mucociliary escalator defects
  • lowered immunity
  • pulmonary oedema
174
Q

Defects in the mucocilliary escalator may cause weakened defence leading to respiratory infection. What kind of defects may occur?

A
  • physical obstruction eg. tumour, foreign body
  • cough reflex
  • ciliary dysmotility eg. Kartagener’s syndrome
  • mucus viscosity eg. CF
175
Q

Lowered immunity may cause weakened defence leading to respiratory infection. Give examples

A
  • hypogammaglobulinaemia
  • lymphomas
  • immunosuppressive drugs
  • AIDS
  • macrophage function - smoking, hypoxia
176
Q

What causes acute bronchitis?

A
  • viral (RSV)
  • H. influenzae
  • strep. pneumoniae
177
Q

What is bronchiolitis obliterans?

A

Rare and life-threatening form of non-reversible obstructive lung disease in which the bronchioles are compressed and narrowed by fibrosis and inflammation

also sometimes used to refer to a particularly severe form of pediatric bronchiolitis caused by adenovirus

178
Q

What do you get in pneumonia?

A

Inflammatory exudate in alveoli and distal small airways (consolidation)

179
Q

What are the 4 different types of classification in pneumonia?

A
  • clinical (primary or secondary)
  • aetiological (bacterial, viral, fungal)
  • anatomical (lobar or broncho)
  • reaction (purulent, fibrinous)
180
Q

Give the main characteristics of bronchopneumonia

A
  • secondary (compromised defences)
  • often low virulence bacteria or occasionally fungi
  • common
  • patchy
  • bronchocentric
  • resolve or heal with scarring
181
Q

What are the characteristics of lobar pneumonia?

A
  • primary (typically male 20-50 years)
  • 90% = virulent step. pneumonia
  • uncommon
  • confluent segments, whole lobe or lobes with overlying pleuritis
  • congestion, red then grey hepatisation, resolution without scarring
  • klebsiella pneumoniae - elderly, diabetic, alcoholic
182
Q

What causes atypical pneumonia in the non-immunosuppressed? (viral causes)

A
  • flu
  • varicella
  • RSV
  • rhino
  • adeno
  • measles
183
Q

What causes atypical pneumonia in the non-ummunosuppressed? (bacterial causes)

A
  • mycoplasma pneumonia (mild, chronic, fibrosis)
  • chlamydia psittacosis
  • coxiella burnetti (Q-fever)
  • legionella pneumophila (systemic, 10-20% fatal)
184
Q

What are the characteristic of atypical pneumonia?

A
  • severely mild to fatal
  • interstitial lymphocytes, plasma cells, macrophages
  • intra-alveolar fibrinous cell-poor exudate
  • diffuse alveolar damage (DAD)
185
Q

Immunosuppressed individuals may be affected by opportunistic infection by low virulence or non-virulence organisms. Give examples

A

Fungi

  • candida
  • aspegillus
  • pneumocystis carinii

Viruses

  • CMV
  • HSV
  • measles
186
Q

Give 3 types of non-infective pneumonia

A
  • aspiration pneumonia
  • lipid pneumoina
  • cryptogenic organising pneumonia and bronchiolitis obliterans organising pneumonia (COP and BOOP)
187
Q

What is aspiration pneumonia?

A

Secondary infection often with mixed anaerobes produces abscesses

188
Q

What are the 2 types of lipid pneumonia?

A
  • endogenous (retention pneumonitis)

- exogenous (aspiration)

189
Q

What causes pulmonary tuberculosis?

A

Mycobacterium tuberculosis

190
Q

What is TB infection associated with?

A
  • socioeconomic deprivation

- immunosuppression (including AIDS)

191
Q

What is the vaccine against TB called?

A

BCG

Bacille Calmette-Guerin

192
Q

What is the fatality of TB if left untreated?

A

50%

193
Q

What do you get in the TB granuloma?

A

Multinucleated Langhan’s giant cells and caseous necrosis

194
Q

What do atypical mycobacteria tend to infect?

A

Lungs with pre-existing pathology such as COPD and are more resistant to treatment than M tuberculosis

195
Q

What is the Heaf and Mantoux test based on?

A

Type IV hypersensitivity to tuberculin

196
Q

What causes pulmonary vascular diseases?

A
  • vessel wall inflammation (vasculitis)
  • obstruction of flow
  • haemodynamic disturbances
197
Q

Give 3 examples of pulmonary vasculitis (uncommon)

A
  • necrotising granulomatous vasculitis
  • goodpasture’s syndrome
  • microvascular damage
198
Q

What is necrotising granulomatous vasculitis?

A

Wegener’s granulomatosis (kidneys and nose, elevated serum ANCA)

Churg-Strauss syndrome (eosinophilia and asthma)

199
Q

What is goodpasture’s syndrome?

A
  • anti-glomerular basement membrane antibodies
  • intra-alveolar haemorrhage
  • glomerulonephritis
200
Q

Give examples of conditions that cause microvascular damage

A
  • ARDS
  • DAD (diffuse alveolar damage, seen in ARDS)
  • SLE
201
Q

Give examples of different types of embolus

A
  • thromboemboli
  • fat
  • air
  • amniotic fluid
  • tumour
  • foreign bodies
202
Q

Explain thromboembolus

A
  • common

- often come from a DVT

203
Q

What determines the symptoms in a thromboembolus? Describe the symptoms

A

The size of the embolus

  • sudden death
  • SOB
  • chest pain
  • pulmonary hypertension
  • right ventricular failure
204
Q

Where does a fat embolus come from?

A

Fat and marrow from bone fractures

205
Q

What may cause localised obstructive pulmonary disease?

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)
206
Q

What is bronchiectasis?

A

Permanent dilation of bronchi and bronchioles caused by the destruction of the muscle and elastic tissue

Results from chronic necrotising infection

207
Q

What are the signs and symptoms of bronchiectasis?

A
  • cough
  • fever
  • copious amounts of foul smelling sputum
208
Q

Which conditions are predisposing to bronchiectasis?

A
  • cystic fibrosis
  • primary ciliary dyskinesia (Kartagener syndrome)
  • bronchial obstruction: tumours, foreign body
  • lupus, RA, IBD, GVHD (autoimmune diseases)
209
Q

Bronchiectasis may be localised and therefore resectable. What are the complications of bronchiectasis?

A
  • pneumonia
  • septicaemia
  • metastatic infection
  • amyloid
210
Q

Obstructive pulmonary diseases can be divided into what 2 categories?

A
  • localised

- diffuse

211
Q

Obstructive pulmonary disease can be localised or diffuse. Give 2 examples of diffuse obstructive pulmonary disease

A
  • COPD

- asthma

212
Q

What is COPD a combination of?

A

Chronic bronchitis and emphysema

213
Q

What defines chronic bronchitis?

A

Cough and sputum for 3 months in each of 2 consecutive years

214
Q

What causes chronic bronchitis?

A
  • chronic irritation

- smoking and air pollution

215
Q

What is the pathology behind chronic bronchitis?

A

Mucus gland hyperplasia and hypertension, secondary infection by low virulence bacteria, chronic inflammation

216
Q

What do chronic inflammation of the small airways (in chronic bronchitis) cause?

A

Wall weakness and destruction thus centrilobular emphysema

217
Q

What is emphysema?

A

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

218
Q

How is overinflation different to emphysema?

A

In just overinflation, there is no airspace wall destruction

219
Q

What are the 3 different classifications of emphysema?

A
  • centrilobular (centiacinar)
  • panlobular (panacinar)
  • paraseptal (distal acinar)
220
Q

What causes centrilobular emphysema?

A
  • coal dust

- smoking

221
Q

What causes panlobular emphysema?

A
  • > 80% a1 antitrypsin deficient (rare, autosomal dominant)

Severest in lower lobe bases

222
Q

What do you get in paraseptal emphysema?

A

Upper lobe subpleural bullae adjacent to fibrosis

Pneumothroax if rupture

223
Q

What is the main symptom of emphysema?

A

Progressive and worsening dyspnoea

224
Q

At what age do you commonly see bronchitis vs emphysema?

A

bronchitis = 40-45

emphysema = 50-75

225
Q

How severe is dyspnoea in bronchitis vs emphysema?

A

bronchitis = mild, late in disease

emphysema = severe, early

226
Q

Describe the cough in bronchitis vs. emphysema

A

bronchitis = early in disease, copious sputum

emphysema = late, scanty sputum

227
Q

How common are infections in bronchitis vs emphysema?

A

bronchitis = common

emphysema = rare

228
Q

How common is cor pulmonale in bronchitis vs emphysema?

A

bronchitis = common

emphysema = rare, terminal

229
Q

What do you see on a chest X-ray of bronchitis vs emphysema?

A

bronchitis = prominent vessles, large heart

emphysema = small heart, hyperinflated lungs

230
Q

What is the stereotype for bronchitis vs emphysema?

A

bronchitis = blue boater

emphysema = pink puffer

231
Q

What is cor pulmonale?

A

Abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels

232
Q

What qualifies coal miners with chronic bronchitis and emphysema for compensation?

A
  • > 20 years underground work
  • compensation depends on degree of disability and smoking history
  • no CXR or history of dust exposure needed
233
Q

What is asthma?

A

Chronic inflammatory disorder of the airways

  • mucosal inflammation and oedema
  • hypertrophic mucous glands and mucus plugs in bronchi
  • hyperinflated lungs
234
Q

What happens in a paroxysmal bronchospasm in asthma?

A
  • wheeze
  • cough
  • variable bronchoconstriction that is at least partially reversible
235
Q

What are the clinicopathological classifications of asthma?

A
  • atopic
  • non-atopic
  • aspirin-induced
  • allergic bronchopulmonary aspergillosis (ABPA)
236
Q

What type of hypersensitivity reaction is atopic asthma?

A

Type I hypersensitivity reaction

237
Q

What may trigger the type I hypersensitivity reaction in atopic asthma?

A
  • allergen (dust, pollen, animal products)

- cold, exercise, reparatory infections

238
Q

What happens in the type I hypersensitivity reaction in atopic asthma?

A
  • many different cell types and inflammatory mediators involved
  • degranulation of IgE bearing mast cells
  • histamine initiated bronchoconstriction and mucus production obstructing air flow
  • eosinophil chemotaxis
239
Q

What are the persistent or irreversible changes in atopic asthma?

A
  • bronchiolar wall smooth muscle hypertrophy
  • mucus gland hyperplasia
  • respiratory bronchiolitis leading to centrilobular emphysema
240
Q

Who gets atopic asthma?

A

Children and young adults

1 in 10 UK children diagnosed with asthma

590,000 teenagers

241
Q

9-15% of adult onset asthma is what?

A

Occupational

the commonest occupational lung disease

242
Q

What would you see on autopsy with acute asthma?

A

Mucus-plugged small bronchus with eosinophils

243
Q

Is interstitial lung disease restrictive or obstructive?

A

Restrictive

244
Q

Interstitial lung diseases are diseases of what?

A

Pulmonary connective tissue (mainly alveolar walls)

245
Q

Give 3 pathological characteristics of interstitial lung disease

A
  • increased tissue in alveolar-capillary wall
  • decreased lung compliance
  • increased gas diffusion distance
246
Q

In interstitial lung disease you get increased tissue in alveolar-capillary wall. Why?

A
  • inflammation and fibrosis
  • limited morphological patterns that differ with site and with time in any individual but with many causes and clinical associations
247
Q

What is the main feature of ACUTE interstitial disease?

A

Diffuse alveolar damage

Exudate and death of type I pneumocytes form hyaline membranes lining alveoli followed by type II pneumocyte hyperplasia

Histologically acute interstitial pneumonia

248
Q

What are the signs and symptoms of CHRONIC interstitial lung diseases?

A
  • dyspnoea increasing for months to years
  • clubbing
  • fine crackles
  • dry cough
  • interstitial fibrosis and chronic inflammation with varying radiological and histological patterns
249
Q

What is “honeycomb” lung?

A

Common end-stage of chronic interstitial lung disease = fibrosed honeycomb lung

250
Q

Give some examples of chronic interstitial lung diseases

A
  • idiopathic pulmonary fibrosis
  • many pneumoconiosis (dust disease)
  • sarcoidosis
  • collaged vascular diseases-associated lung diseases
251
Q

Idiopathic pulmonary fibrosis is a type of chronic interstitial lung disease. What is it also called?

A

Cryptogenic fibrosing alveolitis

252
Q

What is affected first and most severely in idiopathic pulmonary fibrosis?

A

Sub-pleural, lower lobes

253
Q

What is the mortality rate of idiopathic pulmonary fibrosis?

A

3 year = 43%

5 year = 57%

254
Q

How many new cases are there are year in the UK of idiopathic pulmonary fibrosis? (in the middle aged and elderly)

A

5000

255
Q

Idiopathic pulmonary fibrosis is the clinical term for which disease?

A

Usual interstitial pneumonia (UIP)

256
Q

What are the histological findings in idiopathic pulmonary fibrosis/usual interstitial pneumonia?

A
  • interstitial chronic inflammation and variably mature fibrous tissue
  • adjacent normal alveolar walls
  • similar pattern of fibrosis in collagen vascular disease associated interstitial lung disease and in asbestosis
257
Q

What texture do you get on the pleural surface in idiopathic pulmonary fibrosis and why?

A

Bosselated “cobblestone” pleural surface due to contraction of interstitial fibrous tissue

Accentuates lobular architecture

258
Q

What pathology do you get in sarcoidosis?

A

Non-caseating perilymphatic pulmonary granulomas form, then you get fibrosis

259
Q

What parts of the body are involved in sarcoidosis?

A
  • lungs
  • hilar nodes usually involved
  • other organs may be affected (skin, heart, brain)
260
Q

What are the typical symptoms of sarcoidosis?

A
  • tender red bumps on the skin
  • shortness of breath
  • persistent cough
261
Q

Who typically gets sarcoidosis?

A

Typically young adult females affected, aetiology unknown

262
Q

What are the clinical findings of sarcoidosis?

A
  • hypercalcaemia

- elevated serum ACE

263
Q

What are pneumoconioses known as?

A

The dust diseases

264
Q

What were pneumoconioses originally defined as?

A

The non-neoplastic lung diseases due to inhalation of mineral dusts in the workplace

Now also includes organic dusts, fumes and vapours

265
Q

What are the classifications of inhaled dusts that causes pneumoconioses?

A
  • inert
  • fibrogenic
  • allergenic
  • oncogenic (lung carcinoma and pleural mesothelioma)
266
Q

How small must the dust particles be to reach the alveoli? (pneumoconiosis)

A

Less than 3 micrometers to reach the alveoli

267
Q

Coal worker’s pneumoconiosis is the severe state that develops after the milder form of the disease called what?

A

Anthracosis

268
Q

What is the main pathology in coal worker’s pneumoconiosis?

A

Progressive massive fibrosis

269
Q

Give 2 types of coal worker’s pneumoconiosis

A
  • simple macular CWP

- nodular CWP

270
Q

If you have coal worker’s pneumoconiosis and also over 20 years underground mining, what is it diagnosed as?

A

COPD

271
Q

What is silicosis?

A

Type of pneumoconiosis - caused by inhaling large amounts of silica dust (sand and stone dust) usually over many years

Causes inflammation and fibrosis in the lungs

272
Q

What is the pathology in silicosis?

A

Fibrosis and fibrous silicotic nodules

nodular lesions in the upper lobes of the lungs

273
Q

What are the other risks possible in silicosis?

A
  • possible reactivation of tuberculosis

- increased risk of lung carcinoma

274
Q

What is mixed dust pneumoconiosis?

A

Silica with other dusts

275
Q

What does high level of exposure to asbestos produce?

A

Interstitial fibrosis, in a usual interstitial pneumonia pattern

276
Q

Abestosis is histologically like which other diseases?

A
  • idiopathic pulmonary fibrosis
    and
  • collaged vascular disease associated pulmonary fibrosis
277
Q

In asbestosis, what is identifiable in tissue sections?

A

Asbestos bodies

278
Q

Asbestosis is difficult to diagnose with certainty but what is the likely incidence?

A

1000 cases per year in the UK

279
Q

There is an increased risk oh which disease with asbestosis?

A

Lung cancer

280
Q

Hypersensitivity pneumonitis is also known as what?

A

Extrinsic allergic alveolitis

281
Q

What type of hypersensitivity reaction is hypersensitivity pneumonitis/extrinsic allergic alveolitis?

A

Type III hypersensitivity reaction to organic dusts

282
Q

Give 2 examples of hypersensitivity pneumonitis and state what the allergen is

A

Farmer’s lung - actinomycetes in hay

Pigeon fancier’s lung - pigeon antigens

283
Q

What is the pathology in hypersensitivity pneumonitis?

A

Peribronchiolar inflammation with poorly-formed non-caseating granulomas extended to alveolar walls

Repeated episodes leads to interstitial fibrosis

284
Q

What are the 3 major occupational lung diseases?

A
  • COPD in coal miners (4000 UK deaths per year)
  • asbestos related lung cancer (2000 UK deaths per year)
  • asbestos related malignant mesothelioma (2000 UK deaths per year)
285
Q

What is cystic fibrosis?

A

An inherited multiorgan disorder of epithelial cells affecting fluid secretion in exocrine glands and the epithelial lining of the respiratory, GI and reproductive organs

286
Q

What race does CF mostly affect?

A

Caucasians

287
Q

What type of genetic inheritance is CF?

A

Autosomal recessive

288
Q

What is the incidence of CF?

A

0.4 per 1000 live births

289
Q

Cystic fibrosis is caused by a mutation in which gene?

A

CFTR gene

Cystic fibrosis transmembrane conductance regulator gene on chromosome 7q31.2

290
Q

What does the CFTR gene encode?

A

A transmembrane chloride channel protein

291
Q

Cystic fibrosis has a vast phenotypic variation due to what?

A

Variations in mutations, organ specific effects of the gene

292
Q

What is the typical clinical presentation of a cystic fibrosis patient?

A
  • infancy (usually)
  • abnormally viscous mucous secretions
  • recurrent lung infections
  • failure to thrive
  • recurrent intestinal obstruction
  • pancreatic insufficiency
293
Q

What are the effects of cystic fibrosis on the lungs?

A
  • bronchioles distended with mucus
  • hyperplasia of mucus secreting glands
  • multiple repeated infections
  • severe chronic bronchitis and bronchiectasis
294
Q

What are the effects of cystic fibrosis on the pancreas?

A
  • exocrine gland ducts plugged by mucus
  • atrophy and fibrosis of gland
  • impaired fat absorption, enzyme secretion, vitamin deficiencies (pancreatic insufficiency)
295
Q

What are the effects of CF on the small bowel?

A

Mucus plugging - meconium ileus

296
Q

What are the effects of CF on the liver?

A

Plugging of bile cannaliculi - cirrhosis

297
Q

What are the effects of CF on the salivary glands?

A

Similar to pancreas - atrophy and fibrosis

298
Q

95% of males with CF are what?

A

Infertile

299
Q

What kind of tests can you do for CF?

A
  • part of newborn screening in UK
  • sweat test
  • genetic testing
300
Q

What is the median survival for CF in the UK?

A

41 years

301
Q

What can be done to help CF patients?

A
  • physiotherapy
  • mucolytics
  • heart/lung transplants

3. CP - Diseases of the Respiratory System (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions