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respiration > Respiratory pathology > Flashcards

Respiratory pathology Flashcards

1
Q
  1. What are common symptoms of lung cancer?
A

Heamotopsys-coughing blood, chough, chest/shoulder pain, dysnpnae, hoarnsess and finger clubber

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2
Q
  1. How can samples be acquired for cytological analysis?
A

PET scans can see the tumors after being given radioactive glucose
Fine needle aspiration
Brochial brushing, lavage and pleural fluid

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3
Q
  1. What are some features of benign tumours?
A

Tumour is very metabolically active therefore takes radioactive glucose for pet scan fast
Grow slower, no metastase, no invasion

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4
Q
  1. What are the three types of non-small cell carcinoma? What percentage of lung cancers are non-small cell?
A

Small cell lung cancer
Non-small cell lung caner-about 80%
Adenocarcinoma
Large cell carcinoma

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5
Q
  1. How are the incidences of squamous cell carcinoma and adenocarcinoma changing?
A

Squamous cell carcinoma is decreasing, adenocarnioma is increasing

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6
Q
  1. Where do squamous cell carcinomas and adenocarcinomas tend to arise?
A

Squamous near mediastinum-shallow, adenocarcinoma near periphery

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7
Q
  1. State three major risk factors for lung cancer.
A

Smoking, radiation, asbestos

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8
Q
  1. What are the four stages in the pathway to carcinoma?
A

Metaplasia, dysplasia, carcinoma in situ, invasive carcinoma

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9
Q
  1. Why has a precursor lesion for small cell lung carcinoma not been found?
A

Because small cell cancer goes too quicly and metabolises early

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10
Q
  1. How do the cells lining the airways change in squamous cell carcinoma?
A

Ciliated cell undergo metaplasia due to chronic stimulation by cigarette smoke-become squamous

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11
Q
  1. Which type of lung cancer is common in non-smokers?
A

adenocarcinoma

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12
Q
  1. Which types of lung caner are strongly associated with smoking?
A

Small cell carcinoma and squamous cell carcinoma

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13
Q
  1. Describe the cytological features of squamous cell carcinoma.
A

Large nuclei and keratin in cytoplasm

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14
Q
  1. What is the precursor lesion for adenocarcinoma?
A

Atypical adenomatous hyperplasia

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15
Q
  1. At what point does adenocarcinoma in situ become invasive adenocarcinoma?
A

When the cells aquire a mutation allowing to break stomae and invade. Tjis causes inflammation and leads to fibrious tissue

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16
Q
  1. Describe the cytological features of adenocarcinoma.
A

Differentiate to glandular-big atypical nuclei with mucin globules

17
Q
  1. Where does adenocarcinoma usually develop and are they usually multi-focal?
A

They develop near the periphery and are usually multifocal

18
Q
  1. What are the two molecular pathways for adenocarcinoma and which one is associated with smoking?
A

K-ras pathways-smoking

EFGR-responder/resistance mutation

19
Q
  1. Why is it important to differentiate between the different pathways? (kras and EGFR-lung cancer)
A

React very differently to drugs and targeted therapies-kras responds much worse, while EGFR can regress completely

20
Q
  1. What is large cell carcinoma?
A

Poorly differentiated-poor prognosis. Electron microscopy suggests evidence of ssquamous/neuroendocrine

21
Q
  1. What are the cytological features of small cell carcinoma?
A

Look like lymphocytes-large nucleus and little cytoplasm

22
Q
  1. Where does small cell carcinoma tend to arise?
A

Centrally, near the bronchi

23
Q
  1. What does the ERCC1 marker determine?
A

If there marker is there, means advances non-small cell cancer UNLIKELY to respond to cisplatin

24
Q
  1. What type of receptor is EGFR and what is used to block this receptor?
A

Tyrosine kinase like-can use TKL inhbitors

25
Q
  1. What are paraneoplastic syndromes?
A

Systemic effect of tumour due to abnormal expression of factors (eg hormones) not normally in tissue

26
Q
  1. State some endocrine paraneoplastic syndromes.
A 
SIADH (make ADH)
Cushing syndrome (make ACTH
27
Q
  1. What is strongly associated with mesothelioma?
A

asbestos

respiration (15 decks)

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