Respiratory pathology Flashcards

(27 cards)

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
25. What are paraneoplastic syndromes?
Systemic effect of tumour due to abnormal expression of factors (eg hormones) not normally in tissue
26
26. State some endocrine paraneoplastic syndromes.
``` SIADH (make ADH) Cushing syndrome (make ACTH ```
27
27. What is strongly associated with mesothelioma?
asbestos