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Pulmonology Exam > Pulmonary Pathology 5 > Flashcards

Pulmonary Pathology 5 Flashcards

1
Q

carcinogen exposure may be mitigated by genetic variation such as what?

A

P450 polymorphisms and genes responsible for DNA repair

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2
Q

what is the most common type of lung cancer?

A

adenocarcinoma

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3
Q

what is the second most common type of lung cancer?

A

squamous cell carcinoma

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4
Q

what cells do squamous cell carcinomas arise from?

A

basal cells

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5
Q

what cells do small-cell carcinomas arise from?

A

neuroendocrine cells

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6
Q

what cell does adenocarcinomas arise from?

A

type II alveolar cells

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7
Q

which types of lung cancer are heavily linked with smoking?

A

squamous cell carcinoma and small cell carcinomas

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8
Q

how does a neuroendocrine cell become small cell carcinoma?

A

p53 inactivations

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9
Q

which type of cancer is most likely to be found in non-smokers?

A

adenocarcinoma

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10
Q

how does adenocarcinoma develop?

A

normal–> atypical adenoma hyperplasia–> adenoma in situ–> adenocarcinoma

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11
Q

how is atypical adenomatous hyperplasia (AAH) defined?

A

less than 5mm (if it gets any bigger then it is considered to be AIS); dysplastic pneumocytes present along alveoli with some interstitial fibrosis

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12
Q

how is adenocarcinoma in situ defined?

A

less than 3 cm (must be under 3 cms); dysplastic pneumocytes confluently growing along the alveoli

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13
Q

how does pulmonary adenocarcinoma arise?

A

either from precursors or it develops de novo

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14
Q

what does histology of pulmonary adenocarcinoma show?

A

malignant glands invading the lung tissue

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15
Q

what is a test used for pulmonary adenocarcinoma?

A

TTF staining (thyroid-transcription fator-1)

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16
Q

what is mucinous adenocarcinoma?

A

a variant of pulmonary adenocarcinoma; it is not in situ because it extends to far, but it is not invading; very deadly

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17
Q

what does the progression of normal bronchial epithelium require in order to progress to squamous carcinoma?

A

metaplasia

18
Q

what is the progression of normal bronchial epithelium to squamous carcinoma?

A

normal–> squamous metaplasia–> squamous carcinoma in situ (dysplasia)–> invasive squamous carcinoma

19
Q

how do you recognize squamous carcinoma on histology?

A

keratin pearls

20
Q

how do you recognize squamous carcinoma on cytology?

A

orange cytoplasm= keratin

21
Q

what are the characteristic features of squamous carcinoma?

A

more common in men, strong association with smoking, often occurs centrally

22
Q

which lung cancer is almost always associated with smoking?

A

small cell neuroendocrine carcinoma

23
Q

how does small cell neuroendocrine carcinoma appear histologically?

A

small cells with fine blue nuclear chromatin, scant cytoplasm, nuclear “molding”, and characteristic necrosis

24
Q

how do you treat adenocarcinomas?

A

on the basis of molecular testing: EGFR, ALK, or PDL-1

25
Q

so when you know that an adenocarcinoma shows EGFR over expression, what do you do?

A

you know that that EGFR is driving the malignant function- so block it with erlotinib

26
Q

what is there is inversion of that area chromosome 2p where we find our ALK gene?

A

there may be a fusion protein there that sends the cell cycle into over drive/ proliferation; so you block it by using crizotinib

27
Q

what is the general flow chart for adenocarcinoma therapy?

A

look for an EGFR mutation, if it is positive you treat it with an EGFR TKI; if it is negative you look for an ALK rearrangement; if that is positive you treat with crizotinib

28
Q

what should you not use when treating squamous carcinoma?

A

VEGF inhibitors (these tumors are very sensitive to bleeding)

29
Q

what paraneoplastic syndrome is associated with squamous carcinoma?

A

PTH-rP hypercalcemia

30
Q

what paraneoplastic syndrome is associated with small cell carcinoma?

A

SIADH (syndrome of inappropriate ADH secretion) and Cushing’s syndrome (secretion of ACTH)

31
Q

what may be the primary manifestation of the paraneoplastic syndromes?

A

electrolyte disturbances and/or mental status changes

32
Q

what makes up Horner’s syndrome?

A

enophthalmos (sunken eyeball), ptosis, miosis (small pupil), anhidrosis; aka oculosympathetic palsy

33
Q

horner’s syndrome can occur at many sites along the sympathetic pathway; how can you localize it to the thoracic outlet?

A

if the patient is present with brachial plexus symptoms–> wasting, pain, paresthesias, and paresis of arm and hand

34
Q

what are the stages of neuroendocrine tumors?

A

DIPNECH, carcinoid tumor, atypical carcinoid tumor, small cell neuroendocrine carcinoma

35
Q

what does DIPNECH stand for and what is it?

A

diffuse interstitial pulmonary neuroendocrine cell hyperplasia; very small (less than 5 mm) hyperplasia; basically a precursor lesion

36
Q

how do you tell apart DIPNECH and carcinoid tumors?

A

DIPNECH are less than 5 mm and carcinoid tumors are 5 mm or larger

37
Q

what are carcinoid tumors?

A

5 mm or larger, they can metastasize, neuroendocrine carcinoma grade 1

38
Q

what is atypical carcinoid tumors?

A

neuroendocrine carcinoma grade 2

39
Q

how do you tell apart carcinoid tumors and atypical carcinoid tumors?

A

atypical carcinoid tumors have increased mitotic activity, NECROSIS, and disordered growth; increased rates of metastasis

40
Q

what is carcinoid syndrome?

A

flushing, diarrhea, cyanosis

41
Q

which neuroendocrine tumor has the greatest 5 year survival rate?

A

carcinoid tumors, then atypical carcinoid tumors, then small cell carcinoma

42
Q

if a young man is presenting with SOB and hemoptysis and you find metastatic cancer, what two things should you be thinking about?

A

testicular cancer or melanoma

Pulmonology Exam (11 decks)

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