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WI-18 Pulmonary > Pulmonary Oncology > Flashcards

Pulmonary Oncology Flashcards

1
Q

SPN

A

isolated rounded opacity <30 mm on CXR

outlined by normal lung tissue (not in hilar lN)often found incidentally

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2
Q

malignant causes of SPN

A

primary lung CA (adenoCA)

carcinoid tumor

Metastatic dz (melanoma, colon, breast, kidney, testicular)

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3
Q

benign causes of SPN

A

Granuloma (infectious process)

benign tumor (hamaratoma, bronchiole adenoma )

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4
Q

SPN lesion characteristics indicative of malignancy

A
  1. increasing size - rapidly increasing likely CA
  2. SPN composition - solid/subsolid
  3. border characteristics - rougher edges = more likely (corona radiate most)
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5
Q

SPN risk of malignancy pt characteristics (7)

A
  1. increasing age
  2. smoking
  3. prior malignancy
  4. occupation
  5. female sex
  6. upper lobe lesion
  7. family history
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6
Q

risk factors for SPN infection

A
  1. immunocompromised
  2. history of TB or other mycosis
  3. residence or extensive travel in areas of endemic mycosis
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7
Q

work up of SPN

A
  1. non-contrast CT (thin cuts)

2. PET/CT scan

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8
Q

CT SPN imaging

looking for:

A

benign patterns of calcification

estimation of VDT

malignant patterns

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9
Q

SPN CT

benign patterns

A

diffuse homogenous calcification

central calficiation

lamellate calcification

popcorn calficiation

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10
Q

estimation of VDT - benign

A

fast ( <30) suggests infection

slow (>480 days)

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11
Q

malignant patterns of SPN CT

A

peripheral halo

cavitary lesions

Lymphadenopathy

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12
Q

solid nodules SPN

A

dense and homogenous

<8mm = too small for bx, less likely to be malignant

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13
Q

subsolid nodules SOB

A

less attenuation on imaging

normal parenchymal structures can be seen through them

part solid or ground glass (no solid components)

difficult to bx

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14
Q

PET/CT SPN

A

greater than 8 mm

assesses metabolic activity of nodule (most glucose uptake) via SUV

high SUV indicates high FDG, suggestive of malignancy

can exclude cancer

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15
Q

management of SPN

A

growing nodule should always be surgically removed ( > 2mm increase)

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16
Q

when is SPN growth considered stable?

A

solid: stable after 24 months no growth
subsolid: 5 yrs no change

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17
Q

what can we use to determine SPN management?

A

Fleischer guidelines

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18
Q

SPN biopsy

A

sampling to obtain tissue diagnosis

BAL, brushing, directed

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19
Q

indications for resection of SPN

A
  1. growing legion
  2. high probability of malignancy
  3. metabolically active on PET scan
  4. prior sampling nodule has proven malignant
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20
Q

bronchogenic lung carcinoma

A

second most common type of CA diagnosed but number one killer of persons (more than colorectal + breast + prostate CA)

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21
Q

lung CA screening

A

should benefit but hard to screen

annual low dose CT screen for HR individuals

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22
Q

high risk lung cancer defined:

who gets the screening

A

men or women ages 55-79 yrs with 30 pk year history

quit in last 15 yrs

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23
Q

risk factors for bronchogenic lung cancer

A
  1. smoking (90%)
  2. prior h.o. radiation tx (HL or brest)
  3. environmental exposure (second hand smoke, radon)
  4. Other lung dx, 5. HIV, 6. family history, 7. alcohol and diet
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24
Q

epidemiology of bronchogenic lung cancer

A

men > women, lower rates of survival

women: adenoma, high likelihood of local dz, younger age

AA = Caucasian women

AA > men (13% lower)

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25
Q

classifications of lung CA

A
  1. adenocarcinoma (MC, rising)
  2. Squamous cell carcinoma
  3. Large cell carcinoma
  4. Small cell carcinoma
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26
Q

adenosinecarcinoma

A

mucus gland of bronchi, peripheral nodule

predilicition for occurring at pre-existing scars, wounds or inflammation

MC found in non-smokers

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27
Q

bronchoalveolar cancer

A

subtype of adenocarcinoma

arises form type II pneumocystis

profuse, watery sputum

spreads alveolarly, present as an infiltrate or as single/multiple nodules

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28
Q

squamous cell cancer

A

CENTRAL portion

cavitary lesion in lumen of central bronchus

keratin pearls

presents as hemoptysis, exfoliates

most likely to produce hypercalcemia

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29
Q

large cell lung cancer

A

occurs peripherally

lg sheets of atypical cells, focal necrosis (no keratin pearls)

SOME = neuroendocrine component (LCNEC)

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30
Q

small cell carcinoma

A

begins centrally, infiltrates mucosa

spreads rapidly to hilar and mediastinal lymph node

exclusively in smokers

small blue CA cells, sparse cytoplasm

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31
Q

MC presentation of SCLC

A

large mediastinal mass with bulky hilar LAD

hemoptysis and post obstructive PNA uncommon, narrowing and late obstruction of bronchus

neuroendocrine activity

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32
Q

small cell carcinoma spread

A

prone to early hematogenous spread and very aggressive clinical course

sensitive initially to CXR but not durable

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33
Q

presentation of lung CA

A

insidious process

majority of patients will have advanced dz at diagnosis

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34
Q

symptoms of bronchogenic CA (9)

A

related to primary lesion, spread, distant metastasis, paraneoplastic syndromes

  1. new cough/chronic change
  2. dry/scantily productive thin mucoid secretions
  3. post obstructive PNA with thick sputum
  4. dyspnea
  5. change in voice
  6. hemoptysis
  7. chest pain
  8. atelectasis, PNA, malignant pleural effusion
  9. anorexia/weight loss
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35
Q

dyspnea of bronchogenic CA

A

wheezing and stridor

pleural or pericardial effusions (volume loss due to atelectasis)

volume loss and atelectasis/lobe collapse

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36
Q

chest pain in bronchogenic CA

A

dull, intermittent pain on side of tumor

severe or persistent pain = chest wall or mediastinal invasion

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37
Q

SVC syndrome

A

obstruction of superior vena cava causes

  1. superficial venous engorgement of chest
  2. facial edema and plethora
  3. signs of increased ICP, HA, tinnitus, bursting sensation
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38
Q

pancoast’s tumor

A

peripheral tumor (mc NCLC)

invade early and cause local destruction

invasion of nerves of brachial plexus and cervical sympathetic nerves (stellate ganglion) compression of vascular structures

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39
Q

pancoast’s tumor syndrome

A

horner’s syndrome

severe and unremitting pain (upper back and shoulder w/radiation into axilla down inner aspect of arm to hand)

muscle atrophy

compression causing edema

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40
Q

metastatic dz

mc sites

A

brain, bones, liver, adrenals, pericardium and spinal cord

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41
Q

pericardial lesions

A

heart is unable to expand to produce good CO

resulting in tamponade (JVD, HoTN, muffled heart sounds)

42
Q

adrenal lesions

A

destruction of normal adrenal tissue and adrenal insufficiency

HoTN (fluid recesitation decrease), poor stress tolerance, non-specific (weak, tired)

43
Q

symptoms of hepatic metastasis

A

increased transaminases/LFT’s

associated with weight loss

44
Q

symptoms of brain metastasis

A

headache
n/v
seizures
AMS

45
Q

symptoms of spinal cord metastasis

A

paralysis or peripheral weakness

sensory loss of extremity

n. invasion = intense pain

46
Q

symptoms of bone metastasis

A

vertebrae most commonly involved

ribs and pelvis

primary symptoms: severe pain

pathologic fracture may occur

47
Q

paraneoplastic syndromes

A

organ dysfunction related to immune mediated or secretory effects

occurs in 10-20%, may precede, accompany, or follow diagnosis

does not indicate metastasis

48
Q

types of paraneoplastics syndrome

A

SCLC –> SIADH (free water reabsorption)

squamous cell –> hypercalcemia (PTHrP)

trousseau syndrome (adenocarcinoma)

neurological effects (LEMS, SCLC)

cushion’s syndrome (increased ACTH) SCLC

hematologic changes (anemia, thrombocytopenia)

digital clubbing

49
Q

work up of lung mass

A
  1. CT w/contrast, entire area
  2. CBC, electrolytes, LFTs, LDH, albumin
  3. Pulm consult
  4. additional testing/tissue diagnosis
50
Q

tissue diagnosis mechanisms

A
  1. fiberoptic bronchoscopy
  2. CT guided needle bx
  3. FNAB
  4. Sputum cytology
  5. thoracentesis
  6. VATS thoracotomy
51
Q

fiberoptic broncoscapy

A

direct forceps biopsy, brushing

high sensitivity for central, endobronchial lesions

US may assist

52
Q

CT guided needle biopsy

A

evaluation by IR, they skin to get tissue (PTX risk)

good for peripheral tissue

53
Q

FNAB

A

supra-clavicular or cervical lymph nodes

diagnostic

54
Q

thoracentesis

A

malignant pleural effusions, sensitivity 50-60%

may perform twice

55
Q

additional testing for suspected lung CA

A

MRI of brian (CNS symptoms or focal findings)

pulmonary function testing

evaluation of cardiovascular status

PET/CT (look for dz not visible on CT + distant metastasis)

56
Q

which part of node is hardest to visualize on PET/CT?

A

brain

v. difficult bc high uptake of glucose

57
Q

surgical tx options for lung CA

A

NSCLC

  1. Pneumonectomy
  2. Lobectomy
  3. segmentectomy/wedge resection
  4. sleeve resection
58
Q

pneumonectomy

A

removal of ENTIRE lung

MC tumor close to the center of chest

59
Q

lobectomy

A

removal of an entire lobe containing tumor

procedure of choice

60
Q

segmentectomy

A

part of love removed

suboptimal may be used if pt doesn’t have enough lung fxn to withstand lobectomy

61
Q

sleeve resection

A

tx of CA in lg airways

resected with clear margins and distal lung reconnected to proximal airway

preserves lung function

62
Q

FEV1 and surgery determinations

A

use PFTs to determine likelihood a patient will come off vent

good PFTs = radical surgery

63
Q

chemo for lung CA

A

4-6 cycles, given over 1-3 days every 3 weeks

given MC to pts with NCLC, less successful SCLC

64
Q

radiation for lung CA

A

radiation delivered to tumor, must pass thru other tissues to reach target

successful bc CA cells can’‘t recover from DNA result

65
Q

differnt types of XT tx

A

A. conventional external beam: dose fractionation, overtime amount increases

B. stereotactic body radiation: fewer tx of beams, go at tumor from multiple angles

66
Q

NSCLC surgery

stage I/II

A

tx with curative intent

surgical resection (lobectomy)

non-surgical candidates get radiation

67
Q

NSCLC surgery

stage III

A

diverse options, curative intent, mediastinal involvement distinguish

none: surgical resection, adjuvant chemo +/- XT
involvement: definitive chemo-radiation, becomes modality of choice

68
Q

NSCLC surgery

IV

A

tx is palliative intent (prolong survival)

combo platinum based chemo, targeted therapy if possible or after CTX

surgical removal of mets

69
Q

driver mutations

A

tumor growth and progression depend heavily on it

blocking signals allows us to have attack o CA with few effects

EGFR, ALK

70
Q

EGFR

A

driver mutation over expresses EGFR

MC in women, never smoker, adenoma, asians

71
Q

EGFR targeted therapy

A

Tyrosine kinase inhibitors

first line or second line following initial chemotherapy

72
Q

ALK

A

direct mutation promoting growth and spread

light or never smokers, young its with adnoCA and predicts sensitivity to ALK TKI

73
Q

other forms of target therapy

A

molecules that block tumor angiogenesis via decreasing BEGF

decreases blood supply

good option for ALL cancers, not just driver mutations

74
Q

immunotherapy

A

stimulates immune system to recognize and destroy CA cells

PDI ligand is targeted by drugs and destroyed using the body’s T cell/CD8 cells

75
Q

PD-1 inhibitors

A

Pembrolizumab/Keytruda
nivolumab/Opdivo
Atezolizumab/Tecentriq

76
Q

NSCLC prognosis

A

HIGHLY lethal

TMN stage of cancer at time of diagnosis is most imp. prognostic indicator

77
Q

SCLC stages

A

limited (ipsilateral hemithorax, regional nodes) 5 yr <17%

extensive disease (distant mets, pericardial/pleural, contralateral supraclavicular or hilarious LAD) 
2 yr < 5%
78
Q

limited SCLC tx

A

prom tx

limited = NO lymph node = surgical resection/lobectomy + chemotherapy

79
Q

limited SCLC + lymph involvement

A

candidates for chemoradiation

any response prophylactic cranial radiation

80
Q

extensive stage SCLC tx

A

MC presentation

systemic chemotherapy, palliative intent

if responsive: thoracic XT, prophylactic WBRT

81
Q

palliative care for lung CA

A

external radiation
pain control
chemotherapy
hospice control

82
Q

external radiation in palliative care

A

control dyspnea and hemoptysis

pain from bony mets

obstruction from superior vena cava syndrome

symptomatic brain mets

83
Q

chemotherapy palliative care

A

surgical procedures or chemotherapy to control dz

enough to prolong life but no toxicity

84
Q

Neuroendocrine tumors

A

produce and secrete neuropeptides and neuroamines in a variety of places (GI, lungs)

typically slow growing vascular indolent malignant tumors

atypical are aggressive and necrotic

1-2% secrete ACTH causing Cushings

85
Q

Neuroendocrine tumors epidemiology

A

women, caucasians >

before age 60

MC lung tumor in children

ass. with smoking

86
Q

CT of Neuroendocrine tumors

A

well circumscribed centrally located males

25% are peripheral SPN

87
Q

bronchial carcinoid tumors symptoms

A

hemoptysis (vascular tumor)
cough
focal wheezing
recurrent PNA

bc tumor grows centrally, obstructing ariway

88
Q

carcinoid syndrome

A

caused by tumor chemical release, rare in lung NETs (vasoactive instead)

flushing, diarrhea, bronchospasm, wheezing, severe hyper-/hypotension

octreotide = tx

89
Q

bronchial carcinoid tumors metastasis and diagnosis

A

mc site of metastasis is liver

diagnosed using CT, can do PET-CT

serotonin levels unhelpful bc not high enough [ ]

90
Q

tx of bronchial carcinoid tumors

A

surgical excision

adjunct CTX for atypical

91
Q

methods of metastatic spread

A

hematogenous (via blood)

lymphatic (via lymph)

direct extension

common site bc lungs recieve 100% of blood

92
Q

common primaries in lung metastasis (BReAST)

A 
Brest 
Renal 
Anal/Colon 
Skin (multiple melanoma) 
Testes/ovaries
93
Q

metastasis on imaging

A

multiple sharply demarcated solid nodules/masses

Bilateral

lower lung fields

CXR/CT

Lots Little Lower

94
Q

tx of metastasis

A

find and tx PRIMARY CA appropriately (routine screening)

address complications, resection of nodule

95
Q

mesothelioma

A

primary tumor arising from pleura (also peritoneum, pericardium, testes)

begin as a small nodule in lower lung that grows to a sheet encasing pulmonary structures

96
Q

mesothelioma epidemiology

A

men>women , 50-70 y/o

HIGHly associated with asbestos exposure

97
Q

asbestos exposure

A

20-40 yrs prior to mesothelioma exposure

via insulation, shipyard work, building construction and demolition

98
Q

mesothelioma diagnosis

A

typical pulmonary signs

CXR: nodular, irregular unilateral pleural thickening and effusion

Contrast CT to show extent, thoracentesis for effusion

VATS biopsy to confirm

99
Q

mesothelioma course

A

progressive hardening to pericardium and diaphragm/abdomen

progressive pain and dypsena due to decreased lung expansion

100
Q

staging mesothelioma

A

thorascopy +/- MRI

stage i: completely resected, disease free

ii: margins not clear, pleural LAD
iii: local extension, mediastinum and chest cavity
iv: distant mets

WI-18 Pulmonary (11 decks)

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