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Oncology > 15 & 16 - Lung Cancer > Flashcards

15 & 16 - Lung Cancer Flashcards

1
Q

Second most common type of cancer in each men and women

A

Lung Cancer

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2
Q

Leading cause of cancer death

A

Lung Cancer

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3
Q

Screening - CT vs CXR

A

CT catches more, catches them earlier, helps more people survive

More false positives!! (noncalcified granulomas or benign intrapulmonary LN)

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4
Q

Cytology specimens

A

Fine needle aspiration

An assortment of cells

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5
Q

Core biopsy

A

Tissue in context!

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6
Q

Minimally invasive procedures

A

CT guided biopsy - FNA & Core, only peripheral

EBUS - EndoBronchial Ultrasound-Guided Something - FNA, but not Core. Central only. Can stage.

Electromagnetic navigational bronchoscopy - FNA & Core, Peripheral & Central, can’t stage, though

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7
Q

Classifications of Tumors in the Lung

A 
Epithelial
Mesenchymal
Lymphohistiocytic
Ectopic origin
Metastatic
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8
Q

Mesenchymal Tumors

A

Not epithelial cells

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9
Q

Most common Mesenchymal Tumor in Lungs

A

Hamartoma

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10
Q

Hamartoma

A

Tissue elements normally found in lung but occurring as disorganized proliferation
Benign

“Coin lesions” with popcorn calcifications
Well-circumscribed
Slow-growing

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11
Q

Hamartoma - Morphology

A

Varying amounts of mesenchymal elements (Cartilage, fat, connective tissue, bone)
Entrapped respiratory epithelium

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12
Q

Categories of Epithelial Tumors of the Lung

A

Neuroendocrine Tumors
XXX
XXX

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13
Q

Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH

A 
Proliferation of neuroendocrine cells
Confined to mucos aof airways
Invade locally to form tumorlets
Develop into carcinoids
Rarely associated with small cell carcinoma and large cell neuroendocrine carcinoma
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14
Q

Neuroendocrine Tumors - Low-intermediate grade

A

Typical carcinoid

Atypical carcinoid

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15
Q

Neuroendocrine Tumors - High Grade

A

Small cell carcinoma

Large cell neuroendocrine carcinoma

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16
Q

Neuroendocrine - Typical Carcinoid

A

Central Airways > Peripheral
Well-circumscribed
Fill bronchial lumens

Morphology:
Monomorphic
Fine “salt and pepper” chromafin

Immunostains:
Synaptophysin
Chromogranin
CD56

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17
Q

Neuroendocrine - Small Cell Lung Cancer

A

Large central mass with bulky mediastinal adenopathy

Morphology:
Scant cytoplasm
Inconspicuous/Absent nucleoli
Nuclear molding
Crush artifact
Numerous mitoses
Immunostains:
Neuroendocrine markers
Synaptophysin
Chromogranin
CD56
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18
Q

Squamous Cell Carcinoma

A

Preinvasive: Squamous cell carcinoma in situ

Invasive: Keratinizing, Non-Keratinizing, Basaloid squamous cell carcinoma

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19
Q

Adenocarcinoma

A

Preinvasive: Atypical adenomatous hyperplasia (AAH), Adenocarcinoma in situ

Invasive: Adenocarcinoma, classification based on predominant subtype:
Lepidic, acinar, papillary, micropapillary, solid

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20
Q

Squamous Cell Carcinoma - Life cycle

A

Early:
Normal - Ciliated epithelium
Hyperplasia
Squamous metaplasia

Intermediate:
Dysplasia

Late:
Carcinoma in situ
Invasive carcinoma

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21
Q

Squamous Cell Carcinoma - Histo

A

Morphology:
Keratinization
Intercellular bridges

Immunostains:
P40
P63
CK5/6

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22
Q

Adenocarcinoma - Life Cycle

A

Pre-invasive:
Atypical Adenomatous Hyperplasia (AAH) (less than .5cm)
Adenocarcinoma in Situ (less than 3cm)

Invasive:
Minimally invasive adenocarcinoma

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23
Q

Adenocarcinoma - Histo

A

Morphology:
Glands/acini
(micro)papillae
Mucin

Immunostains
TIF-1
Napsin A

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24
Q

Which two molecular tests do you do on an adenocarcinoma?

A

EGFR Mutation

ALK rearrangement

25
Q

Large Cell Carcinoma

A

Non-small cell carcinoma
Lacks cytological architectural and immunohistochemical features of small cell carcinoma, adenocarcinoma and squamous cell carcinoma

Catch-all

26
Q

Sarcomatoid Carcinoma

A

Pleomorphic Carcinoma

Non-small cell carcinoma, with at least 10% spindle and/or giant cells

27
Q

Lung Metastases - Presentation

A

Single or multiple
Lymphangitic
Lung parenchyma or pleura>endobronchial mass

28
Q

Lung Metastases - Common sites

A 
Breast
Prostate
GI tract
Gynecological
Head & Neck
29
Q

Lung Metastases - Pathological Diagnosis

A

Clinical
Morphological
Immunohistochemical

30
Q

Lung Cancer Presentation - Local Symptoms

A 
Cough
Dyspnea
Hemoptysis
Chest pain
Hoarseness (recurrent laryngeal nerve)
SVC Syndrome
Wheezing
31
Q

Lung Cancer Presentation - Systemic Symptoms

A

Constitutional:
Weight loss
Malaise

Skeletal:
Clubbing
Hypertrophic Pulmonary Osteoarthropathy

Endocrine:
SIADH (SCLC)
Hypercalcemia (Squamous)
Cushings Syndrome (SCLC)

Neurologic:
Horner’s Syndrome
Eaton-Lambert Syndrome (SCLC)

Vascular:
Hypercoagulable state of malignancy
Thrombophlebitis
DIC

32
Q

NSCLC Staging - Determination

A

Size
Invasion of adjacent structures
Separate nodules with the same morphology

33
Q

Lung Cancer - Clinical Staging

A

PET scan

MRI

34
Q

TNM - Nodes N1 vs N2

A 
N1 = Double Digit Station (more peripheral)
N2 = Single Digit Station (more central)
35
Q

Dr. Bosl’s Rules of Cancer

A

It’s not cancer until proven to be cancer
If it’s cancer, it’s curable until proven otherwise
If it’s not curable, the cancer is treatable until proven otherwise
Even if the cancer is not treatable, the patient is always treatable.

36
Q

Definitive Management - Early Stage Disease

A

Surgery

Anatomical resections:
Pneumonectomy - High M&M, especially a right pneumonectomy. MAJOR functional consequences (60% function loss)
Lobectomy - Preferred surgical option for most patients

Lung-preserving surgery:
Wedge Resection - Least morbidity, commonly done, but recurrence rate higher. Can be safe in patients with limited lung function. First surgical step if pathology is unclear.

Techniques:
Conventional open
VATS (Video-Assisted Thoracoscopic Surgery)
Robotic

37
Q

Adjuvant Treatment

A

Given after surgery to decrease risk of recurrence

Chemotherapy (eliminate micrometastatic disease)
Radiotherapy (eliminate localized disease at resection margins/mediastinal nodes)

Curative intent, but no guarantee

38
Q

Lung Cancer - Adjuvant Treatment (Stage I - II)

A

Platinum Doublet
No major difference in efficacy between various chemotherapy doublets in advanced disease

Cisplatin with:
Premetrexed
Docetaxel
Gemcitabine
Etc

4cm cutoff for adjuvant chemotherapy

39
Q

Lung Cancer - Adjuvant Treatment (Stage III)

A

Involves local and distant therapy

Surgery → Adjuvant chemo → PORT
Neoadjuvant Chemo → Surgery → +/- PORT
Chemo + XRT → Surgery
Chemo + XRT

40
Q

PORT

A

Post-Operative RT
When you discover mid-surgery that there is N2 lymph node involvement, causing them to be a higher stage than you thought.

PORT has not been shown to improve survival
Increases mortality in N0 and N1

41
Q

Stage IIIB

A

Involvement of the contralateral lymph nodes
Prognosis poor
They are essentially at stage 4, so only treat with chemo & XRT or XRT alone. No surgery.

42
Q

Platinum Doublets for Stage IIIB treatment

A

Cisplatin and Paclitaxel
Cisplatin and Gemcitabine
Cisplatin and Docetaxel
Carboplatin and Paclitaxel

Which platinum doublet is best?
THEY ARE ALL THE SAME

43
Q

Cisplatin - Mechanism

A

Platinum agent

Inhibits DNA synthesis by the formation of DNA cross-links, disrupts DNA function

44
Q

Cisplatin - Side effects

A 
Neurotoxicity
Nausea/vomiting
Ototoxicity
Nephrotoxicity (must hydrate)
Electrolyte disturbances
45
Q

Paclitaxel - Mechanism

A

It’s a taxane

Disrupts microtubule function (stabilizer), cell cycle arrest & apoptosis

46
Q

Paclitaxel - Side Effects

A 
Alopecia
Decreased blood count
Neuropathy
Hypersensitivity reaction
Arthralgias/myalgias
Fatigue
Nail changes
47
Q

Pemetrexed - Mechanism of Action

A

Antimetabolite
Inhibits folate-dependent enzymes involved in purine & pyrimidine synthesis:
Thymidylate Synthase (TS)
Dihydrofolate Reductase (DHFR)
Glycinamide Ribonucleotide Formyltransferase (GARFT)

Multi-targeted folate analogue

Adenocarcinoma does better with this than other drugs

48
Q

Premetrexed - Side Effects

A 
Well tolerated, for the most part
Decreased blood counts
Nausea
Fatigue
Rash
Supplementation with B12 and folic acid to reduce side effects.
49
Q

EGFR Pathway

A

Member of the HER family of cell surface TKRs
Downstream signaling via RAS/MAPK, PI3K/AKT pathways
Inappropriate signaling leads to:

Increased/uncontrolled cell proliferation
Decreased apoptosis
Enhanced cancer cell motility
Angiogenesis

50
Q

Lung cancer with an EGFR mutation

A

Predictive AND prognostic
Better prognosis
Responds well to an EGFR TKI

51
Q

Give an EGFR TKI to Lung Cancer with EGFR mutation

A

Higher response rates in:
Females
Never smokers
Asians

52
Q

ALK+ NSCLC - Treatment

A

Crizotinib (WAY BETTER THAN CHEMO)

53
Q

Small Cell Lung Cancer - Staging

A

Limited Vs Extensive stage disease based on radiation fields

Limited:
40% of patients
14 - 20 months median survival
40% 2-year survival
10 - 20% long-term survival
Extensive:
60% of patients
8 - 12 months median survival
5 - 10% 2-year survival
Very few long-term survivors
54
Q

Limited Stage Small Cell Lung Cancer - Treatment

A 
Surgery is rarely an option
Standard of care: Chemo & XRT
Chemo = Platinum + Etoposide (4 - 6 cycles)
Concurrent > Sequential
BID may be more effective than daily RT?
55
Q

Limited Stage Small Cell Lung Cancer - During Remission

A

Give Prophylactic Cranial Irradiation (PCI)
10 - 30% of patients entering complete remission relapse with isolated CNS mets
PCI (20 - 40 Gy) improves survival
Long-term neuropsychiatric defects commonly noted

56
Q

Extensive Stage SCLC

A

Very poor outcome
9 - 12 months medical survival

Standard treatment is chemo (4 - 6 treatments of platinum/etoposide)
60 - 80% response rate
Patients quickly relapse

2nd line chemotherapies provide only short-term benefits

57
Q

Etoposide - Mechanism of action

A

Topoisomerase inhibitor
Forms complex with DNA andtopoisomerase II
Prevents re-ligation of DNA strands causing breakage

58
Q

Etoposide - Side effects

A 
Alopecia
Nausea
Decreased blood counts
Fatigue
Secondary leukemia

Oncology (23 decks)

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