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MOD 3 > Lung Cancer Path and Phys > Flashcards

Lung Cancer Path and Phys Flashcards

1
Q

Primary bronchogenic carcinomas are divided into these two categories. What are these categories based on, and what is the break up

A
  1. Non-Small Cell Lung Carcinoma (75%)
  2. Small Cell Lung Carcinoma (20%)

Based on their response to available surgery

NSCLC: surgery

SCLC: chemotherapy

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2
Q

What are the 5 types of Non small cell carcinoma?

A
  1. Sqamous Cell Carcinoma
  2. Adenocarcinoma
  3. Large Cell Carcinoma
  4. Bronchioloalveolar carcinoma
  5. Carcinoid
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3
Q

Adenocarcinoma of the lung:

  • characteristic histology
  • association
  • location
A
  • glands or mucin, papillary pattern
  • most common tumor in nonsmokers and female smokers
  • peripheral
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4
Q

lepidic growth pattern

A

usually seen in bronchioloalveolar carcinoma

  • “butterflies sitting on a fence”
  • grows along preexisting structure i.e. bronchioles, alveolar septa, without destroying alveolar architecture (no invasion)
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5
Q

Sqamous cell carcinoma of the lung:

  • characteristic histology
  • association
  • location
  • comment
A
  • keratin pearls or intercellular bridges (desmosomal connections between the cells)
  • most common tumor in male smokers, usually see tumor suppressor Loss Of Function (LOF)
  • central
  • may produce PTHrP (hypercalcemia)
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6
Q

large cell carcinoma of the lung

  • characteristic histology
  • association
  • location
  • comment
A
  • poorly differentiated LARGE cells, anaplastic (NO kertain pearls, intercellular bridges, glands or mucin)
  • smoking
  • central OR peripheral (can be variants of squamous and adenoma)
  • poor prognosis
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7
Q

Small cell carcinoma of the lung

  • characteristic histology
  • assocation
  • location
  • comment
A
  • poorly differentiated small cells; arises from neuroendocrine (Kulchitsky) cells
  • male smokers
  • central
  • rapid growth and early metastasis; may produce ADH or **ACTH **or cause Eaton-Lambert syndrome (paraneoplastic syndrome)
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8
Q

oat cells

A

small cells that characterize small cell carcinoma

  • look like lymphocytes, uniform in shape and size, but theyre infact 2-3x larger in size
  • hyperchromatic nuclei
  • chromatin “salt and pepper” appearance
  • scarce cytoplasm
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9
Q

Clinical manifestations of:

Adenocarcinoma

What is the 5 year survival?

A

pleuritic chest pain (since peripheral), effusion, weight loss, dyspnea

5 year survival = 10%

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10
Q

Clinical manifestations of:

Squamous cell carcinoma

What is the 5 year survival?

A

cough (since central), dyspnea, weight loss

5 year survival: 10%

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11
Q

Clinical Manifestations of:

Small cell carcinoma

What is the 2 year survival?

A

paraneoplastic syndromes, cough, hemoptysis, weight loss, dyspnea

2 year survival = 25%

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12
Q

In metatastases of lung cancer, no organ is spared, but the 4 major sites (and percentage of cases) are the following:

Which type of lung cancer characteristically involves the bone marrow?

A

“BLAB”

  1. Brain (20%)
  2. Liver (30-50%)
  3. Adrenals (>50%)
  4. Bone (20%)

Small cell lung carcinoma characteristically has widespread focal involvement of bone marrow

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13
Q

diagnosis of lung cancer (5)

A

1) chest radiograph and CT scanning
2) sputum cytology and bronchial lavage
3) fiberoptic bronchoscopy
4) needle biopsy
5) molecular pathology, fluorescence bronchoscopy, endobronchial ultrasound, spiral computed tomogrpahy

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14
Q

T4 (general meaning of status)

A

Tumor of any size invading mediastinum, heart, esophagus, trachea, etc.

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15
Q

List 4 main carcinogens in tobacco smoke

A

1) polycyclic aromatic hydrocarbons: penzopyrene from tars
2) nitrosamines
3) aromatic amines
4) free radicas and nonradical oxidants

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16
Q

5 major molecular pathways in the pathogenesis and progression of lung cancer

A

1) inactivation (or silencing) of tumor suppressor genes
2) activation of oncogenes
3) evasion of apoptosis
4) DNA repair defects
5) telomerase dysregulation

17
Q

List the changes in epithelium as it goes from early to intermediate to late stages

A

normal epithelium –> hyperplasia –> squamous metaplasia –> dysplasia (intermediate) –> carcinoma in situ (late) –> invasive carcinoma

18
Q

For each change in epithelium, list the molecular changes/markers observed:

Normal epithelium:

Hyperplasia:

Squamous metaplasia:

Dysplasia:

Carcinoma In situ/Invasive Carcinoma:

A

Normal epithelium: 3p21-9b21 LOH

Hyperplasia: telomerase inactivation

Squamous metaplasia: P15/NK4a methylation

Dysplasia: FHIT inactivation 8p22-24 LOH

Carcinoma In situ/Invasive Carcinoma: Tp53 inactivation, 5q22 LOH

19
Q

What are the major mutations/molecular pathology of lung adenocarcinoma? (5)

A
  1. EGFR mutation
  2. EML4-ALK rearrangements (anaplastic lymphoma kinase)
  3. KRAS mutations (kirsten rat sarcoma viral oncogene)
  4. MET amplifications (mesenchymal epithelial transition factor)
  5. ROS-1
20
Q

What do all of the EGFR (HER/ERbB) have in common?

A

Tyrosine kinase domains on the opposite site of where the lingand binds (intracellular)

21
Q

5 effects of signaling pathway of EGFR

A
  1. angiogenesis
  2. differentiation
  3. motility
  4. proliferation
  5. survival
22
Q

Current therapy for lung cancer (4)

A
  1. Surgery
  2. Radiation
  3. Chemotherapy
  4. Targeted therapy
23
Q

3 main NEW targeted therapies for lung cancer

A

1) EGFR family inhibitors
2) ALK tyrosine kinase inhibitors
3) immune checkpoints blockade

24
Q

5 less important new targeted therapies

A
  1. inhibitors of angiogenesis
  2. inhibitors of signal transduction
  3. inducers of apoptosis
  4. inhibitors of eicosanoid pathway
  5. demethylating agents
25
Q

3 promising treatments for immune checkpoint blockade:

  • mAb anti-CTl-4
  • mAb anti-PD-1
  • mAb anti-PD-L1
A
26
Q

2 ways to create immunosuppressive microenvironment

A
  1. production of immunosuppressive cytokines (TGF-B, IL-10, VEGF)
    * TGF-B normally inhibits the cell cycle
    2) expression of co-inhibitory immune checkpoint molecules (CTLA-4, PD-1)
27
Q

3 most common sources (cancers) of osteoblastic metastases

A
  1. small cell lung cancer
  2. prostate gland carcinoma
  3. breast carcinoma
28
Q

Molecular pathology of squamous cell carcinoma (7)

A
  1. loss of p16 and cyclin overexpression in earlier lesions
  2. loss of FHIT (tumor suppressor gene)
  3. Bcl2 overexpression
  4. abnormal expression / mutation of **p53 **
  5. telomerase dysregulation
  6. EGFR overexpression (86%)
  7. cyclin D1 over expression and 2q, 18q, HER-2 neu, bcl-2 gene alterations occur at the transition to invasive cancer
29
Q

this cancer may produce ADH or ACTH (cushing’s: body exposed to increased cortisol levels)

A

small cell carcinoma

-pt can have greatly increased free cortisol urine levels

30
Q

Molecular testing for these two markers is indispensible for lung adenocarcinomas

A

EGFR and ALK

MOD 3 (19 decks)

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