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Neoplasia Flashcards

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1
Q

Neoplasia definition

A

Uncontrolled growth of cells
Normal regulation of proliferation fails
Cell growth is autonomous, excessive, and disorganized

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2
Q

Tumor definition

A

Proliferation of neoplastic cells that forms a mass

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3
Q

Cancer definition

A

Malignant neoplasms

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4
Q

Benign versus malignant neoplasm

A

Benign: limited growth potential, typically good outcome, no metastases
Malignant: uncontrolled growth and spread, potential to kill host, can metastases

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5
Q

Metastasis definition

A

Spread of a neoplasm from one site in the body to another

Only malignant neoplasms are capable of doing this

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6
Q

Gross appearance of benign versus malignant tumors

A

Benign: smooth borders, looks the same throughout
Malignant: infiltrative border, spreads into other tissues, hemorrhage and necrosis, can get into blood and lymph vessels

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7
Q

Epithelial tumors

A

Benign ones are often called adenomas
Benign ones in the skin, urinary bladder, and larynx that protrude above the surface are often called papillomas
Malignant ones are called carcinomas

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8
Q

Epithelial tumor classification:

  1. Glands/ducts
  2. Squamous epithelium
  3. Transitional cells
  4. Neuroendocrine cells
  5. Liver cells
  6. Kidney cells
A
  1. B: adenoma, M: Adenocarcinoma
  2. B: Squamous papilloma, M: squamous cell carcinoma
  3. B: Transitional cell papilloma, M: transitional cell carcinoma
  4. B: neuroendocrine tumor, M: small or large cell neuroendocrine carcinoma
  5. B: Hepatocellular adenoma, M: hepatocellular carcinoma
  6. B: Renal adenoma, M: renal cell carcinoma
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9
Q

Mesenchymal tumors

A

Neoplasms originating from connective tissues such as adipose, bone, muscle
Ending in -oma

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10
Q

Mesenchymal tumor classification:

  1. Fibroblast
  2. Fat cell
  3. Blood vessel
  4. Smooth muscle
  5. Striated muscle
  6. Cartilage
  7. Bone
A
  1. B: fibroma, M: fibrosarcoma
  2. B: lipoma, M: liposarcoma
  3. Hemangioma, angiosarcoma
  4. Leiomyoma, leimyosarcoma
  5. Rhabdomyoma, Rhabdomyosarcoma
  6. Chondroma, chondrosarcoma
  7. Osteoma, osteosarcoma
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11
Q

Benign versus Malignant tumors in:

  1. Neural cells
  2. Glial and neural support cells
  3. Germ cells
  4. Melanocytes
  5. Mesothelium (only M)
A
  1. Ganglioneuroma, neurblastoma
  2. Glioma, glioblastoma multiforme
  3. Teratoma, seminoma or embryonal carcinoma
  4. Melanocytic nevus, melanoma
  5. M = mesothelioma
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12
Q

Teratoma

A

Benign tumor derived from germ cells
Contains tissue formed from all 3 germ layers (ecto, meso, endoderm)
Ovary most common
Contain teeth, hair, skin, etc

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13
Q

Blastoma

A

Tumors composed of embryonic cells originating from embryonic primordia
Mostly in children

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14
Q

Eponymic tumors (3 examples)

A

Carry name of physicians who described them first
Hodgkin’s disease: a type of lymphoma
Ewing’s sarcoma: type of bone sarcoma
Kaposi’s sarcoma: type pf vascular malignancy

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15
Q

What is grading versus staging based on?

A

Grading: based on histologic examination
Staging: based on clinical assessment during gross examination, surgery, x-rays, etc

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16
Q

What does TMN stand for?

A 
T = size and local invasiveness of tumor
N = presence of lymph node metastases
M = distant metastases
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17
Q

Grading

A

Degree of differentiation (well to poor)
Based on tissue architecture, mitoses, degree of cell atypia
Low grade looks like normal tissue
Less important than staging with a few exceptions

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18
Q

Staging

A

TNM
T1-4 based on size of tumor or depth of invasion
N0-N3 based on number and location of involved lymph nodes
M0-M2 based on presence, location, and number of metastases
More prognostic significance than grade (usually)

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19
Q

Metastasis definition

A

The process of malignant cells moving from one site in the body to another site

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20
Q

3 pathways of metastasis

A
  1. Lymphatics
  2. Blood (hematogenous spread)
  3. Seeding of the surface of the body cavities
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21
Q

To metastasize, a tumor (clone) must be able to…

A

Escape the immune system
Be capable of entering the bloodstream/lymph/body cavity
Arrive at the new site, invade and be capable of forming a new blood supply (angiogenesis)

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22
Q

3 general classes of exogenous causes

A

Chemical agents
Physical agents
Biologic agents

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23
Q

2 classes of endogenous causes

A

Oncogenes

Tumor suppressor genes

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24
Q

Examples of chemical carcinogens (4)

Study These Flashcards
A
  1. Polycyclic aromatic hydrocarbons (3,4-benzopyrene from tobacco tar, aflatoxin from fungus)
  2. Aromatic amines (Beta napthylamine from rubber and dye industry)
  3. Nitrosamines (nitrates from food additives)
  4. Steroid hormones (estrogens from hormone replacement therapy)
25
Carcinogen
Absorbed either preformed or in the form of procarcinogen (transformed into active carcinogen)
26
Carcinogen action
1. Initiation (genetic change induced in cell) 2. Promotion (initiated cell promoted to grow) 3. Coversion (change into new cell type) 4. Progression (cells proliferate following removal of initiating carcinogen and promoters) 5. Clonal expansion
27
4 physical carcinogens
1. UV light 2. X-rays 3. Radioactive isotopes 4. Atomic bomb
28
3 Natural biologic carcinogens
1. Aflatoxin (derived from fungus Aspergillus flavus; contaminated peanut a source, acts as liver carcinogen) 2. Schistosoma haematobium (parasite; acts as urinary bladder carcinogen) 3. Opisthorchis sinensis (chinese liver fluke; acts as carcinogen for bile duct or liver)
29
Human carcinogenic DNA (3) and RNA (1) viruses
1. HPV (warts, cervical cancer, oropharynx cancer) 2. Epstein-Barr virus (lymphomas, nasopharyngeal carcinoma) 3. Hep B (liver cancer) 4. Human T-cell leukemia/lymphoma virus
30
Clinical manifestations of neoplasia
Local (effects due to invasion or compression of adjacent normal tissues) Systemic (cachexia and paraneoplastic syndromes)
31
Cachexia
Wasting caused by cancer | Weight loss, weakness, fatigue
32
Paraneoplastic syndromes
Caused by substances secreted by cancer (often hormones)
33
Incidence
Number of new registered cases over specific time in a defined population
34
Prevalence
Number of all cases, new and old, within defined population at defined time
35
Oncogenes
Genes that promote autonomous cell growth in cancer cells | Abnormally activated forms of proto-oncogenes
36
Proto-oncogenes
Normal genes Have roles in normal cells that are related to growth and proliferation Proteins encoded by them may be growth factors, their receptors, signal transducers, transcription factors, or cell cycle components
37
Oncoproteins
Protein products of oncogenes Similar to normal products of proto-oncogenes, but lack important internal regulatory elements Act independently of growth factors and other external signals Can make cell growth autonomous
38
4 mechanisms of the transformation of proto-oncogenes into oncogenes
1. Point mutation 2. Gene amplification 3. Chromosomal rearrangment 4. Insertion of viral oncogene
39
Point mutation
A single base substitution in the DNA Results in a miscoded protein, typically with an amino acid substituted with another Common mutations in RAS and RAF gene families
40
Gene amplification
The cell acquires an increased number of copies of the proto-oncogene The more copies of the oncogene, the more malignant the cell becomes
41
Chromosomal rearrangements
A translocation can occur where one chromosome fragment attaches to another, juxtaposing two genes A deletion can also result in a juxtaposition The resulting gene complexes can cause overexpression of proto-oncogenes, due to stimulation by the adjacent promoter gene
42
Insertion of viral genome
Insertion of portions of the viral genome disrupts normal chromosomal architecture Changes can accumulate gradually in slow transforming viruses such as hep B
43
Tumor suppressor genes
Normal cells have regulatory mechanisms that protect cells against activated or newly acquired oncogenes Their products apply brakes to cell proliferation
44
Retinoblastoma gene (RB-1)
Found in patients with pediatric eye tumor retinoblastoma Its a tumor suppressor gene Hereditary version - already only have 1 copy of the gene Often die of other tumors - osteosarcoma Product regulates the checkpoint between G1 and S When it is not functioning, the cell will proliferate without regulation
45
TP53
p53 is the protein product | Probably the most important TSG
46
3 actions p53 does after sensing DNA damage
1. Activates temporary cell cycle arrest (quiescence) 2. Induces permanent cell cycle arrest (senescence) 3. Triggers apoptosis
47
Neurofibromatosis 1
Numerous subcutaneous neural sheath tumors (neurofibromas) and cafe-au-lait macules Patients can develop other tumors NF1 is a TSG inactivating signal transduction by the RAS proto-oncogene NF1 gene which is defective or lost results in tumor formation
48
Familial Adenomatous Polyposis Coli
Defects in the tumor suppressor gene APC Innumberable colonic polps by age 20 Most patients will die of colon cancer without colectomy at an early age
49
Wilms' tumor
Malignant kidney tumor of childhood | Caused by defects in the tumor suppressor gene WT1
50
Hereditary breast cancer
Most common cause is defects in TSG Braca 1 and 2 Much higher chance of getting breast cancer Many elect to have a prophylactic bilateral mastectomy
51
What are CEA and AFP markers for?
CEA (carcinoembryonic antigen): marker for adenocarcinoma of colon AFP (Alpha-fetoprotein): marker for heptaocellular carcinoma and certain germ cell tumors that contain yolk sac components
52
Keytruda (pemrolizumab)
Inhibit PD-1 receptor, cannot interact with ligand on tumor cells, immune cells can kill! Just induces remission for a couple of months Can get hypersensitivity reactions to it
53
Cushing's syndrome
Small cell carcinoma of the lung
54
Hypercalcemia
Squamous cell carcinoma of the lung
55
Polycythemia
Renal cell carcinoma
56
Venous thrombosis
Pancreatic carcinoma
57
Myasthenia gravia
Thyoma
58
BCG
Attenuated tuberculosis bacillus of Calmette-Guerin used for treatment of bladder cancer

Pathology (19 decks)

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