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USMLE Step I Pathology > Principles of Neoplasia (Pathoma) > Flashcards

Principles of Neoplasia (Pathoma) Flashcards

1
Q

Basic Principles of Neoplasia

A

Unregulated, irreversible, and monoclonal.

Distinct from hyperplasia and repair.

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2
Q

Monoclonal

A

Neoplastic cells are derived from a single mother cell

*Clonality can be determined by G6PD isoforms (or androgen receptor isoforms). –> ratio of A:B G6PD will not be 1:1 in neoplasia, but will be 1:1 in hyperplasia.

All tumors are monoclonal (benign and malignant)

Clonality of B cells is determined by Ig light chain phenotype (kappa to lambda). Ratio is normally 3:1 .

In infection hyperplasia occurs, and 3:1 ratio stays the same. In neoplasia (i.e. lymphoma) ratio will be changed (i.e. 20:1)

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3
Q

Adenoma

A

Benign tumor of the epithelium w/ glandular differentiation.

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4
Q

Papilloma

A

Benign tumor of the epithelium finger like projections.

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5
Q

Adenocarcinoma

A

Malignant tumor of the epithelium w/ glandular differentiation.

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6
Q

Papillary carcinoma

A

Malignant tumor of the epithelium w/ finger like projections.

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7
Q

Lipoma

A

Benign tumor mesenchyme

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8
Q

Liposarcoma

A

Malignant tumor of mesenchyme

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9
Q

Lymphoma/Leukemia

A

Malignant lymphocyte proliferation (automatically malignant)

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10
Q

Nevus

A

Benign melanocyte tumor (mole)

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11
Q

Melanoma

A

Malignant melanocyte tumor.

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12
Q

Causes of death in adults:

A

1 Cardiovascular disease

  1. Cancer
  2. Cerebrovascular disease
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13
Q

Causes of death in children

A
  1. accidents
  2. cancer
  3. congenital defects
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14
Q

MC cancers in adults (excluding skin)

A
  1. Breast/ Prostate
  2. Lung
  3. CRC
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15
Q

MC cancer killers in adults

A
  1. Lung
  2. Breast/prostate
  3. CRC

Shows principled of early detection –> Can screen for breast, prostate, crc. Not for lung –> thus the jump in mortality.

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16
Q

Cancer progression

A

Begins w/ a single mutated cell

Approximately 30 cell divisions occur before earliest sx arise.

Each division (doubling time) results in increased mutations.

Cancers that don’t produce sx until late in disease will have undergone additional divisions and mutations.

Cancers that are detected late tend to have a poor prognosis (ovarian, pancreatic, lung)

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17
Q

Goal of screening

A

Catch dysplasia before it becomes carcinoma (i.e. pap smear)

Detect carcinoma before clinical sx arise (before additional mutations have occured) (i.e. mammography to catch ductal carcinoma in situ or tumors that are only 1cm (1/2 the size that is clinically found)

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18
Q

Pap smear

A

Detect CIN dysplasia before it becomes carcinoma

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19
Q

Mammography

A
  1. Detect ductal carcinoma in situ before it has had the chance to invade locally
  2. Detect tumors that are smaller (1cm) than can be found clinically (2cm). thus lowering their propensity to metastasize.
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20
Q

PSA and DRE

A

Prostate cancer tends to grow in the posterior and peripheral prostate –> thus is often a clinically silent disease (vs. BPH which grows periurethral causing urinary sx).

Digital Rectal Exam allows for palpation of posterior peripheral prostate.

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21
Q

Hemoccult and colonoscopy.

A

Goal is to remove the adenomas before they progress to carcinoma

Or detect carcinoma before it is clinically symptomatic.

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22
Q

Carcinogens

A

Carcinogens damage cell DNA

Important carcinogens include chemicals, viruses, and radiation.

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23
Q

Aflatoxins

A

Carcinogen derived from Aspergillus which can contaminate stored grains.

Risk for hepatocellular carcinoma (MC cancer in some areas in the world Asia/Africa due to this)

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24
Q

Alkylating agents

A

Side effect of chemotherapy that increases risk for Leukemia/Lymphoma

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25
Alcohol
Squamous cell carcinoma of oropharynx and upper esophagus, pancreatic carcinoma (chronic pancreatitis), and hepatocellular carcinoma (cirrhosis)
26
Arsenic
Squamous cell carcinoma of skin (women in England putting on arsenic to cover up tan) Lung cancer Angiosarcoma in liver
27
Asbestos
Lung cancer Mesothelioma Exposure to asbestos are FAR MORE LIKELY to develop LUNG CANCER than mesothelioma
28
Cigarrette smoke
Carcinoma of oropharynx Esophagus Lung kidney Bladder MC carcinogen worldwide; polycyclic hydrocarbons are particularly carcinogenic.
29
Nitrosamines
Stomach carcinoma (intestinal adenocarcinoma) Found in smoked foods; responsible for high rate of stomach CA in Japan.
30
Napthylamine
Urothelial of carcinoma of bladder. Derived from cig. smoke
31
Vinyl chloride
Angiosarcoma of the liver. Occupational exposure to make PVC for use in pipes.
32
Nickel, chromium, beryllium, of silica
Lung CA Occupational exposure.
33
EBV
Nasopharyngeal carcinoma (chinese male or African child) Burkitt lymphoma CNS lymphoma in AIDS
34
HHV-8
Kaposi Sarcoma 1. Older eastern European males (rx w/ excision) 2. ) AIDS patients (antiretrovirals --> immune system kills tumor) 3. ) Transplant patients (reduce immonsuppression)
35
HBV and HCV
Hepatocellular carcinoma
36
HTLV-1
Adult T cell leukemia/lymphoma
37
HPV (16,18,31,33)
SCC of vulva, vagina, anus, and cervix. Adenocarcinoma of cervix
38
Ionizing radiation (nuclear reactors and radiotherapy)
AML, CML, and papillary carcinoma of the thyroid Generates hydroxyl free radicals
39
Nonionizing radiation (UVB sunlight is MC source)
Basal Cell, SCC, and Melanoma of skin Results in formation of pyrimidine dimers in DNA, which are normally excised by restriction endonuclease (mutated in Xeroderma Pigmentosum!)
40
Systems disrupted by carcinogens
Proto-oncogenes TS genes Regulators of apoptosis
41
Proto-oncogenes
Genes that are essential for cell growth and differentiations Mutations form oncogenes which leads to unregulated cell growth. Categories: 1. ) Growth factors (PDGFB) 2. ) Growth Factor Receptors 3. ) Signal transducers 4. ) Cell cycle regulators
42
Platelet Derived Growth Factor B (PDGFB)
Overexpression due to mutation causing an autocrine loop (PDGF binds to its own PDGFR causing overgrowth of astrocytes). Drives creation of Astrocytoma
43
ERBB2 (HER2/NEU)
Epidermal growth factor receptor Causes Amplification of normal signal --> increased cell growth Subset of breast cancers Treatable with Trastuzumab.
44
RET
Neural Growth Factor Receptor Point mutation MEN 2A; MEN 2B and sporadic medullary carcinoma of thyroid. (test if concerned of MEN --> prophylactic removal of thyroid)
45
KIT
Stem cell growth factor receptor Point mutation Gastrointestinal stromal tumor (GIST) Can treat w/ Imatinib
46
RAS gene family
Signal transducer *GTP-binding protein Point mutation --> GAP (GTPase Associated Protein) mutation --> RAS doesn't shut itself off --> uncontrolled growth Carcinomas, melanoma, and lymphoma Mutated in 70% of cancers
47
ABL
Signal Transducer Tyrosine kinase t(9:22) with BCR --> BCR:ABL aka Philadelphia chromosome CML and some types of AML (poor prognosis AML)
48
c-MYC
Nuclear regulator Transcription factor t(8;14) involving IgH causes Burkitt's lymphoma (massive overproduction of MYC due to being translocated onto IgH which is constitually on) Massive cell ovegrowth --> Burkitt's lymphoma --> Starry Sky --> White is
49
N-MYC
Nuclear regulator Transcription factor Amplification Neuroblastoma (N-myc = Neuroblastoma)
50
L-MYC
Nuclear regulator Trascription factor Amplification Small cell carcinoma of the Lung (L-myc = Lung)
51
CCND1 (Cyclin D1)
Cell cycle regulator Cyclin (key regulator of G1 --> S phase). t(11;14) --> Mantle Cell (region next to the follicle) Lymphoma. Translocation of cyclin D(11) to IgH (14) (which is constituitively active)
52
CDK4
Cell Cycle Regulator Amplification of Cyclin Dependent Kinase (CDK4). Causes Melanoma
53
p53
Regulates cell cycle progression from G1-->S. Monitors for DNA damage and can signal DNA repair or apoptosis (via BAX destroying Bcl-2) Both copies of p53 must be knocked out for tumor formation (two brakes) Loss is seen in >50% of cancer Germline mutation in Li-Fraumeni sydrome; increased risk for multiple carcinomas and sarcomas
54
RB
RB binds E2F. If RB is phosphorylated by Cyclin D/CDK4 it releases E2F allowing E2F to facilitate G1 to S. If mutated E2F constituitively active. Rb mutation results in constituitvely free E2F and uncontrolled G1-->S progression. Sporadic mutation - unilateral retinoblastoma Germline mutation (familial) - bilateral RB and osteosarcoma Need two hits!
55
Bcl2
Normally stabilized mitochondrial membrane blocking release of cytochrome C Disruption of Bcl2 allows cytochrome c to leave mitochondria and activate apoptosis Overexpressed in follicular lymphoma t(14:18) moves Bcl2 (18) to IgH (14); results in increased Bcl2 Need B-cell apoptosis in follicle where somatic hypermuation is occuring.
56
Telomerase
Normally telomeres shorten w/ serial cell divisions resulting in senescence Cancers have upregulated telomerase --> preserves telomeres.
57
Angiogenesis
FGF and VEGF are commonly produced by tumor cells to supply needed nutrients
58
Avoiding immune surveillance
Tumor cells can evade immune surveillance by downregulation of expression of MHC I. Immunodeficiency (primary and secondary) increases the risk for cancer.
59
Characteristics of Progression of Malignant Neoplasia and Metastasis
Downregulation of E-cadherin --> cadherins normally keep cells attached to each other. Tumor cells attach to laminin and destroy BM (collegniase type IV) Attaches to fibronecting --> spreads locally. Gains access into vascular/lymphatic space.
60
Lymphatic spread
Characteristic of carcinomas. Intitial spread is to regional draining lymph nodes (sentinel node)
61
Hematogenous spread
Characteristic of sarcomas and some carcinomas ``` Exceptions: Renal Cell carcinoma (renal vein) Hepatocellular carcinoma (hepatic vein) Follicular carcinoma of Thyroid Choriocarcinoma (malignancy of trophoblasts --> cells programmed to find vasculature) ```
62
Seeding of body cavities
Characteristic of ovarian carcinoma Results in "caking" of omentum
63
Benign tumor clinical features
Slow growing Well circumscribed Distinct Mobile (can move it upon palpation) Biopsy or excision is required for confirmation
64
Malignant tumors clinical features
Rapid growing Poorly circumscribed Infiltrative (i.e. nerve involvement) Fixed to surrounding structures. Biopsy or excision is required for confirmation
65
Benign tumor histologic features
Well differentiated Organized growth Uniform Nuclei Low nuclear to cytoplasmic ratio Minimal mitotic activity Lack of invasion No metastatic potential
66
Malignant tumors histologic features
Poorly differentiated Disorganized growth Nuclera pleomorphism w/ hyperchromasia High nuclear to cytoplasmic ratio High mitotic activity Invavsion
67
The absolute distinction between benign and malignant?
Ability to metastasize = malignant.
68
Immunohistochemistry
Used to characterize malignant tumors that are difficult to classify. Add antibodies and brown stains for specific cell types.
69
Keratin Positive
Carcinoma (Malignant epithelium)
70
Vimentin Positive
Sarcoma (Malignant mesenchyme)
71
Desmin positive
Muscle
72
GFAP positive
Neuroglia
73
Neurofilament positive
Neurons
74
PSA positive
Prostatic eptihelium
75
Estrogen Receptor positive
Breast epithelium
76
Thyroglobulin positive
Thyroid follicular cells
77
Chromogranin positive
**Neuroendocrine cells (i.e. small cell CA of lung and carcinoid tumors)
78
S-100 positive
Melanoma
79
Serum tumor markers
Proteins released by the tumor that can be useful as: 1. ) Screening (PSA) 2. ) Monitoring response to treatment (PSA CA-19) 3. ) Monitoring for recurrence (prostate cancer w/ bone pain after remission --> PSA elevated) Elevated levels require tissue biopsy for dx of carcinoma because other things can elevate tumor marker.
80
Grading of cancer
Microscopic assessment of differentiation Takes into account architectural and nuclear features. Well differentiated: resembles parent tissue (good prognosis) Poorly differentiated: does not resemble parent tissue.(poor prognosis) Important for determining prognosis
81
Staging of cancer
Key prognostic factor (more important than grading) Determined after final resection of tumor. Uses TNM system T - tumor size (solid organs) or depth (hollow organs) N - Spread to regional lymph nodes; second most important prognostic factor* M- Metastasis; MOST IMPORTANT PROGNOSTIC FACTOR**

USMLE Step I Pathology (14 decks)

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