Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

Principles of Neoplasia (Pathoma) Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

Basic Principles of Neoplasia

A

Unregulated, irreversible, and monoclonal.

Distinct from hyperplasia and repair.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Adenoma

A

Benign tumor of the epithelium w/ glandular differentiation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Papilloma

A

Benign tumor of the epithelium finger like projections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Adenocarcinoma

A

Malignant tumor of the epithelium w/ glandular differentiation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Papillary carcinoma

A

Malignant tumor of the epithelium w/ finger like projections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lipoma

A

Benign tumor mesenchyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Liposarcoma

A

Malignant tumor of mesenchyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Lymphoma/Leukemia

A

Malignant lymphocyte proliferation (automatically malignant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Nevus

A

Benign melanocyte tumor (mole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Melanoma

A

Malignant melanocyte tumor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Causes of death in adults:

A

1 Cardiovascular disease

  1. Cancer
  2. Cerebrovascular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of death in children

A
  1. accidents
  2. cancer
  3. congenital defects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

MC cancers in adults (excluding skin)

A
  1. Breast/ Prostate
  2. Lung
  3. CRC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pap smear

A

Detect CIN dysplasia before it becomes carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Carcinogens

A

Carcinogens damage cell DNA

Important carcinogens include chemicals, viruses, and radiation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Alkylating agents

A

Side effect of chemotherapy that increases risk for Leukemia/Lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Alcohol

A

Squamous cell carcinoma of oropharynx and upper esophagus, pancreatic carcinoma (chronic pancreatitis), and hepatocellular carcinoma (cirrhosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Arsenic

A

Squamous cell carcinoma of skin (women in England putting on arsenic to cover up tan)

Lung cancer

Angiosarcoma in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Asbestos

A

Lung cancer

Mesothelioma

Exposure to asbestos are FAR MORE LIKELY to develop LUNG CANCER than mesothelioma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Cigarrette smoke

A

Carcinoma of oropharynx

Esophagus

Lung

kidney

Bladder

MC carcinogen worldwide; polycyclic hydrocarbons are particularly carcinogenic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Nitrosamines

A

Stomach carcinoma (intestinal adenocarcinoma)

Found in smoked foods; responsible for high rate of stomach CA in Japan.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Napthylamine

A

Urothelial of carcinoma of bladder.

Derived from cig. smoke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Vinyl chloride

A

Angiosarcoma of the liver.

Occupational exposure to make PVC for use in pipes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Nickel, chromium, beryllium, of silica

A

Lung CA

Occupational exposure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

EBV

A

Nasopharyngeal carcinoma (chinese male or African child)

Burkitt lymphoma

CNS lymphoma in AIDS

34
Q

HHV-8

A

Kaposi Sarcoma

  1. Older eastern European males (rx w/ excision)
  2. ) AIDS patients (antiretrovirals –> immune system kills tumor)
  3. ) Transplant patients (reduce immonsuppression)
35
Q

HBV and HCV

A

Hepatocellular carcinoma

36
Q

HTLV-1

A

Adult T cell leukemia/lymphoma

37
Q

HPV (16,18,31,33)

A

SCC of vulva, vagina, anus, and cervix.

Adenocarcinoma of cervix

38
Q

Ionizing radiation (nuclear reactors and radiotherapy)

A

AML, CML, and papillary carcinoma of the thyroid

Generates hydroxyl free radicals

39
Q

Nonionizing radiation (UVB sunlight is MC source)

A

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
Q

Systems disrupted by carcinogens

A

Proto-oncogenes

TS genes

Regulators of apoptosis

41
Q

Proto-oncogenes

A

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
Q

Platelet Derived Growth Factor B (PDGFB)

A

Overexpression due to mutation causing an autocrine loop (PDGF binds to its own PDGFR causing overgrowth of astrocytes).

Drives creation of Astrocytoma

43
Q

ERBB2 (HER2/NEU)

A

Epidermal growth factor receptor

Causes Amplification of normal signal –> increased cell growth

Subset of breast cancers

Treatable with Trastuzumab.

44
Q

RET

A

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
Q

KIT

A

Stem cell growth factor receptor

Point mutation

Gastrointestinal stromal tumor (GIST)

Can treat w/ Imatinib

46
Q

RAS gene family

A

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
Q

ABL

A

Signal Transducer

Tyrosine kinase

t(9:22) with BCR –> BCR:ABL aka Philadelphia chromosome

CML and some types of AML (poor prognosis AML)

48
Q

c-MYC

A

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
Q

N-MYC

A

Nuclear regulator

Transcription factor

Amplification

Neuroblastoma (N-myc = Neuroblastoma)

50
Q

L-MYC

A

Nuclear regulator

Trascription factor

Amplification

Small cell carcinoma of the Lung (L-myc = Lung)

51
Q

CCND1 (Cyclin D1)

A

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
Q

CDK4

A

Cell Cycle Regulator

Amplification of Cyclin Dependent Kinase (CDK4).

Causes Melanoma

53
Q

p53

A

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
Q

RB

A

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
Q

Bcl2

A

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
Q

Telomerase

A

Normally telomeres shorten w/ serial cell divisions resulting in senescence

Cancers have upregulated telomerase –> preserves telomeres.

57
Q

Angiogenesis

A

FGF and VEGF are commonly produced by tumor cells to supply needed nutrients

58
Q

Avoiding immune surveillance

A

Tumor cells can evade immune surveillance by downregulation of expression of MHC I.

Immunodeficiency (primary and secondary) increases the risk for cancer.

59
Q

Characteristics of Progression of Malignant Neoplasia and Metastasis

A

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
Q

Lymphatic spread

A

Characteristic of carcinomas.

Intitial spread is to regional draining lymph nodes (sentinel node)

61
Q

Hematogenous spread

A

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
Q

Seeding of body cavities

A

Characteristic of ovarian carcinoma

Results in “caking” of omentum

63
Q

Benign tumor clinical features

A

Slow growing

Well circumscribed

Distinct

Mobile (can move it upon palpation)

Biopsy or excision is required for confirmation

64
Q

Malignant tumors clinical features

A

Rapid growing

Poorly circumscribed

Infiltrative (i.e. nerve involvement)

Fixed to surrounding structures.

Biopsy or excision is required for confirmation

65
Q

Benign tumor histologic features

A

Well differentiated

Organized growth

Uniform Nuclei

Low nuclear to cytoplasmic ratio

Minimal mitotic activity

Lack of invasion

No metastatic potential

66
Q

Malignant tumors histologic features

A

Poorly differentiated

Disorganized growth

Nuclera pleomorphism w/ hyperchromasia

High nuclear to cytoplasmic ratio

High mitotic activity

Invavsion

67
Q

The absolute distinction between benign and malignant?

A

Ability to metastasize = malignant.

68
Q

Immunohistochemistry

A

Used to characterize malignant tumors that are difficult to classify.

Add antibodies and brown stains for specific cell types.

69
Q

Keratin Positive

A

Carcinoma (Malignant epithelium)

70
Q

Vimentin Positive

A

Sarcoma (Malignant mesenchyme)

71
Q

Desmin positive

A

Muscle

72
Q

GFAP positive

A

Neuroglia

73
Q

Neurofilament positive

A

Neurons

74
Q

PSA positive

A

Prostatic eptihelium

75
Q

Estrogen Receptor positive

A

Breast epithelium

76
Q

Thyroglobulin positive

A

Thyroid follicular cells

77
Q

Chromogranin positive

A

**Neuroendocrine cells (i.e. small cell CA of lung and carcinoid tumors)

78
Q

S-100 positive

A

Melanoma

79
Q

Serum tumor markers

A

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
Q

Grading of cancer

A

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
Q

Staging of cancer

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions