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Physiology & Pathology > Basic Pathological Mechanisms April 27-May 1 > Flashcards

Basic Pathological Mechanisms April 27-May 1 Flashcards

1
Q

Define neoplasm.

Define tumor.

A

new growth (indicates autonomy with a loss of response to growth control)

tumor = swelling

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2
Q

What are the predominant female cancers? male?

A

breast and thyroid

esophagus and pancreas

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3
Q

Which cancer types show increased incidence during childhood?

A

Rb and Wilm’s

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4
Q

What disorders predispose to cancer?

A

liver cirrhosis, Barret’s esophagus, and liver hepatitis

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5
Q

Define neoplasm.

What are basic components of a neoplasm?

A

an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of normal tissue and persists after cessation of stimuli which evoked the change.

parenchymal tissue, supportive stroma: made up of connective tissue, blood vessels, and variable numbers of cells of the adaptive and innate immune system (desmoplasia- hyalinization)

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6
Q

How can neoplasms be classified?

A

by embryonic origin, by biological activity (benign v. malignant), cellular features, and differentiation status (grading)

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7
Q

What is the cell or tissue of origin for mesenchymal tumors (sarcomas)?

A

fibroblast, fat, blood vessels, smooth muscle cell, striated muscle cell, cartilage, and bone

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8
Q

What is the cell or tissue of origin for epithelial tumors (carcinomas)?

A

squamous, transitional, glandular epithelium; neuroendocrine cells (specifically liver and kidney)

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9
Q

What is the embryonic origin of blastomas? teratomas? choristomas? hemartoma? papilloma?

A

embryonic primordial tissue; mixed tumors (from all three germ layers; must have at least two); nest of normal tissue in another location; deranged tissue in a normal location; epithelium

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10
Q

What is a feature of squamous cell carcinomas? adenocarcinomas?

A

keratin; mucin (PAS-Alcian blue stain)

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11
Q

What are polyps? papillomas?

A

are benign or malignant neoplasm(s) that produces macroscopically visible projection(s) above a mucosal surface

are benign epithelial neoplasms producing macroscopically or microscopicially visible fingerlike or warty projection(s) from an epithelial surface

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12
Q

T/F: all leukemias are malignant?

A

T

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13
Q

What are uses of IHC in cancer biology?

A

categorization of intermediate filament proteins; classification of hematopoeitic malignancies (with flow cytometry); for diagnosis of metastatic lesions; for assessment of biomarkers

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14
Q

What are the intermediate filament proteins and what type of tissue are they found in?

A

cytokeratins (epithelial); GFAP (astrocytes); desmin (muscle); vimentin (mesenchymal)

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15
Q

What are the biomarkers discussed in lecture?

A

estrogen receptor (breast cancer), alpha fetoprotein (hepatocellular carcinoma)

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16
Q

Describe benign neoplasms.

A

slow, expansive growth (no metastases); smooth surface, capsular, without necrosis and hemorrhage; resembles tissue of origin, with well differentiated cells (few mitotic events and nuclei or normal size and shape)

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17
Q

Describe malignant neoplasms.

A

fast, invasive growth (with metastases); irregular (not encapsulated and evidence of both necrosis and hemorrhage); does not resemble tissue of origin with poorly differentiated cells (many irregular mitotic events and pleomorphic nuclei)

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18
Q

What are examples of benign neoplasms?

A

lipoma, adenoma, fibroma, hemangioma, polyps, papillomas, hemartomas, and choristomas

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19
Q

What are examples of malignant neoplasms?

A

carcinoma (adenocarcinoma, squamous cell carcinoma), sarcoma (liposarcoma, fibrosarcoma, and angiosarcoma), and teratomas

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20
Q

T/F: teratomas may contain nerve, hair, and teeth?

A

T

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21
Q

Describe generalized grading scheme of neoplasms.

A

Grade 1: well differentiated
Grade 2: moderately differentiated
Grade 3: poorly differentiated
Grade 4: nearly anaplastic?

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22
Q

What are methods of metastasis?

A

seeding of body cavities; lymphatic spread (carcinomas); hematogenous spread (sarcomas)

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23
Q

T/F: angiogenesis equates to good prognosis?

A

F

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24
Q

What is cachexia? How is it correlate to cancer?

A

progressive weakness, loss of appetite, anemia, and profound weight loss (equal loss of both fat and lean muscle);

often correlates with tumor size or extent of metastases

etiology includes generalized increase in tumor metabolism and central effects of tumor on hypothalamus (IL-1, IL-6, and TNFalpha)

evidence of systemic inflammation as seen by an increase in acute phase reactants

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25
Q

What are paraneoplastic syndromes?

A

Cushing’s (ACTH), hypercalcemia (PTH-like polypeptide), polycythemia (EPO), venous thrombosis (thromboplastin)
Lambert-Eaton syndrome (antibodies to NMJ; cross-reaction with tumor associated antigens), Myasthenia gravis (antibodies to NMJ)

ECTOPIC HORMONE PRODUCTION

26
Q

What is the suffix given to benign lesions?

A

In general, benign tumors are designated by attaching the suffix -oma to the name of the cell type from which the tumor originates.

27
Q

Describe papillomas.

A

Benign epithelial neoplasms producing microscopically or macroscopically visible fingerlike or warty projections from epithelial surfaces are referred to as papillomas

28
Q

Describe polyps.

A

When a neoplasm—benign or malignant—produces a macroscopically visible projection above a mucosal surface and projects, for example, into the gastric or colonic lumen, it is termed a polyp

29
Q

What is the most common pathway for initial dissemination of carcinomas?

A

transport through lymphatics

also mode of transport for sarcoma

30
Q

What organs are involved in hematogenous dissemination?

A

liver and lungs

31
Q

Can leiomyomas progress to leiomyosarcoma?

A

No

32
Q

Describe the metastatic cascade.

A

clonal expansion, growth, diversification, and angiogenesis (bulk of tumor); metastatic subclone arises followed by adhesion to and invasion of the basement membrane (subsequent passage through the ECM); intravasation, interaction with host lymphoid cells, and generation of tumor cell embolus (bound to platelets); adhesion to basement membrane, extravasation, and deposition of the cells (followed by angiogenesis and growth)

33
Q

T/F: any tumor, even a benign one, may cause morbidity and mortality?

A

T; location is a critical determinant of the clinical effects

34
Q

Can benign or malignant tumors produce hormones?

A

Yes (more typical of benign lesions)

35
Q

Describe cancer stating methodology.

A

The staging of solid cancers is based on the size of the primary lesion, its extent of spread to regional lymph nodes, and the presence or absence of blood-borne metastases.

36
Q

What are epidemiological trends in cancer?

A

incidence of most cancers is going down (particularly stomach cancer); exception is lung cancer

37
Q

Describe sarcomas.

A

fleshy, mesodermal origin, associated with lots of connective tissue;

spindly morphology

38
Q

How is dysplasia represented?

A

incidence of pleomorphic cells

39
Q

What is a carcinogen?

A

an agent whose administration to previously untreated animals leads to a statistically significant increased incidence of malignant neoplasms as compared with that in appropriate untreated control animals

chemicals, radian energy (sunlight and ionizing radiation), and viruses (or microbes)

40
Q

What are chemical carcinogens?

A

polycyclic hydrocarbons (common in fossil fuels and smoked meats)

electrophilic intermediates (following metabolic activation)

41
Q

What are features of most carcinogens?

A

are not species specific

are organ specific

need metabolic activation

42
Q

What are genetic predispositions to cancer?

A

autosomal dominant inherited cancer syndromes (point mutation of a tumor suppressor gene; example: Rb)

defective DNA repair syndromes (autosomal recessive; example: ataxia-telangiectasia)

familial cancers (multiple low penetrance genes; example: BRCA1/BRCA2)

43
Q

T/F: Cancers usually result from a series of mutations in a single cell?

A

T (generally a mutation in tumor suppressor, followed by an oncogene mutation, and subsequent tumor suppressor mutations)

44
Q

Are gain of function mutations singular events? loss of function?

A

Yes

loss of one copy reduces activity but loss of both alleles eliminates the tumor suppressor gene

45
Q

What are functions of proto-oncogenes?

A

signal transduction, cell cycle regulation, and cell differentiation (growth factors, growth factor receptors, and transcription factors)

46
Q

T/F: mutations convert proto-oncogenes into oncogenes?

A

T (self-sufficient cell growth)

47
Q

What was the first oncogene identified?

A

src from retrovirus

48
Q

What are properties of transformed cells in culture?

A

altered morphology, loss of contact inhibition, ability to grow without attachment to solid substrate, immortilization, reduced requirement for mitogenic growth factors, increased transport of glucose, and tumorigenicty

49
Q

How can retroviruses transform?

A

insertional mutagenesis

50
Q

How are oncogenes discovered?

A

shotgun cloning (generation of a focus of transformed cells and transplantation into immunocompromised mice

51
Q

T/F: oncogenes are loss of function mutations?

A

F

52
Q

Describe the autocrine loop. Give examples

A

Cancer Cells acquire the ability to synthesize growth factors to which they are responsive

PDGF, TGFalpha

not sufficient for transformation

53
Q

How do growth factor receptors become oncogenic? Examples?

A

are constitutively activated (dimerization) by mutations, translocations, or overexpression (or deletion of extracellular domain)

MEN2A and MEN2B

54
Q

Describe HER2/neu

A

cell surface receptor protein (class of EGF receptor)

no known ligands (forms heterodimers with EGFR)

overexpressed in breast cancer (worst prognosis)

treated with trastuzumab or Tarceva

55
Q

What is the most important mutated signal transducing proteins?

A

RAS (3 genes)

small GTPase (downstream: MAPK)

mutations that destroy GTPase activity or prevent GAP binding

56
Q

How are GTPases activated? inactivated?

A

guanine nucleotide exchange factor

GTPase activating protein (NF-1)

57
Q

What transcription factors are oncoproteins?

A

myc, myb, jun, fos, and rel

58
Q

Describe myc

A

thought to activate genes involved in proliferation

target genes: cyclin D2

other activities: histone acetylation, decreased cell adhesion, and increased protein synthesis

part of iPS cocktail

can be overexpressed, dysregulated by translocation (Burkitts), or amplification

very poor prognosis

59
Q

What is the Philadelphia chromosome?

A

brc/abl fusion in CML and ALL

Gleevec (Imatinib)

60
Q

Describe oncogene addiction.

A

Cancer cells may rely more heavily on certain oncogenic mutations than others for their growth, proliferation, and survival

examples: Her-2/neu, Kras, beta catenin, and cyclin D1

61
Q

Describe oncometabolites.

A

Mutations in the enzyme cytosolic isocitrate dehydrogenase (IDH1) are common in brain cancer

reduction of a-ketoglutarate to R(-)2-hydroxyglutarate (2HG) (normally converts isocitrate to alpha ketoglutarate)

Physiology & Pathology (40 decks)

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