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Pathophysiology I > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

tumor also known as

A

neoplasm

new growth/swelling

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2
Q

what did galen do? 167 AD

A

natural-pregnant uterus
unnatural-pus, bone callus
contrary to nature-neoplasms

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3
Q

what are tumors?

A

attempt by body (under a stimulus) to make a new, useless organ

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4
Q

what do tumor cells arise from?

A

a single cell

  • usually due to mutation
  • can also be due to chromosomal abnormalities
  • wrong shape, wrong place, etc.
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5
Q

tumors similarities to normal

A
  • functional (parenchyma) and supporting (stroma) tissues
  • cells look similar (usually) to those of organ in which tumor arose
  • cells continue to perform some same functions
  • cells continue to produce some same proteins
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6
Q

tumors differences from normal

A
  • don’t contribute to maintenance of homeostasis
  • grow more rapidly (usually) than surrounding normal origin
  • some benign and all malignant tumors never stop growing
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7
Q

what types of cells are tumors?

A

overgrowths of cells bearing cumulative genetic injuries

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8
Q

Nowell’s law

A

each mutation confers a growth advantage over the neighbors

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9
Q

what are tumors a failure of?

A

division control
senescence (immortalization)
proper apoptosis (cell suicide)
(at least some of these have already gone bad in the seemingly-normal cells from which tumors arise)

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10
Q

what is the great acquired genetic disease of humans?

A

cancer

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11
Q

benign tumors characteristics

A
  • cells resemble normal cells and tumor architecture resembles parent organ
  • usually spherical (grossly) and compress surrounding tissues
  • have a surrounding capsule
  • grow slowly
  • never metastasize
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12
Q

malignant tumors characteristics

A

-cells differ from normal and tumor architecture disorganized
-tumor bears tendrils (crab claws) and grows into surrounding tissue
-grow more rapidly than benign
-will eventually metastasize (some exceptions)
malignant=cancer

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13
Q

what gives a tumor its name?

A

cell of origin

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14
Q

differentiation

A

degree of resemblance to normal cell counterpart

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15
Q

examples of differentiation terms

A

well, moderate, poorly

basis for “grading” malignant tumors

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16
Q

what are cancers of epithelium called?

A

carcinomas

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17
Q

what are cancers of mesenchyme called?

A

sarcomas

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18
Q

anaplasia

A

ugly cells, a marker for cancer or “pre-cancer”

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19
Q

dysplasia

A

ugly cells in epithelium with no invasion

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20
Q

other terms for dysplasia

A

carcinoma in-situ
intraepithelial neoplasia
pre-cancer
intraepithelial lesion

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21
Q

where do squamous carcinomas arise?

A

where stratified squamous is normal or metaplastic

  • skin, esophagus, mouth, anal canal, others
  • cervix, bronchi
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22
Q

what do pathologists see in squamous carcinomas?

A
  • keratin
  • pearls (little hairs)
  • desmosomes (intracellular junctions)
  • single-cell apoptosis (cells think they’re at the top of the epidermis)
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23
Q

where do adenocarcinomas arise?

A

anywhere there are glands, even single-cell glands

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24
Q

what are the most common cancers?

A

adenocarcinomas

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25
Q

what do pathologists see in adenocarcinomas?

A

-lumens (intercellular, intracellular)
-“glands within glands” or even “glands inside-out” glands (“papillary growth)
-mucin (intercellular or intracellular “lakes)
-other secretory products, depending on gland of origin
-cells sticking to one another
-signet-ring cells (distended with a product), alone or in clusters
microvilli

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26
Q

adenomas

A

many features of adenocarcinomas but appear benign
no invasion
often functional

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27
Q

can adenomas show dysplasia?

A

yes without invasion

pre-malignant

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28
Q

appearance of benign tumors

A

typically spherical

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29
Q

appearance of malignant tumors

A

exophytic-“lump” with a cauliflower-like surface
endophytic-appears as an ulcer
infiltrating-diffuse spread through organ without change in shape
often will have areas of hemorrhage and necrosis

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30
Q

exophytic

A

“lump” with a cauliflower-like surface

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31
Q

endophytic

A

appears as an ulcer

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32
Q

infiltrating

A

diffuse spread through organ without change in shape

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33
Q

why do malignant tumors have areas of hemorrhage and necrosis?

A

tumor invades its own blood supply

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34
Q

malignant tumors-potential for metastasis

A

spread of malignant tumor cells to distant sites

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35
Q

four routes of metastasis

A

carcinomas-typically spread via lymphatics
sarcomas-typically spread via blood vessels
seeding of serosal surfaces from pleural or peritoneal fluids
mechanical transplantation (rare, typically iatrogenic)

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36
Q

where do certain cancers go?

A

certain cancers have unexplained predilection for certain metastatic sites

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37
Q

common sites of metastasis

A

lymph nodes, liver, bone, brain

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38
Q

grading and staging

A

used to determine prognosis and treatment

both usually represented by roman numerals (I=good; III, IV, V=bad)

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39
Q

grading

A

done by pathologists
requires tissue
reflects degree of differentiation (similarity to normal organ)

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40
Q

staging

A

done by clinicians
reflects size and extent of tumor spread
elaborate systems for each tumor type

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41
Q

TNM staging

A

T for tumor
N for regional lymph nodes
M for metastases

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42
Q

what determines stage?

A

TNM combination

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43
Q

what suffix for tumors?

A

end in -oma

non-neoplasms also: hematoma, granuloma, gossypiboma, etc.

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44
Q

what do you add to a tumor name if malignant?

A

add carcin if epithelial
add sarc if mesenchymal
if benign, add nothing (just oma no middle)

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45
Q

additional roots

A

describe cell of origin

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46
Q

what to add to name for glandular epithelium

A

add adeno-

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47
Q

squamous or transitional epithelium and benign

A

add papill-

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48
Q

non-glandular epithelium and malignant, what do you add to the tumor name?

A

cell of origin

ex. basal cell carcinoma, squamous cell carcinoma, renal cell carcinoma, choriocarcinoma

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49
Q

additional roots to describe cell of origin non-epithelial examples

A 
fibr-fibroblasts
chondr-cartilage
oste-osteoblasts
lip-fat
leiomy-smooth muscle
rhabdomy-striated muscle
hemangi-blood vessels
lymphangi-lymphatics
mesotheil-mesothelium
meningi-arachnoid granulation
lymph-lymphocytes
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50
Q

malignant tumor with “benign” names

A 
lymphoma
leukemia
melanoma
hepatoma (now hepatocellular carcinoma)
pheochromocytoma (adrenal medulla)
mesothelioma
myeloma ("multiple", plasma cell)
astrocytoma
glioma
ependymoma
seminoma
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51
Q

tumors or unknown (or used to be) origin have eponyms

A

Hodgkin’s disease
Ewing’s sarcoma
Wilm’s tumor

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52
Q

non-tumors

A

hamartoma-tissue in right location but in wrong proportions

choristoma-tissue in right proportion but in wrong location

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53
Q

hamartoma

A

tissue in right location but in wrong proportions

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54
Q

choristoma

A

tissue in right proportion bu t in wrong location

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55
Q

what causes cancer?

A 
multiple genetic injuries conferring growth advantages
clones within clones within clones
less subject to growth controls
learn how to do things they shouldn't
grow faster than die off
carcinogenesis
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56
Q

things cancer cells learn to do but shouldn’t

A

invade basement membrane

induce own blood supply

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57
Q

carcinogenesis

A

events leading up to malignant phenotype

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58
Q

karyotype changes

A

many cancers have hallmark chromosomal abnormalities

“genetic fingerprint”

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59
Q

t (9;22)

A

chronic myelogenous leukemia

Philadelphia chromosome

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60
Q

t(8, 14)

A

Burkitt’s lymphoma

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61
Q

del 3p

A

renal cell carcinoma (VHL) and almost all lung cancers

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62
Q

del 13q

A

retinoblastoma (Rb)

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63
Q

del 11p

A

Wilms tumor (WT1)

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64
Q

monosomy 22

A

meningioma (NF-2)

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65
Q

chemical carcinogenesis-initiator

A

induces genetic damage but not phenotype (yet)
mutagen “genotoxic carcinogen”
avoid these as much as possible

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66
Q

chemical carcinogenesis-promotor

A 
causes initiated cells to become tumors
only "work" after initiation
stimulate cell division, promote Nowell's law
"non-genotoxic carcinogen"
lots of common substances
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67
Q

which carcinogens are genotoxic?

A

initiators

avoid these

68
Q

complete carcinogen

A

acts as both initiator and promoter

69
Q

chemical carcinogens-scoot

A

scrotal cancer “chimney sweep’s cancer”

70
Q

chemical carcinogens-chemotherapy

A

acute leukemias (promoters)

71
Q

chemical carcinogens-polycyclic hydrocarbons (stuff in tobacco smoke)

A

lung, larynx, mouth, throat, esophagus, pancreas, bladder, kidney

72
Q

chemical carcinogens-aflatoxin (moldy grain and peanuts)

A

hepatocellular carcinoma

COMPLETE CARCINOGEN

73
Q

chemical carcinogens-asbestos

A

lung cancer, mesothelioma

74
Q

chemical carcinogens-estrogen

A

endometrial carcinoma, post-menopausal breast cancer (maybe, current thinking increases probability)

75
Q

what if you are asked “does substance X cause cancer?”?

A

you have to do the research

approach same way as “does a drug work?”

76
Q

radiation carcinogenesis

A

induces breaks in DNA

-direct or free radical formation

77
Q

what types of radiation cause radiation carcinogenesis?

A

ultraviolet and ionizing

78
Q

carcinogenesis-ultraviolet radiation

A

most skin cancers

79
Q

carcinogenesis-ionizing radiation

A

remember leukemias

80
Q

occupations more susceptible to radiation carcinogenesis

A

radiologists

uranium miners

81
Q

what patient population is at risk for radiation carcinogenesis?

A

patients receiving therapeutic radiation

82
Q

viral carcinogenesis

A

important in a few human cancers

83
Q

viral carcinogenesis-HPV (certain strains)

A

benign warts, cancer of cervix, vulva, penis

-viral proteins inactivate tumor-suppressor proteins

84
Q

viral carcinogens-epstein-barr

A

Burkitt’s lymphoma

85
Q

viral carcinogenesis-hep b and c

A

promotors for hepatocellular carcinoma

86
Q

are common human cancers caused by viral carcinogenesis contagious?

A

no

87
Q

what can predispose to squamous cell carcinoma?

A

bad or repetitive skin trauma

Marjolin’s ulcer

88
Q

proto-oncogenes (mitogenes)

A
  • essential genes that govern normal tissue growth, differentiation and apoptosis
  • hormone or vitamin receptors or their signal transduction pathways
  • general cell “turn-ons”
  • roughly 200 known
89
Q

oncogenes

A

mutated (“activated”) proto-oncogenes that help transform a benign cell into a cancer cell

90
Q

oncogenes-mechanisms of activation

A

point mutation
translocation
amplification
receptor tyrosine kinases

91
Q

oncogenes MOA point mutation

A

gene product is stuck on the “on” position (“gain of function”)

92
Q

oncogenes MOA translocation

A 
gene product is under control of the wrong promoter
fusion gene (half-one gene, half-another) produces a fusion gene product that promotes cell division
93
Q

oncogenes MOA amplification

A

too many copies of the gene

94
Q

oncogenes-receptor tyrosine kinases

A

epidermal growth factor receptor family

  • erbB-squamous cell cancers
  • HER2-adenocarcinomas (especially breast)
  • RET-endocrine tumors (remember MEN IIa and IIb), mucosal neuromas
95
Q

what was the first inherited oncogene discovered?

A

RET-endocrine tumors (MEN IIa and IIb), mucosal neuromas

96
Q

oncogenes-cytoplasmic tyrosine kinases

A

c-abl-translocated from 9 to 22 (Philadelphia chromosome) in CML and other leukemias

97
Q

what is MEN?

A

multiple endocrine neoplasias

98
Q

oncogenes-g proteins

A

ras family-involved in initiation of mitosis
characteristic point mutations at codons for AA
loss of GTPase activity-stuck in “on” position-keep dividing
mutations found in large proportion of human cancers (pancreatic, others)

99
Q

ras family

A

involved in initiation of mitosis

100
Q

oncogenes-DNA binding proteins

A

myc family-involved in DNA synthesis
amplification and/or translocation
c-myc translocated from 8 to 14 in Burkitt’s lymphoma (next to an immunoglobulin gene)
amplified in oat cell lung carcinomas

101
Q

myc family

A

involved in DNA synthesis

102
Q

what are tumor suppressor genes also known as?

A

anti-oncogenes

103
Q

what do tumor-suppressor genes do?

A

prevent cells from overgrowing, even with activated oncogenes

104
Q

what must happen for tumor suppressor genes to lose effect?

A

both alleles must be altered

105
Q

knudson’s “two-hit” law

A

one hit: cell with an increased propensity to turn neoplastic
two hits: tumor cell

106
Q

tumor-suppressor gene deletion syndrome

A 
"tumor-susceptibility syndrome"
mutant allele is inherited
autosomal dominant
all somatic cells carry mutation
greatly increased risk for particular cancer
107
Q

tumor-suppressor genes malignant phenotype

A

2nd allele mutated in cell of origin
autosomal recessive (now 2 bad copies)
OR
both mutations can also occur spontaneously

108
Q

tumor-suppressor genes

retioblastoma

A

RB1-13q14

  • gene product central to regulating cell cycle
  • binds to nuclear proteins
  • DNA tumor viruses bind and inactivate gene product (HPV)
109
Q

what is p53 (TP53)?

A

most common genetic injury in human cancer

110
Q

what does p53 do?

A

gene product binds DNA and prevents mitosis during cell injury

111
Q

what is p53 known as?

A

guardian of the genome

112
Q

what can p53 induce?

A

apoptosis

113
Q

what is p53 mutation linked to?

A

hepatocellular carcinoma

aflatoxin induces p53 mutation

114
Q

what do astrocytomas become with p53 mutation?

A

astrocytomas (low-grade) become glioblastomas (high-grade) with p53 mutation

115
Q

what do benign tumors cause problems by?

A

-compressiong surrounding structures “malignant by location”
-over-secreting a substance (adenomas)-hormones
-existing in multiple places
transformation into malignant tumor

116
Q

are benign tumors lethal?

A

rarely

117
Q

benign tumor problems-malignant by location

A
  • pituitary adenomas crushing the normal gland and optic nerves
  • atrial myxoma blocking blood flow through the heart
  • meningiomas compressing the brain
  • pleomorphic adenoma of the parotid gland encasing the facial nerve
118
Q

benign tumor problems-hormone production

A

pituitary and adrenal adenomas

insulinomas and glucagonomas

119
Q

benign tumor problems-multiple tumors

A

Von Recklinghausen’s neurofibromatosis

classical autosomal defect

120
Q

benign tumor problems-large size

A

100-pound ovarian cystadenomas

121
Q

benign tumor problems-torsion and infarction

A

ovarian tumors

122
Q

malignant tumors-local effects (primary or metastasis)

A
  • brain damage and herniation
  • pulmonary edema
  • bone fractures
  • cytopenias
  • hemorrhage
  • bowel obstruction-
  • pleural effusions and pericardial effusions
123
Q

malignant tumors local effects brain damage and herniation

A

tumors growing inside the brain

124
Q

malignant tumors local effects pulmonary edema

A

cancer blocking pulmonary lymphatics

125
Q

malignant tumors local effects bone fractures

A

cancer metastasis to the bone

126
Q

malignant tumors local effects cytopenias

A

bone marrow replacement by tumor

127
Q

malignant tumors local effects hemorrhage

A

thrombocytopenia and/or vascular invasion

128
Q

malignant tumors local effects bowel obstruction

A

large tumors

129
Q

malignant tumors local effects pleural effusions and pericardial effeusions

A

both quite common

130
Q

paraneoplastic syndromes

A

result from elaboration of substances by tumor

131
Q

examples of paraneoplastic syndromes

A
  • fever
  • cushing’s syndrome
  • masculinization
  • feminization
  • hyponatremia
  • hypokalemia
  • hypercalcemia
  • carcinoid syndrome
  • erythrocytosis
  • hyperviscosity syndrome
  • autoimmune hemolytic anemia
  • eaton-lambert syndrome
  • venous thrombosis
132
Q

paraneoplastic syndrome elaboration fever

A

mostly lymphomas, suspect in “fever of unknown origin”

133
Q

paraneoplastic syndrome elaboration cushing’s syndrome

A

excess cortisol, common adrenal cortical tumors and oat cell carcinoma of lung

134
Q

paraneoplastic syndrome elaboration masculinization

A

common in certain ovarian and adrenal tumors

135
Q

paraneoplastic syndrome elaboration feminization

A

breast development in a male, postmenopausal uterine bleeding; testicular or ovarian tumors

136
Q

paraneoplastic syndrome elaboration hyponatremia

A

oat cell carcinoma, hypersecretion of ADH

137
Q

paraneoplastic syndrome elaboration hypokalemia

A

villous adenoma of the colon, hypersecretion of potassium

138
Q

paraneoplastic syndrome elaboration hypercalcemia

A

bone mets from any tumor or PTH-like substances produces by squamous cell carcinoma of lung

139
Q

paraneoplastic syndrome elaboration carcinoid syndrome (paroxyms of flushing, wheezing and diarrhes)

A

production of serotonin and bradykinin by certain APUDomas

140
Q

paraneoplastic syndrome elaboration erythrocytosis (excessive red cell mass)

A

excessive erythropoietin from renal cell carcinoma

141
Q

paraneoplastic syndrome elaboration hyperviscosity syndrome

A

erythrocytosis or cancers that elaborate IgM, thick blood sludges in the brain

142
Q

paraneoplastic syndrome elaboration autoimmune hemolytic anemia

A

lymphomas

143
Q

paraneoplastic syndrome elaboration eaton-lambert syndrome (NMJ problem like myasthenia gravis)

A

oat cell lung cancer, autoantibody against calcium channels blocks release of acetylcholine

144
Q

paraneoplastic syndrome elaboration venous thrombosis

A

pancreatic cancer (“Trosseau’s other sign”) and many others

145
Q

cancer death examples

A 
pneumonia
sepsis
hemorrhage
pulmonary embolism
paraneoplastic syndromes
iatrogenic
suicide and active euthanasia
146
Q

cancer death-pneumonia

A

most common, multifactorial

  • neutropenia (bone marrow replacement)
  • airway obstruction
  • atelectasis (alveolar collapse)-bedridden, pleural effusions
  • aspiration
  • narcotics
147
Q

cancer death-sepsis (gram-negatives)

A

pneumonia, UTI

remember stercoraceous ulcer from constipation

148
Q

cause of sepsis-stercoraceous ulcer

A

frequently missed-stercoraceous ulcer-pain treated by narcotics, cause constipation, erodes rectal wall, rectal ulcer provides path to bloodstream, frequently avoidable cause of sepsis

149
Q

cancer death-hemorrhage

A

thrombocytopenia

150
Q

cancer death-iatrogenic

A

surgery, radiation, chemotherapy

151
Q

cancer death-pulmonary embolism

A

DVTs lead to pulmonary embolus

152
Q

tumor markers

A

substances produced by tumors, useful in diagnosis or detection of recurrence

153
Q

tumor markers Ig light chains

A

plasma cell (multiple) myeloma

154
Q

tumor markers carcinoembryonic antigen (CEA)

A

various adenocarcinomas; used to detect recurrence of colon cancer
IMPORTANT ONE

155
Q

tumor markers alpha-fetoprotein (AFP)

A

hepatocellular carcinoma

156
Q

tumor markers calcitonin

A

medullary thyroid carcinoma

157
Q

tumor markers prostate-specific antigen (PSA)

A

prostate cancer, only marker used for screening

158
Q

what is the only tumor marker used fo screening?

A

PSA

159
Q

tumor markers CA-125

A

ovarian cancer

160
Q

tumor markers-CA-19-9

A

stomach, colon, especially pancreatic cancer

161
Q

what type of genetic disorders are genetic cancer syndromes?

A

autosomal dominant

162
Q

genetic cancer syndromes-familial polyposis coli (familial adenomatous polyposis, FAP)

A 
APC gene (tumor suppressor), 5q22
hundreds of colon polyps, premalignant
colonoscopy early and often
colon cancer before 40
prophylactic colectomy by age 25
163
Q

genetic cancer syndromes-multiple endocrine neoplasia (MEN) syndromes MENI

A

MEN I
“PPP”, “Wermer’s syndrome”
-chromosome 11, gene MENI, protein menin, tumor suppressor
parathyroid
-hyperplasia/adenoma(s) (95%)
-pituitary adenoma (15-90%)
-pancreatic endocrine tumors (usually gastrinoma) (30-80%)

164
Q

genetic cancer syndromes-multiple endocrine neoplasia (MEN) syndromes MEN IIa

A

MEN IIa
“PPM”, “Sipple’s syndrome”
-chromosome 10, gene RET, protein tyrosine kinase, proto-oncogene
-parathyroid adenoma(s) (50%)
-pheochromocytoma (33-50%)
-medullary thyroid cancer (100%)
these people get prophylactic thyroidectomy

165
Q

genetic cancer syndromes-multiple endocrine neoplasia (MEN) syndromes MEN IIb

A

MEN IIb
“PMM”, “Wagenmann-Froboese syndrome”
-chromosome 10, gene RET, protein tyrosine kinase, proto-oncogene
-pheochromocytoma (50%)
-medullary thyroid cancer (85%)
-mucosal neuromas (100%), also Marfanoid body habitus
these people get prophylactic thyroidectomy as well

166
Q

genetic cancer syndromes-breast and ovary cancer

A

BRCA1

  • 17q2
  • tumor suppressor
  • 60% get breast or ovarian cancer by age 50
  • breast lifetime risk 60-70%, ovarian 40-50%
  • common in male breast cancers
  • prophylactic mastectomy/oophorectomy

Pathophysiology I (10 decks)

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