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Anatomy (AIM) > Pathology E2 > Flashcards

Pathology E2 Flashcards

1
Q

Neoplasia

A

New growth
Clonal proliferation of cells (benign or malignant)
Common progenitor (but not all cells ID)

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2
Q

Neoplasm

A

physical manifestation of neoplasia

solid mass OR dispersed

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3
Q

Benign characteristics

A

Well differentiated
Progressive, slow growth. May halt or regress
Mitotic figures –> rare, normal
Usu cohesive, expansile circumscribed masses
Absent metastasis

Exp. Benign nevus

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4
Q

Malignant characteristics

A 
Lack of differentiation (anaplasia) 
Atypical structure
Erratic growth - slow to rapid
Mitotic figures --> numerous, abnormal
Locally invasive
Metastasis present

Exp. malignant melanoma

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5
Q

Benign vs malignant dx and tx

A

Definitive dx req. pathologic evaluation

Benign tumors –> often tx w/ surgery alone

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6
Q

Leiomyoma

A

Benign

  • often cause sx
  • may become lg
  • well differentiated, demarcated
  • slow growing
  • freq multiple
  • typically no metastasis
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7
Q

Leiomyosarcoma

A

Malignant

  • often cause sx
  • may become lg
  • poor differentiation
  • usu single
  • commonly metastasize
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8
Q

Local vs distant recurrence

A

Local recurrence –> not ness malignant, could just be that didn’t remove all at initial tx
Distant recurrence –> metastasis

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9
Q

Epithelium neoplasm nomenclature

A

Malignant: carcinoma

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10
Q

Squamous papilloma

A

Benign proliferation of squamous epithelium

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11
Q

Colonic Adenoma

A

Benign lesions, most grow as exophytic polyps
Can progress to carcinoma
- detection by colonoscopy –> imp in prep adenocarcinoma

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12
Q

Colonic adenocarcinoma

A

Malignant, invasive tumor glands

Malignant glands have invaded the wall of the colon and the potential for metastasis is established

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13
Q

Most, not all “oma’s” are benign

Exceptions?

A

hepatoma, lymphoma, seminoma, melanoma, mesothelioma

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14
Q

In situ carcinoma

A

lack metastatic potential, but are treated as malignant because still phenotypic/genotypic char of invasive tumor cells. If no removal –> some will progress to invasive cancer

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15
Q

Ductal “carcinoma” in situ of the breast

A

Duct filled with neoplastic cells

  • Often look poorly differentiated
  • Sim to invasive ductal carcinoma, just cant break through basement membrane
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16
Q

Nomenclature: Mesenchymal neoplasms

A

Benign: -oma
Malignant: -sarcoma

Exp. osteoma vs osteosarcoma

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17
Q

Mixed epithelial / mesenchymal neoplasms

Benign exp?

A

Fibroadenoma, breast

Pleomorphic adenoma, salivary gland

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18
Q

Mixed epithelial / mesenchymal neoplasms

Malignant exp?

A

Carcinosarcoma, any location

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19
Q

Hematopoietic neoplasms

A

Lymphoma

  1. Hodgkin’s lymphoma
  2. Non-Hodgkin’s lymphoma

Pre-malignant lymphoid: “lymphoproliferative disorders”

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20
Q

Spectrum of lymphoid disorders

A

Non-neoplastic (hyperplasia)
Lymphoma (low grade)
Lymphoma (high grade)

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21
Q

Nomenclature: Hematopoietic neoplasms

A

Leukemia - malignant; arise in bone marrow, blood

  1. Acute (myeloid, lymphoid)
  2. Chronic (myeloid, lymphoid)

Pre-malignant entities: “myelodysplastic syndromes” and “myeloproliferative disorders”

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22
Q

Teratoma

A
  • neoplasm composed of cell types derived from 2-3 germ layers
  • arise via totipotent cells
  • mature elements=benign, immature –> indeterminante course
  • malignancies (teratocarcinoma) rare
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23
Q

Hamartoma

A

benign, proliferation of 1 or more tissue types indigenous to the site of origin, but disorganized.

  • once thought congenital malformations, but many –> neoplastic (recurrent translocations)
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24
Q

Heterotopia / Choristoma

A
  • ectopic rest of normal tissue.
  • congenital anomaly; not neoplastic

GI most common

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25
Q

Incidence

A

of new CAs of specific site/type, arising in a specific time period

(typically expressed as the number of cancers per 100,000 population at risk)

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26
Q

Prevalence

A

New and pre-existing patients alive during specific time period

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27
Q

Cancer incidence

A

Estimated 15M new CAs worldwide, 9M deaths (25K deaths/day)

worldwide: lung, stomach, liver (men); breast, cervix, lung (women)

50% of cancer DXs (and deaths) in US: lung, breast, prostate and colorectum

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28
Q

Men vs women cancer incidence by site

A

Lung is #1 in both men and women

Men: prostate, lung, colon and rectum
Women: breast, lung, colon and rectum

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29
Q

Men vs women cancer deaths by site

A

Lung is #1 in both men and women

men: lung, prostate, colon and rectum
women: lung, breast, colon and rectum

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30
Q

Cancer survival

A

proportion of patients alive at some point after CA DX

overall survival –> alive
disease free survival –> alive without disease recurrence

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31
Q

Hereditary tumors

A

↓ age at DX

multiple tumors

bilateral tumors in paired organs

syndromes with Mendelian inheritance

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32
Q

TSGs

A

encode proteins critical for normal growth inhibitory pathways (misnomer)

  • Knudson “two hit” hypothesis: both TSG alleles must be effected to lose function
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33
Q

Loss of heterozygosity

A

Many CA’s with hereditary component: 1 defective allele inherited, “predisposing” to CA; only 1 more “hit” needs to be acquired somatically

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34
Q

BCL-2

A

Regulate membrane permeability

↓↓ apoptosis in 85% of follicular lymphomas by t14:18 (juxtapose Ig heavy chain & BCL-2 genes)

Most hematopoietic & solid tumors overexpress at least 1 member of the BCL-2 family

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35
Q

Hereditary non-polyposis colon CA (HNPCC) or Lynch Syndrome

A

most common CA predisposition syndrome; autosomal dominant - mutations in MMR genes

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36
Q

Hallmarks of Cancer

A
  • self-sufficiency in growth signal
  • insensitivity to growth inhibitory signal
  • altered metabolism (Warburg effect = switch to aerobic glycolysis)
  • avoid apoptosis
  • immortality (stem-cell like characteristics)
  • ability to induce sustained angiogenesis (primary, mets)
  • ability to invade, metastasize
  • ability to evade immune system
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37
Q

Carcinogenesis initiation

A

acquire non-lethal, irreversible & transmissible genetic change in CA-related gene

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38
Q

Carcinogenesis promotion

A

reversible biologic processes that do not result in genetic damage, but favor devel of CA (estrogen in breast CA)

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39
Q

Tumor Growth Rate

A

determined primarily by % cells in growth phase (growth fraction)

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40
Q

Tumor Growth Fraction

A

% cells in growth phase

directly proportional to tumor’s susceptibility to chemoRX

Tumors with ↑TGR are ↑↑ responsive

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41
Q

Most common CA’s have doubling times of …

A

2-3 months

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42
Q

Breast molecular therapy genetic target. Predictive factor in responding to tx

A

mutated HER2

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43
Q

4 classes of regulatory genes (principal targets of CA)

A
  • growth-inhibiting tumor suppressor genes (gatekeeper)
  • growth-promoting proto-oncogenes (gatekeeper)
  • apoptosis related genes (gatekeeper)
  • DNA repair genes (caretaker)
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44
Q

RB associated tumor and action

A

retinoblastoma
osteosarcoma

action: cell cycle regulation

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45
Q

BRCA 1,2 associated tumor and action

A

TSG
breast
ovarian
prostate CA

action: DNA repair

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46
Q

p53 associated tumor and action

A

TSG
many common CAs

action: cell cycle, apoptosis

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47
Q

APC associated tumor and action

A 
TSG
colon CA (FAP)

action: inhibit signal transduction

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48
Q

TSGs

A 
RB
BRCA1,2
p53
APC
NF1
NF2
WT1
p16
DPC
DCC
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49
Q

role of RB in regulating the G1-S checkpoint

A

Hypo-phosphorylated: RB-E2F complex binds to DNA, recruits histone enzymes –> inhibits transcription

Growth factor gene products –> hyperphosphorylated RB: release of E2F, activation of S-phase genes

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50
Q

Cervical metaplasia (physiological)

A

Prepuberty –> glandular mucosa

Post puberty –> squamous mucosa

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51
Q

pre-cancerous lesions

A

Neoplastic

  • dysplasia
  • atypical hyperplasia
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52
Q

Dysplasia

A

applied to cervix, GI tract, GU tract, squamous lesions of the lung

architecture:
cellular and nuclear pleomorphism
nuclear hyperchromasia (dark)
increased mitotic activity with abnormal mitoses
intact basement membrane (Don’t have metastatic potential YET)

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53
Q

Atypical Hyperplasia

A

synonymous with “endometrial intraepithelial neoplasia”

applied to endometrium, breast and glandular lung lesions

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54
Q

3 ways to handle usual/atypical ductal hyperplasia/atypical lobular hyperplasia/lobular carcinoma in situ

A
  1. follow it, adhere to yearly mammograms. Possibly MRI
  2. tx prophylactically (tamoxifen, anti-estrogen therapy)
  3. In very high risk women (FHx or genetic defect), bilateral prophylactic mastectomy
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55
Q

Tumor grade

A

Degree of differentiation

exp.
- squamous cell CA (intercellular bridges, keratinization)
- adeno CA (gland formation)

Cytologic features
-mitotic rate, abnormal mitosis, nucleus abnormalities

HIGHER GRADE –> MORE AGGRESSIVE

56
Q

Well differentiated (G1) squamous cell CA

A

intercellular bridges
stratified, flattened cells
cytologically bland
↓ mitoses

57
Q

Moderately differentiated (G2) squamous cell CA

A

more cellular, less organized
↓ flattened cells
↓ stratification
↑ mitoses

58
Q

Poorly differentiated (G3) squamous cell CA

A

↓ morphologic evidence of
squamous differentiation
pleomorphic cytology
↑ mitotic activity

59
Q

Undifferentiated (G4) squamous cell CA

A
  • no evidence of squamous differentiation

- need IHC to prove squamous differentiation (cytokeratin 5/6, p40, p63)

60
Q

Staging of tumors

A

Extent of tumor based on patho and clinical findings

TNM Classification
T: Site and extent of primary tumor
N: Involvement of regional lymph nodes
M: Distant metastasis

AJCC Classification
0 to IV - (tumor size, nodal spread, and distant metastasis)

61
Q

Breast CA staging

A 
0 – carcinoma in situ, 100% survival rate
I - no nodal/distant metastases
II - no distant metastases 
III - distant metastases 
IV - distant metasteses present
62
Q

Immunohistochemistry (IHC)

A

Using Abs to test for specific proteins

  • categorize undifferentiated malignant tumors
  • assess for invasion, metastases
  • determine site of origin of occult primary tumors
  • classify leukemias and lymphomas
    assess prognostic and predictive factors
63
Q

Immunohistochemistry process

A

Primary antibody detects a specific cellular epitope in tumor
Detection step localizes the site of primary antibody binding (secondary Ab (has dye) binds primary antibody)

64
Q

Prognostic factors

A

prognosis of tumor INDEPENDENT of tx

  • Presence / absence of metastases
  • Tumor grade
  • Tumor size
  • Tumor proliferative activity
65
Q

Predictive factors

A

likelihood of response to a specific tx

  • ER in breast CA (TAMOXIFEN)
  • HER2/neu in breast CA (TRASTUZUMAB and PERTUZUMAB)
  • EGFR mutation in lung ACA (ERLOTINIB and GEFITINIB)
66
Q

Flow Cytometry

A

immunophenotyping hematologic malignancies

spun through laser
tase with Abs
look at tons of Abs at same time

67
Q

Cytogenetics

A

req culture of living tumor cells

68
Q

FISH

A

using DNA probe to look for gene

  • Can assess status of a single gene
  • Primarily prognostic/predictive uses
  • Applied to routine histologic sections
69
Q

Oncotype Dx

A

Multi-gene assessment
- Reverse transcriptase PCR assay – RNA based

Calculates “recurrence score” = risk assessment for distant recurrence in patients with breast CA

70
Q

circulating tumor cells (CTCs)

A

Tumor cells often in blood circulation before metastasis

71
Q

NF1

A

TSG
inhibits signal transduction
- neurofibromas

72
Q

Proto-oncogenes

A

mediate cell prolif/diffrent in normal cells
- non-lethal mutation –> oncogenes that promote cell growth

  • NO 2 hit requirement
abl
ras
HER2
EGFR
MEN 1,2
c-myc
l-myc
n-myc
bel-2
73
Q

Rb mechanism of cancer

A

hypO-P Rb binds E2F (trace for S genes)

hypEr-P Rb does NOT bind E2F –> proceeds to S phase

mutation in Rb ^ no checkpoint, all goes to S

74
Q

p53 mechanism of cancer

A

activation of normal p53 –> arrest of cell cycle in G1 and DNA repair

mut –> genetically damaged cells proliferate –> malignant tumors

75
Q

E7/E6 mechanism of cancer

A

E7 bind to Rb –> inactivation

E6 binds to p53 –> inactivation

76
Q

Common distant mets for liver

A

colon, stomach, pancreas, breast, lungs

77
Q

Common distant mets for brain

A

lung, breast, melanoma, kidney, GI tract

78
Q

Common distant mets for bone

A

breast/prostate, lung, kidney, thyroid, testis

79
Q

Common distant mets for peritoneum

A

ovation, primary peritoneal CA, lonular Ca of breast, appendices CA, melanoma

80
Q

CK

A

cytokeratin, common epithelial marker
carcinoma
(breast, prostate, lung, colon)

81
Q

LCA

A

leukocyte common antigen

lymphoma

82
Q

S-100

A

common neuroendocrine marker

melanoma

83
Q

PSA

A

prostate CA marker

84
Q

CEA

A

colorectal, pancreatic, gastric, breast CA marker

85
Q

CA-125

A

ovarian CA marker

86
Q

AFP

A

hepatocellular CA, NS-GCT serum marker

87
Q

lymphatic spread is characteristic of

A

carcinomas

88
Q

hematogenous spread is characteristic of

A

sarcomas

89
Q

chromogranin

A

neuroendocrine IHC stain

90
Q

germ cell tumor

A

ß-HCG, AFP, PLAP

91
Q

vimentin

A

soft tissue/sarcoma

92
Q

markers of bone formation

A

alkaline phosphatase
precollagen peptides P1NP
osteocalcin

93
Q

markers of bone resorption

A

urinary calcium

N- and C-telopeptides (collagen crosslinkers)

94
Q

lung squamous cell CA

A

a paraneoplastic syndrome
mediator: PTH
systemic effect: hypercalcemia

95
Q

lung small cell CA

A

a paraneoplastic syndrome
mediator: ACTH
systemic effect: Cushing syndrome (hypercortisol)

96
Q

osteoblasts

A

bone formation via secreting organic bone matrix proteins

regulate osteoclasts

97
Q

osteoclasts

A

resorb bone, form respiration pits
differentiation mediated via RANK/RANKL –> binding activates osteoclasts (OPG binds RANK and stops osteoclast inhibition)

98
Q

Regulation of osteoclast differentiation

A

via RANK/RANKL
RANKL on both osteocytes and osteoblasts.
OPG normally binds RANKL so RANKL doesn’t activate osteoclasts

99
Q

Vitamin D deficiency

A

decreased Ca/phosphate absorption
poor bone mineralization
sx: leg bowing in kids

100
Q

osteomalacia

A

adults, softened bones

101
Q

rickets

A

via vitamin D deficiency in kids

102
Q

osteoporosis

A

kyphosis, height loss, fragility fractures

dx: dual energy XR absorpitometry (DXA)
tx: bisphosphonates (antiresorptives, inhibit osteoclasts)

103
Q

Paget’s

A

chronic, progressive skeletal disorder
focal abnormal inc in bone resorption via osteoclasts
compensation –> increased osteoblast activity
result: disorganized bone with woven/lamellar bone in certain sites

sclerotic lesions of bone marrow replaced by vascular fibrous tissue

risks: inc with age, genetic component

can get osteosarcoma

tx: antiresorptives

104
Q

Achondroplasia

A

recipe disease
most comm form of hereditary dwarfism (1/30,000), AD, fully penetrant
Defect in FGFR3, point mutation
^ usually acts like brake to slow bone growth (during endochondral ossification) in resting cartilage

sx: small stature, gene VARUM, frontal bossing, foramen magnum stenosis (prevents CSF from getting out)

prenatal dx: 90% new mut
related to paternal age (mut from father)

affected individuals –> 50% chance affected child

no cure

105
Q

osteogenesis imperfecta

A

ingredient disease
bone fragility due to defective type I COLLAGEN

most common defect is quantitative, AD pattern, likely premature stop codon

blue sclera –> sign of abnormal collagen

variation in severity (normal intelligence, broad forehead, etc)

ineffective tx: ca, phosphorous…
effective tx: bracing, bisphosphonates (inhibit osteoclast resporption, which is inc in OI) combine w growth hormone

Prenatal: fractures in utero are concerning for severe OI

106
Q

Blout’s disease

A

“oven” disorder

result of abnormal compression of bone leading to growth retardation

histo changes in ZONE OF RESTING CARTILAGE

genu VARUm, internal rotation of tibia

107
Q

Morquio’s disease

A

cleanup disorder
AR mucopolysaccaridosis
cant degrade GAG (keratin sulfate –> cornea and cartilage) –> thickening of tissues, dysfunctional cell/organ formation, accumulation of lysosomes and extracellular tissue

–> skeletal dysplasia

ODONTOID HYPOPLASIA
genu VALGUM (medial epiphyseal plate issue)
108
Q

synovial fluid analysis (inflammation)

A

wbc: 5,000 - 75,000
neutrophils: >50%

109
Q

synovial fluid analysis (bacterial infection)

A

bacterial infection:

> 50,000->100,000
70%

110
Q

type A synovial cell

A

phagocytic, produce synovial fluid, exchange waste and solute between synovium and vessels in CT beneath

111
Q

type B synovial cell

A

fb-like, secrete proteins

112
Q

articular cartilage

A

hyaline cartilage
Type II collagen
chondrocytes
destroyed via IL-1/TNF signaling (trigger chondrocytes)
lacks blood supply, lymphatic drainage, innervation

113
Q

osteoarthritis

A

noninflammory, wbc under 2000
loss of articular cartilage with possible osteophyte formation
chondrocytes –> dec type II collage/proteoglycan, inc catabolic metalloproteases
–> bone fibrillation and eburnation
- majority cases IDIOPATHIC

  • pain often worst during activity and at night after days activities
  • seen in large, weight bearing joints
  • ganglion and synovial cysts
114
Q

RA

A

chronic, systemic inflammatory disorder
I response and CD4 mediated non-suppurative synovitis

destruction of articular cartilage 
ankylosis of joints
panes formation
synovium with papillary proliferative growth
rheumatoid nodules 
swan neck deformity
ulnar deviation
boutonniere deformity of thumb 
synovial cysts (usually baker's cyst)
115
Q

avascular necrosis

A

osteonecrosis, ischemic necrosis

direct damage to bone vasculature 
- ischemia (fracture, corticosteroids..)
creeping substitution to attempt to replace infarct
- TRIANGULAR SHAPE OF BONE NECROSIS
- YELLOW BONE
- glucocorticoids and xs alcohol --> 80% of cases
- alc osteonecrosis * men
- SLE osteonecrosis * women
116
Q

gout

A

articular deposition of monosodium rate crystals in joints, subcutis, kidney

top formation

long needles, yellow, - birefringence

117
Q

pseudogout

A

intra-articular accumulation of any insoluble crystal (like Ca pyrophosphate)

rhomboid in shape, weakly birefringent
blue, + birefringence –> pseudo gout
ELDERLY

118
Q

most common tumors in bones are

A

metastatic

originate via prostate, breast, thyroid, lung, kidneys

119
Q

most common site of infection

A

long bone (rich vascular supply)

120
Q

Diaphysis

which tumors commonly here

A

Ewing’s sarcoma, lymphoma, myeloma, fibrous dysplasia, enchondroma, osteoid osteoma

121
Q

Metaphysis

A

non-ossifying fibroma, osteoid osteoma, osteosarcoma, chondrosarcoma, osteoblastoma, enchondroma, fibrous dysplasia, bone cysts, osteochondroma

122
Q

Epiphysis

A

chondroblastoma, giant cell tumor

123
Q

cartilage forming tumors

A

osteochondroma, enchonroma, chondrosarcoma

124
Q

bone forming tumors

A

osteoma, osteoid osteoma, osteoblasto, osteosarcoma

125
Q

cartilage and other tumors

A

Ewing sarcoma, giant cell tumor, tumors of adipose tissue

126
Q

osteochondroma

A 
most common benign tumor of bone
young patients
location: physes
perpendicular lesion
carilingous cap looks normal
127
Q

endochondroma

A

benign
adults
small bones of hand
radiolucency, hypercellular, sclerotic ring

128
Q

chondrosarcoma

A

malignant
most common cartilaginous tumor
middle aged population
large lesions, small irregular nuclei, abnormal mitoses

129
Q

osteoid osteoma

A

relieve pain with NSAIDs
benign, younger adults
only in bones formed via endochondral ossification
presents with woven bone, central nidus (XR), sclerotic rim

130
Q

osteosarcoma

A 
conman triangle on xray 
most common primary malignancy of bone
under 20 and elderly (elderly usu w/ syndrome like paget's) 
Rb mut --> higher risk 
CODMAN'S TRIANGLE
131
Q

Ewing sarcoma

A 
onion skin appearance on XR 
population = teens
location: femur, long bones 
small round blue cells
t(11;22)(q24;q12)
132
Q

Giant cell tumor

A

soap bubble
adults over 20
location: all bones
osteoclast-type giant cells, pigmented villonodular synovitis involvement, soft tissue mass, hemorrhagic

133
Q

chondrosarcoma

A

malignant cartilage-forming tumor

134
Q

lipoma

A

subQ

benign

135
Q

liposarcoma

A

LE, retroperitoneum

Anatomy (AIM) (13 decks)

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