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EXMD504 > 5. Cancer Pathology > Flashcards

5. Cancer Pathology Flashcards

1
Q

what is a lesion?

A

any change in tissue or organ from injury or disease that impairs normal function

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2
Q

what is a tumour/mass/lump/nodule/polyp?

A

swelling caused by abnormal growth of tissue

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3
Q

what is cancer?

A

malignant neoplasm

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4
Q

what is oncology?

A

branch of medicine that deals with cancer

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5
Q

difference between polyp and tumour

A

polyp has a stalk

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6
Q

are all growths neoplasm?

A

no

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7
Q

what are 5 types of growth that are not neoplasm?

A
  1. malformation
  2. repair from excessive healing
  3. hypertrophy
  4. hyperplasia
  5. metaplasia
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8
Q

3 examples of malformations:

A
  1. Choristoma/ectopic tissue/heterotopia –> normal tissue misplaced in abnormal tissue
  2. Hamartoma –> benign disorganized growth of cells and tissues
  3. Vascular malformation
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9
Q

hypertrophy

A

increase in cell size

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10
Q

hyperplasia

A

increase in cell number

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11
Q

what would you see with pancreatic heterotopia in stomach?

A

pancreatic tissue in stomach –> ie tissue in wrong location

not neoplastic!

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12
Q

what mediates hyperplasia?

A

hormones, growth factors

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13
Q

why does hyperplasia differ from neoplasia? (3)

A
  1. cells are genotypically and phenotypically normal
  2. organ involved is usually diffusely enlarged –> not a localized mass
  3. reversible –> stops when stimulus stops
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14
Q

can hyperplasia become neoplasia?

A

yes –> hyperplasia can be precursor in some cases

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15
Q

what is metaplasia?

A

replacement of 1 type of normal adult cell/tissue with another type

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16
Q

what causes metaplasia? (3)

A
  1. tissue damage
  2. tissue repair
  3. tissue regeneration
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17
Q

what causes metaplasia in epithelial tissue?

A

inflammation

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18
Q

is metaplasia neoplastic?

A

no but often becomes malignant

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19
Q

what causes neoplasm?

A

accumulation of genetic changes

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20
Q

what is neoplasm?

A

cells grow out of control, independent of physiological growth signals and controls

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21
Q

what are 2 components of neoplasm?

A
  1. abnormal neoplastic cells
  2. non-neoplastic stroma
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22
Q

what is stroma? (3)

A
  1. connective tissue
  2. inflammatory cells
  3. blood vessels
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23
Q

are all neoplasms the same?

A

no, there is heterogeneity within and between neoplasms

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24
Q

2 steps when patient has tumour

A
  1. neoplasm or not?
  2. if neoplasm: benign, borderline, or malignant
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25
Q

what is malignant tumour?

A

tumour is more invasive and destroys surrounding tissue

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26
Q

what is differentiation?

A

how closely neoplastic cells have similar morphology and function to normal cells

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27
Q

what is anaplasia?

A

lack of differentiation

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28
Q

what does it mean for cells to be highly differentiated?

A

cells resemble the tissue they arise from

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29
Q

does a benign tumour have differentiation or lack of differentiation?

A

benign tumours are differentiated

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30
Q

does a malignant tumour have differentiation or lack of differentiation?

A

variable differentiation –> well/moderately/poorly/un-differentiated

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31
Q

5 morphological changes of malignant cancer cells

A
  1. pleomorphism (varied cell size and shape)
  2. abnormal nucleus
  3. increased and atypical mitosis
  4. loss of polarity, disorganization
  5. ischemic necrosis
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32
Q

describe difference in colon tissue with benign and malignant tumour:

A

BENIGN: nuclei at basal layer, cytoplasm outward –> nicely organized

MALIGNANT: lots of cells, poor orientation of cells, big nuclei/nucleoli –> active cells

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33
Q

describe the 7 steps of neoplasia development

A
  1. normal cell has genetic change
  2. abnormal, transformed neoplastic cell
  3. becomes malignant: dysplasia + neoplasia
  4. invasion
  5. overt malignancy
  6. metastasis
  7. drug resistance, production of hormones, production of receptors
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34
Q

what is dysplasia?

A

disordered growth

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35
Q

can dysplasia become malignant?

A

dysplasia can become malignant if not treated

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36
Q

how can you prevent malignancy from dysplasia?

A
  1. change habit
  2. remove with surgery
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37
Q

what is carcinoma in situ?

A

severe dysplasia involving the ENTIRE thickness of the epithelium but not yet invaded thru basement membrane –> high probability of progressing to invasive cancer

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38
Q

how can carcinoma in situ become invasive carcinoma?

A

metastasize by breaking thru basement membrane to access blood and lymph vessels

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39
Q

is benign tumour invasive?

A

no –> grows slowly, may compress surrounding tissue and stop growth at a point

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40
Q

4 ways for metastases to occur

A
  1. direct seeding of body cavities/surfaces
  2. lymphatic spread
  3. hematogenous spread (lung, liver)
  4. other: CSF, implantation
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41
Q

3 types of body cavities/surfaces where metastases can occur

A
  1. peritoneum
  2. pleura
  3. pericardium
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42
Q

why does metastases occur via body cavities/surfaces?

A

no barrier to breach, tumour can easily travel

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43
Q

what is the most common type of metastases?

A

lymphatic spread

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44
Q

is sarcoma or carcinoma most common for hematogenous spread?

A

sarcoma

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45
Q

overall summary of differentiation of benign vs malignant

A

benign: well-differentiated, structure typical of normal tissue

malignant: some anaplasia/lack of differentiation, structure atypical

46
Q

overall summary of growth rate of benign vs malignant

A

benign: progressive and slow, may stop or regress, normal mitosis

malignant: erratic growth, slow to rapid, abnormal mitosis

47
Q

overall summary of local invasion of benign vs malignant

A

benign: cohesive, does not invade

malignant: locally invasive

48
Q

overall summary of metastasis of benign vs malignant

A

benign: no metastases

malignant: common, more likely with large undifferentiated primary tumours

49
Q

how are neoplasms classified? (5)

A
  1. organ or precise type
  2. origin of cell type
  3. benign vs malignant
  4. histological type
  5. additional subtyping
50
Q

what are 3 ways of additional subtyping?

A
  1. immunohistochemistry
  2. flow cytometry
  3. molecular and genetic features
51
Q

what does immunohistochemistry show if malignant tumour?

A

when cells lose differentiation, use IHC to identify specific proteins that match a cell type to identify the origin

52
Q

2 types of malignant neoplasm

A
  1. carcinoma
  2. sarcoma
53
Q

what is carcinoma?

A

malignant tumour from epithelium

54
Q

what is sarcoma?

A

malignant tumour from mesenchymal (cartilage, adipose, bone)

55
Q

tumours of mesenchymal origin: benign vs malignant suffixes

A

benign = -OMA
malignant = -SARCOMA

56
Q

tumours of epithelium origin: malignant suffixes

A

-CARCINOMA

57
Q

what are mixed tumours?

A

more than one neoplastic cell type, derived from 1 germ cell layer

58
Q

more than one neoplastic cell type derived from MORE THAN 1 germ cell layer =?

A

teratogenous

59
Q

what is the paradigm shift in cancer treatments?

A

we treat patients based on genetic profiling rather than cell origin and morphology

60
Q

why do we try to treat patients based on genetic profiling now?

A

different types of cancers in different places can have same mutation

61
Q

6 clinical aspects of benign neoplasm

A
  1. cosmetic
  2. local symptoms/signs: obstruction, pressure, pain
  3. distant endocrine effects
  4. complications: bleeding necrosis, ulceration, perforation
  5. can cause morbidity
  6. can cause malignant transformation
62
Q

2 diseases of malignant neoplasm

A
  1. cachexia
  2. paraneoplastic syndrome
63
Q

what occurs with cachexia?

A

HYPERCATABOLIC STATE

64
Q

when does cachexia occur?

A

in 50% of cancer patients

65
Q

6 symptoms of hypercatabolic state

A
  1. extreme weight loss
  2. fatigue
  3. muscle atrophy
  4. anemia
  5. anorexia
  6. edema
66
Q

cachexia is responsible for how many cancer deaths? why?

A

responsible for 30% of cancer deaths due to atrophy of diaphragm and respiratory muscles

67
Q

even though the cause of cachexia is unknown, what is thought to play an important role?

A

inflammatory mediators affecting muscles

68
Q

what is paraneoplastic syndrome?

A

unexplainable hormone secretion and other unexpected function that leads to clinical symptoms from the tumour

69
Q

5 results of paraneoplastic syndrome

A
  1. endocrinopathies
  2. neuromyopathic paraneoplastic syndromes
  3. skin changes
  4. skeletal and joint abnormalities
  5. hypercoagulability
70
Q

what are endocrinopathies?

A

ACTH, PTH, insulin or similar substances unexpectedly secreted by tumour

71
Q

what are neuromyopathic paraneoplastic syndromes associated with?

A

cancer-induced immunologic attack on normal tissues which leads to muscle weakness or neuropathy

72
Q

2 types of skin changes from paraneoplastic syndromes

A
  1. acanthosis nigricans
  2. multiple seborrheic keratosis
73
Q

neuromuscular changes in paraneoplastic syndromes?

A

changes in bone but unknown pathogenesis

74
Q

how is cancer diagnosed?

A

integration of clinical and imaging features with pathological assessment by biopsy

75
Q

what 6 things do we look at in cancer diagnosis?

A
  1. clinical history
  2. physical exam
  3. radiology/imaging
  4. lab results
  5. tumour markers
  6. assays of circulating tumour cells, RNA/DNA
76
Q

what are tumour markers?

A

specific hormone/substances are secreted that we can measure and correlate to tumour presence

77
Q

are tumour markers good enough to use for diagnosis? why

A

no –> not specific or sensitive enough bc substance may change in other conditions

78
Q

how can we use tumour markers?

A

if level decreases with treatment, you know tumour is responding to treatment

if level goes back up, tumour may have returned

79
Q

4 macroscopic findings of neoplasms

A
  1. mass/swelling/diffuse enlargement
  2. circumscribed or invasive and metastasizing
  3. pale, white
  4. ulceration/bleeding/necrosis
80
Q

how do we use ink to look at tumour?

A

marks the margins to know if tumour is fully excised

81
Q

what type of tumour is necrosis common in?

A

necrosis common in malignant tumour

82
Q

once we see the tumour, what diagnostic techniques do we use when looking at cells?

A
  1. cytologic methods/cytopathology
  2. biospy/histopathology
83
Q

describe cytopathology

A

examines individual cell changes –> quick and less invasive

84
Q

3 types of cytopathology

A
  1. direct smear
  2. analysis of fluids
  3. fine needle aspiration from solid organs
85
Q

describe biopsy/histopathology methods

A

examines individual cells and architecture by taking the tissue with surrounding tissue –> very invasive

86
Q

cytology or biospy first?

A

cytology first, then if abnormal use biopsy to see invasion

87
Q

describe quick frozen section and the benefit

A

tissue is quick frozen in cryostat and prepared for microscopy

benefit: very quick diagnosis during surgery

88
Q

2 things we learn from quick frozen section

A
  1. look at margins of excised tumour
  2. decide additional studies other than histology
89
Q

4 ancillary diagnostic techniques

A
  1. IHC
  2. flow cytometry
  3. circulating tumour cells
  4. molecular/cytogenetic analyses
90
Q

3 roles of IHC

A
  1. histologic categorization of malignant tumours
  2. determining site of origin of malignant tumours
  3. detecting molecules with prognostic or therapeutic significance
91
Q

1 role of flow cytometry

A

for immunophenotyping of lymphomas / leukemias

92
Q

4 examples of molecular/cytogenetic analyses

A
  1. FISH
  2. PCR
  3. chromosomal analysis
  4. NGS
93
Q

molecular/cytogenic analyses tell us: (6)

A
  1. diagnosis
  2. prognosis
  3. detection of minimal residual disease
  4. hereditary predisposition
  5. guiding therapy
  6. mechanisms of drug resistance
94
Q

2 parameters to determine how well/poorly a patient with cancer will do

A
  1. grading
  2. staging
95
Q

what is grading?

A

degree of differentiation –> how closely does neoplasm resemble original tissue

96
Q

what does a low grade mean? better or worse prognosis?

A

well differentiated, closest resemblance to parent tissue

better prognosis

97
Q
A
98
Q
A
99
Q
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100
Q
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101
Q

how is grading done?

A

by light microscopy

101
Q

what is grading based on? (2)

A
  1. cytology (nuclear and cytoplasmic changes)
  2. histology (architecture, gland formation, mitosis)
101
Q

is staging or grading more important?

A

staging!

101
Q

why are there different grading schemes?

A

for each carcinoma –> each scheme has different criteria

102
Q

what is staging?

A

extent of malignant neoplasm

103
Q

how is staging done?

A

examining surgical specimen/pathological staging) and integration of other information

104
Q

what is the main system for staging? is it the same for all cancers?

A

TNM system –> varies for specific forms of cancer

105
Q

what is TNM system?

A

T = primary Tumour characteristics
N = regional lymph Node involvement
M = distant Metastases

106
Q

what is the difference in staging for breast cancer and prostate cancer?

A

in breast cancer can easily see the size of tumour but prostate cancer, can’t measure size so must look at invasion

107
Q

4 goals of cancer treatment

A
  1. cure
  2. debulking
  3. adjuvant, neo-adjuvant
  4. palliative
108
Q

5 types of cancer treatment

A
  1. surgery
  2. radiation
  3. chemotherapy
  4. immunotherapy
  5. targeted molecular therapy
109
Q

6 things that affect chances of survival

A
  1. histological type of neoplasm
  2. location
  3. staging, grading
  4. biological/molecular properties
  5. degree of angiogenesis
  6. state of host

EXMD504 (12 decks)

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