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EXMD 504 > Lecture 4: pathology of cancer > Flashcards

Lecture 4: pathology of cancer Flashcards

1
Q

what is a lesion

A

modification of tissue or organ from injury or disease, often resulting in impairment of normal function

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2
Q

what is a tumor/masslump/nodule/polyp

A

a swelling caused by an abnormal growth of tissue

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3
Q

true or false: a cancer is a malignant neoplasm

A

true

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4
Q

what is oncology

A

a branch of medecine that deals with the study, treatment, diagnosis and prevention of cancer

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5
Q

what is a polyp

A

a growth with a stalk

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6
Q

name some malformations

A

-choristoma
-hamartoma
-vascular malformation

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7
Q

what is a choristoma

A

misplaced normal tissues in abnormal location

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8
Q

what is a hamartoma:

A

a benign disorganized growth of cells and tissues notmally found in the area

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9
Q

what can cause a keloid

A

repair if excessive healing

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10
Q

what is hypertrophy

A

increase in cell size

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11
Q

what is hyperplasia

A

increase in cell number in response to a stimulus, physiological or pathological; mediated by hormones and growth factors

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12
Q

give examples of hyperplasia

A

-in epithelial cells in the female breast during pregnancy
-hepatocytes to regenerate liver parenchyma after oartial resection
-

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13
Q

what cause prostatic hyperplasia?

A

androgens

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14
Q

what can cause endometrial hyperplasia in postmenopausal women

A

they receive estrogens

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15
Q

true or false: hyperplasia differs from neoplasia

A

true

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16
Q

why is hyperplasia different from neoplasia

A

-the cells are genotypically and phenotypically normal
-the organs involved is usually but not always diffusely enlarged aka it does nor form a localized mass
-the hyperplasia ends when the stimulus ends and is usually reversible

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17
Q

true or false: hyperplasia may be a precursor of neoplasia

A

true
ex: endometrial hyperplasia may become carcinoma

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18
Q

what is metaplasia

A

replacement of one type of normal adult cell/tissue with another type
-in response to tissue damage, repair and regeneration
-in epithelial tissues, often mediated by inflammation

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19
Q

give examples of metaplasia

A

-squanmous metaplasia in bronchial epithelium from smoking or endocervix
-glandular: intestinal metaplasia in stomach caused by h pilory and intestinal metaplasia in gastro esophageal junction caused by acid reflux

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20
Q

true or false; metaplasia is prone to ,malignant transformation

A

true

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21
Q

what is a neoplasm

A

-a new growth of cells and stroma
-a genetic disorder of cell growth trigerred by aquired or less commonly inherited mutations
-characterized by an excessive and unceasing proliferation of cells, independant of physiologic growth signals and controls

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22
Q

what happens with the neoplastic cells

A

-the abnormal neoplastic cells with variable degrees of differenciation
-a non neoplastic stroma of connective tissue , inflammatory cells and blood vessela

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23
Q

where are the characteristics of neoplastic cells

A

they are in the dna transmitted genetically to progeny cells

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24
Q

true or false: there is heterogeneity within and between neoplasm

A

true

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25
Q

true or false: you are either a malingnat neoplastic cell or you are not

A

false there is a spectrum in the neoplastic cells whether they are benign or not

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26
Q

what is the difference between the cells whether they are cancerous or nor

A

-beningn: they are fully differenciated
-malingnant: they are undifferenciated

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27
Q

morphologic changes of cancer cells

A

-pleomorphism: variation in cell size and shape
-abnormal nuclear morphology; dark, thick, irregular, conspicuous nuclei, coarsely clumped chromatin
-mpre nuclei than citoplasm
-more mitose
-loss of polarity
-ischemic necrosis

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28
Q

what is dysphasia

A

-disorganized growth aka pre malingnant
-cytologic features of malignancy, partically involving the epithelium
-may be the precursor to malingnant transformation but not always to progress to cancer aka reversible

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29
Q

what is carcinoma in situ

A

-severe dysphasia involving the full thickness of the epithelium
-considered pre malingnat or pre invasive
-has the biological genotype and phenotype of a malingnancy but has not yet invaded through the basal malingnacy
-

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30
Q

true or false: carcinoma in situ has no probability of progression to cancer

A

false it has a high probability of progression to invasive cancer if untreated

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31
Q

what are the pathways of spread of metastases

A

-direct of seeding of body cavities/surfaces like peritoneum, pleura and pericardium
-lymphatic spread: most common in carcinoma/ folllows the natuiral routes of lymphatic drainage
-hematogenous spread: typical in sarcoma but also in carcinoma/lung and liver is most frequently involved

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32
Q

true or false: benign lesions do not infiltrate or infiltrate the normal tissues

A

true

33
Q

what is the difference between carcinoma and sarcoma

A

-carcinoma is of epithelial origin
-sarcoma is of mesenchymal origin

34
Q

what do you add at the end of a cancer name of mesebchynmal origin

A

sarcoma

35
Q

what do you add at the end of epithelial origin

A

carcinoma

36
Q

what are mixed tunours

A

more than one neoplastic cekkl type, derived from one germ cell layer
-found in salivary gland and renal anlage

37
Q

what is the name oftumor that has more than one neoplastic cell type derived from more tyhan one germ cell layer

A

teratogenous
-ex: totipotential cells in gonads or in embryonic rests

38
Q

What is the paradigm shift un therapeutic targets in cancer

A

-cancer classification according to therapeutic targets rather than cell origin and morphology

39
Q

cancer cachexia is found in …% of cancer patients

A

50%

40
Q

what is cancer cachexia

A

-hypercatabolic state: extreme weight loss, fatigue, muscle atrophy, anemia, anorexia

41
Q

cancer cachexia is responsible for ….% of all cancer deaths

A

30%
due to the consequences of the atrophy of the diaphram and other respiratory muscles

42
Q

what are the vcauses of cancer cachexia

A

-precise causes unknown but inflammatory mediators like tnf, il1 and 6 appear to have important roles

43
Q

what is a paraneoplastic syndromes

A

basically symptoms that are not associated to ur cancer`

44
Q

what can endocrinopathies cause

A

neoplastic cells lose og functions but have weird functions insead

45
Q

what is possibly assocuated with cancer induced immunologic attack on normal tissues

A

neuromyopathic paraneoplastic syndromes

46
Q

can neoplasms cause hypercoagulability

A

yeah

47
Q

name 2 paraneiplastic syndromes

A

-acanthosis nigrantis aka skin discoloration
-hypertrophoc osteoarthropathy: fucked up joints

48
Q

what is cancer diagnosis

A

integration of clinical and imaging features with a pathological assessment by biopsy or rekated techniques
aka there are so many things that can be done

49
Q

what are the tumor markers clinically used

A

psa, cea, afp, hcg, ca125 and monoclonal ig

50
Q

macroscopic findings of neoplasms

A

-mass, swelling and diffuse enlargement
-often pale or white

51
Q

what are the secondary changes of neoplasms

A

-ulceration
-bleeding
-necrosis

52
Q

pathologic or tissue diagnosis necessary and defenite aka them slay mathods

A

-cythopathology and biopsy/histopathology

53
Q

what is cytologuc mathods aka cythopathology:

A

-rapid and less invasive; examines exfoliative cell changed
-direct smears; aka pap smears for cervical cancer
-analysis of fluids
-fine needle aspiration frok solid organs like breast, lung, pancreas etx

54
Q

what is a biopsy/histopathology methods

A

-assessing individual cells and architecture
-variable biopsies(core, incisional or excisional
-resection

55
Q

what is quick frozen sections

A

-establish rapid diagnosis within minutes mostrly during an operayion
-tissue quickfrosen in a cryostat and prepared for a microscopy
-good to determine nature of lesion, eval of margins of an excised tumour
-deciding addictional studies other than histology

56
Q

what is immunohistochemistry

A

-hostolpgic xategorization of malignant tumours
-determination of site of origin of metastati tumopus
-detection of molecules that have pronostic or therapeutic significance like receptors

57
Q

what is flow used for in cancer detectiopn

A

mostly for immunophenotyping of lymphomas/leukemias

58
Q

can u use pcr to detect cancer

A

yeah you can also use molecular/cytogenic analyses like fish, ngs and chromosomal analysis

59
Q

Molecular/cytogenetic analyses in Neoplasm is used for….

A
  • Diagnosis of malignant neoplasms.
  • Prognosis of malignant neoplasms.
  • Detection of minimal residual disease.
  • Diagnosis of hereditary predisposition to cancer: BRCA1, BRCA2, RET proto-oncogene
  • Guiding therapy with oncoprotein-directed drugs: BRAF, EGFR, ALK, BCR-ABL, PML-RARA
  • Identifying mechanisms of drug resistance: liquid biopsies.
60
Q

Next-generation DNA sequencing of cancer genome:

A

rapidly transitioning to standard clinical practice and routinely performed for
targeted sequencing to identify therapeutically actionable gene

61
Q

Parameters to determine how well or poorly a patient with cancer will do?

A

grading and staging

62
Q

what is grading in malignant neoplasms

A

-degree of differenciation aka how closely the neoplastic cells resemble to their normal counterparts
aka low grade is grade one and is the closest to parent tissie

63
Q

how is grading done in in malignant neoplasms

A

-light microscopy based on:
cytology; nuclear and cytoplasmic changes
histology; architecture of cells, gland formation and mitotic figures

64
Q

true or false: grading is organ specific

A

yes especially for breast, prostate and sarcome

65
Q

shit gland formation=////

A

cancer

66
Q

Nottingham grading system for breast carcinoma

A
  • Tubule formation
    – Majority of tumor, > 75%: 1
    – Moderate degree, 10-75%: 2
    – Little or none, < 10%: 3
  • Mitotic count
    – 0-9 mitoses/HPF: 1
    – 10-19 mitoses/HPF: 2
    – ≥ 20 mitoses/HPF: 3
  • Nuclear pleomorphism (grade)
    – Nuclei small compared with normal cells, regular outlines, chromatin, little variation in size: 1
    – Cells larger than normal, open vesicular nuclei, visible nucleoli, moderate variation in size and shape: 2
    – Vesicular nuclei, large nucleoli, marked variation size, shape: 3
67
Q

what is the grading for prostate adenocarcinoma:

A

gleason grading

68
Q

what is the grading for colon adenocarcinoma

A

degreee of gland formation

69
Q

TROJANI Grading System/the French Federation of Cancer Centers Sarcoma Groups (FNCLCC) is based on what

A

based on points
Differentiation:
a) Resembles normal cell type: 1
b) Easily recognized sarcoma: 2
c) Undifferentiated sarcoma: 3
Mitotic activity per mm²:
a) 0-9: 1
b) 10-19: 2
c) ≥ 20: 3
Necrosis:
a) No necrosis: 0
b) Necrosis < 50%: 1
c) Necrosis > 50%: 2
Grade I: 2-3
Grade II: 4-5
Grade III: 6-8

70
Q

what is staging

A

-extent of a malingnant neoplasm

71
Q

true or false: grading is of greater clinical value than staging

A

flase staging is more importantw

72
Q

what is staging done

A

-done by examination of a resected syrgical specimen and integration of other infos like imaging and clinical lan

73
Q

what is staging based on

A
  • TNM system(American Joint Committee on Cancer
    Staging)
    – T for Primary tumor characteristics
    – N for regional lymph node involvement
    – M for distant metastases
74
Q

true or false: TNM staging varies for specific forms of cancer

A

true

75
Q

what are the cancer treatment goals

A
  • Curative
  • Debulking
  • Adjuvant,neo-adjuvant
    -palliative
76
Q

what are the modalitioes of cancer treatment

A
  • Surgery
  • Radiation therapy
  • Chemotherapy
  • Immunotherapy
  • Targeted molecular
    therapy
77
Q

what are Prognostic Factors in Neoplasia
(chances of survival(survival rate)) based on

A
  • Histological type of neoplasm
  • Location
  • Staging, grading
  • Biological/molecular properties
  • Degree of angiogenesis
  • State of the host
78
Q
A

EXMD 504 (12 decks)

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