Terminology and classification of tumors Flashcards

1
Q

Clinicopathologic groups:

A
  • preneoplastic/dysplastic lesions
  • neoplasias
  • tumor-like lesions
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2
Q

Types of neoplasias

A
  • benign
  • semimalignant (borderline)
  • in situ carcinoma
  • malignant
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3
Q

Nomenclature of tumors

A

benign neoplasias are usually called by tissue of origin with “-oma” at the end (lypoma)
Can be tricky because malignant tumors also can end eitj -oma (lymphoma) or tumor-like lesions (granuloma, haematoma, actinobacilloma)

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4
Q

Epithelial malignant tumors are usually called …

A

carcinoma

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5
Q

Mesenchymal malignant tumors are usually called …

A

sarcoma

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6
Q

What does ending -blastoma mean in case of tumor?

A

highly undifferentiated tumors (nephroblastoma, retinoblastoa etc)

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7
Q

Dysontogenic tumors - ?

A

individual category somewhere between neoplasias and developmental anomalies

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8
Q

2 big groups of dysontogenic tumors

A

Choristoma and Hamartoma

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9
Q

Choristoma

A

type of heterotopia. Normally differentiated tissue developed at a WRONG LOCATION

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10
Q

Hamarthoma

A

Focal malformation. Abnormally differentiated tissue at anatomically normal location.
Teratomas are kind of hamarthomas

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11
Q

Teratoma

A

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12
Q

Differentiation of neoplasias?

A

More differentiated tumor is, more it resembles tissue of origin, more benign characteristics it has

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13
Q

Benign vs. Malignant basic characteristics

A
  • localized (capsule), slower growth, well-removable, no recurrence usually <-> faster growth, invasion into surrounding tissues
  • no invasion or metastasis <-> metastasis to distant organs
  • can cause compression but usually does not harm patient’s life <-> can cause death
  • benign tumors are genetically “simple” and stable (less mutation and less variation in genetic structure over time)
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14
Q

Can types of tumors overlap?

A

Yes. Criteria for differentiation are:
- differentiation
- pace of growth
- local invasion
- metastasis

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15
Q

Can benign tumors become malignant?

A

Yes they can. Also there can be functional malignancy

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16
Q

Is it always possible to distinguish between malignant and benign tumors?

A

No. E.g. tumor is growing, invading the tissue but doesn’t give metastasis -> SEMIMALIGNANT TUMORS

17
Q

Semimalignant tumors

A

Have mostly characteristics of benign tumors BUT they are locally invasive, infiltrating surrounding tissues ! also tend giving recurrence
NO metastasis

18
Q

In situ carcinoma - ?

A
  • Pre-invasive phase of an epithelial malignancy
  • localized process
  • proliferation will no go through basement membrane !! (won’t affect dermis)
  • skin -> Bowen or multicentric in situ carcinoma
  • mammary gland -> intraductal and intralobular carcinoma
  • in case of mucosas - if it does not go through lamina muscularis mucosae
  • important to make several slides !!
19
Q

Neoangiogenesis

A
  • Neoplasm will form new small blood vessels that will be O2 source for tumor.
  • if cell proliferation rate > rate of neoangiogenesis -> hypoxia -> necrosis
20
Q

Grade of differentiation

A

Level of cell differentiation of the tumor’s parenchyma is variable
-G1 well-differentiated
-G2 moderately differentiated
-G3 Poorly differentiated / anaplastic
(growing ability, invasion ability, prognosis of disease, therapy modality)

21
Q

Anaplasia - ?

A

lack of differentiation. Tissue will lose original functions but can gain new ones.

22
Q

Characteristics of anaplasia:

A
  • anisocytosis, anisokaryosis, kariomegaly, increased nuclear:cytoplasmic ratio, hypo/hyper chromasia,
  • prominent NUCLEOLUS,
  • increased mitotic activity,
  • irregular chromosomes
23
Q

Anisocytosis - ?

A

Difference in size and shape of cells

24
Q

Anisokaryosis - ?

A

Variation in nuclear size and shape

25
Q

Karyomegaly - ?

A

enlargement of the nucleus (2-3x normal size)

26
Q

Nuclear : cytoplasmic ratio

A

nuclei- cell and nuclear cytoplasm ratio 1:1 instead of 1:4/1:6

27
Q

Hypo- / hyperchromasia

A

Lack or hyper staining of the nuclei

28
Q

pre-neoplastic lesions

A

Genetic deformities can be already marked with molecular methods but there are no clinical signs

reversible pre-neoplastic lesions (dysplasia, metaplasia) are frequently precursors to neoplastic progression

29
Q

Acquired pre-neoplasia

A

some chronic regenerative cell proliferation (e.g. liver cirrgosis)

30
Q

Tumor-like lesions. Examples

A
  • macroscopically look like tumors
  • e.g.
  • idiopathic nodular hyperplasia (liver, pancreas, spleen, adrenal gland)
  • cystic mucinous hyperplasia in gall bladder
  • chronic inflammatory tissue proliferation
  • hyperregeneration
  • follicular cyst in skin