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PATHOANA > Precancers. Dysplaisa of squamous and glandular epithelium > Flashcards

Precancers. Dysplaisa of squamous and glandular epithelium Flashcards

1
Q

definition of precancer

A

on-invasive lesion that has genetic abnormalities, loss of cellular control funciton and some phenotypic charchterisitc of inavsive cancer, and is very likely to develop tint inasvive canver

or
genetically induved, non invasive lesion which with some probability leads to development of malignancy

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2
Q

criteria of precancer

A
  1. evidence exista thta precancer is associated with increased risk of cancer
  2. when precancer progresses to cancer, the resulting cnacer arises from cells
  3. precancer is different form normal tissye it arises form
  4. precancer is different form the cnacer into which it develops
  5. there are methods by which is can be diagnosed
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3
Q

inborn syndromes with high risk of malignancy

A

Li fraumeni s.: defect of p53

lynch s: defect of DNA repair genes

immunodeficinect

ecposition to carcinogens

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4
Q

disorder with high risk of developmetn of malignancy

A

cholescystolithasis

cryptorchidism (undescended testicle)

feature of clinical manifestation of malignancy-paraneoplastic phenoma

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5
Q

what is dysplasisa

A
  • most common morphological featur eof precancer
    -disturbances of normal tissue structure or normal cell morpholgy
    -cells are larger, nuceli are larger aka increased N:C ratio, pleomorphism of cells and distinct nucleoli and so one
    -can be reversible
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6
Q

what is reactive chnages

A

rversible chnages of tissue by injury, morphologically mimicking true dysplasia, distinguishing reactive atypia form true dysplasia can be difficul or immpossible

  • these are seriously altered morpholoy
  • ## not DNA induced lesions, only DIRECT INJURY OF TISSUE
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7
Q

hyperplasia

A

-progressive chnage in which ther eis increased number of cells in tissye
-pathological hyperplasia can develop into malognancy like of Lymphoid tissue in AIS, HP, induced MALT hyperplasia, atypical ductal hyperplasia in breats
- AIDS thing can bear risk of lymphoma–>precancerous
-gastritis of endometrial mucosa=MOST COMMON kind which is precancerous lesion

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8
Q

metaplasia

A

change of one differentiated tupe of tissye to antoher differentiated type of tissye

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9
Q

what is most crucial feature of precancerous

A

invasive growth/ infiltration
- It is a non-invasive lesion. it doesnt infiltrate

it is DNA induced

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10
Q

info about cells of precancerous

A
  1. are active and are able to proliferate withoug growth support
  2. proliferaet and growth is automatic(autonomous)
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11
Q

classification of precancers-according to importance

A
  1. stacionar/facultative
  2. progredient/obligatory
  3. absolute progredient precancers
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12
Q

stacionar/facultative

A

-transformation <20% of lesions, time inetrval >5y
-usually chronic tissueirritation-resp chronic proliferation of cells
-neurofibromatosis, endometrial hyperplasia
-not true precancers, only diseases which high tisk of mlignancy exceot the two mentioned

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13
Q

progredient/obligatiory

A
  • transformation >20% of lesion, time interval <5y
  • serous alteration of genetif information
    -cornu cutaneum, cervical intraepithelial neoplasin-cin, prostatic intraepileila neoplasia-PIN, atypical endometrial hyperplasia
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14
Q

absolute progredient precancers

A

-100% occurence of malignancy
-FAP-familial adenomatous polyposis, XP-ceroderma pigmentosum

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15
Q

classifciation of precancers to morphology and development

A
  1. acquired microscopic precancers
  2. acquired large lesions with morphologic atypia
  3. precursors lesion occuring with inherited hyperplasic syndorme thta often progress into cancer
  4. acquired diffuse hyperplasia and diffuse metaplasia
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16
Q

acquired microscopic precancers

A

-msot commen
-mainly intraepi neoplasia
-need time to developm bc acc of DNA mutations
- multifocal lesions, atypical cells replace epi without formation of distinct tumor mass

baretts esophagus-only metaplasia

17
Q

acquired large lesions with morphologic atypia

A
  • often without lesions(dont chnage their apperance)
  • macroscopic visbile mass,
  • crowding of cells, irregualr growth pattern, marked cellular atypia , usually displastic cells
    -irreversible
18
Q

precursors lesion occuring with inherited hyperplasic syndorme thta often progress into cancer

A
  • inborn muation
    -casual genetic mutation
    -younger people
    -hyperplasia of cells without serious dysokasia
    -usually multiple/resp. bilateral: in all kinds of tissye, basically 2 sided organs the tumors will occur in both sides (bilat)
    -EX
    A. multiple nedocrine neoplasia syndorme(MEN:hyperplasia of endrodrine cells in GITS–>increased nr cells..>neuroendocrine tumors
    B. herediatry medullary thyroid carcinoma: hyperplasia of parafollicular cells which produce calcitonin–>attach both lobes of TG bilaterally
19
Q

acquired diffuse hyperplasia and diffuse metaplasia

A

-diffuse chnage of mucosa/organ
-affect all teh tissue, not focal lesion
- increased nr cells, enlargment of tissue structures,, chnage of cells/tissue without serous dysplasia
-irrverible
-ex: endometrial hyperplasia

20
Q

carcinogenesis- two basic types of mutations

A

causal and accompanying

21
Q

causal (drivers)

A
  • these mutations affect the genes whoch really progress to canver=responsible for carcnogenesis
  • on or severl needed
    -oncogene: normal genes in our body which reg increased proliferation of cells when needed
    -antionocgne: normal which suppress prolif of cells
22
Q

ypes of causal mutation

A

activation of oncogenes

inhibition of anti-oncogene

ianctivation of apoptosis

inactivation of DNA repair

23
Q

accompanied(passengers)

A
24
Q

precancers number

A

2-4 in precancerous
3-5 in carcinogenesis
invasive malignancy: 4-6 causal genetic mutationa +genetic instavbility

25
Q

precancer is a …

A

genetic stable lesion

26
Q

hematologic neoplasma

A

-only malignant
-usually only one cadual muattion charcteristic for distinct malignancy(bcr/abl)–>CML–>FL–>MCL–>AML-M3

chronic myelegenous leukemia has bcr/abl translocation(philadelphia chromosome)

follicular lymohima has translocation form chromosome 14–>18

27
Q

hemopoiesis/ lymphopoiesis

A
  1. high cell prolifeation
  2. spread into peripheral blood(metastasing)
  3. infiltartion of organs
28
Q

persistnece

A

-most of prescancers
-patinet ill get it and die with it

29
Q

progression

A

-cells toward malignancy by acc of new DNA muation–>carcninogenesis
- cytological atypisa, mitotix act, formaiton of multiple lesions

30
Q

regression

A

-mechnism: increased antigenicity of cells and increased apoptosis of cells

31
Q

diagnosis of precancers by morphology

A

1) epithelial lesions
- most common
-clearly defined architerctur
-distrubances of cell stratification, differentiation, shape and size, chnages of cell nuclei(hyperchromia, pleomorphy, nucleoli), mitotic activity
- cells on BM-limiting facotr of infiltration

2)mesenchumal
- absence of BM
- criteria of assesment of dignity: size and nr of lesion, pleomorpjology of cells, number of cells, mititic act, necrosis

32
Q

importance of precancer diagnostic

A
  1. early detection of precancer
    -you have time to influence
  2. cnacerogenesis is dynamic process: can be stopped or reversed
  3. possibilities for therapy
    -like surgery
33
Q

actinic keratosis/squamos cell carcinoma in situ

A

Bowens precancer
squamous carcinoma of skin

34
Q

atypical endometrial hyperplasia

A

endometrioid adenocarcinoma

35
Q

myelodysplastoc syndorme

A

leukemia

36
Q

progressive transformaiton of germinal centers

A

lymphocyte predominant Hodgkins disease

PATHOANA (13 decks)

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