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Pathology Pre-Midterm > Module 4 Path > Flashcards

Module 4 Path Flashcards

1
Q

What are the cellular adaptations to stress?

A

Atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia

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2
Q

A neoplasm can be classified as what two things?

A

Benign

Malignant: sarcoma, carcinoma. other (mixed, teratoma, etc)

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3
Q

What are some general characteristics of tumors?

A 
Differentiation 
Anaplasia
Rate of Growth 
Invasion 
Metastasis
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4
Q

The phases of malignant tumor growth, each card will go into details of these phases. 1st phase is transformation

A
  1. Transformation: monoclonal proliferation

- additional mutations over time can lead to subclones –> increases resistance to chemo

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5
Q

The next phase is tumor growth, explain some characteristics

A
  1. Tumor Growth- requires 30 doubling times for clinical significance
    - Angiogenesis via FGF,PDGF,VEGF to maintain blood supply
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6
Q

The third phase of malignant tumor growth is local invasion, explain some characteristics

A
  1. Local Invasion -resistant tissues -mature cartilage and elastic tissue in arteries
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7
Q

What are the steps to local invasion

A
  1. Detachment of tumor by downregulating E-cadherin and mutation of catenins
  2. Attachment of ECM proteins - laminins, integrins, fibronectin
  3. ECM protein degradation -type IV collagenase
  4. Generation of new sites -MMP2 and MMP9 secreted by the tumor
  5. Movement through ECM proteins -autocrine motility factors
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8
Q

The fourth and final step in malignant tumor growth is distant metastasis, what are some features?

A

via lymphatics, hematogenously or seeding

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9
Q

what is atrophy?

A

Decrease in size and function of cell; decreased size of whole organ
if persistent: cell death

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10
Q

What is hypertrophy?

A

Increase in size and augmented function of cell

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11
Q

What is hyperplasia?

A

Increase in number of cells

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12
Q

What is metaplasia?

A

Conversion of one differentiated cell type to another

both types of cells are normal

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13
Q

What is dysplasia?

A

Alteration in size, shape, organization of cells

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14
Q

What is aplasia, hypoplasia and agenesis?

A

Aplasia: absence of an organ (only rudiment present)
Hypoplasia: decrease size due to incomplete development
Agenesis: complete lack of organ

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15
Q

What is a neoplasm?

A

Abnormal mass of tissue
growth exceeds and is uncoordinated with that of normal tissue
persists in the same excessive manner after cessation of the stimulus which evoked the change

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16
Q

How are neoplasms named?

A
  1. type of neoplastic cells:indicate tissue of origin

2. nature of tumor (Whether benign or malignant)

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17
Q

In regards to classifying tumors there are two ways in which this is done, grading and stage. How are tumors graded?

A

Level of differentiation (well, moderately, or poorly differentiated), mitoses and character of tumor
Grade based on I-IV on histological appearance
Problems with variation of histology of various areas and observer variation

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18
Q

How are tumors staged?

A

Extent of spread (more important then grade)

  • clinical staging: based on evidence acquired before treatment
  • Pathological staging- obtained at surgery via examination tissues
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19
Q

In regards to staging, what does T,M and N stand for?

A

Size of the primary tumor = T
Extent of spread to regional lymph nodes (N)
Presence or absence of metastases (M)

20
Q

What are the two major systems of categorization?

A

TNM: Union Internationale Contre Cancer
-clinical staging:based on evidence acquired prior to decision of definitive trust
-pathological staging: includes info obtained at surgery and from examination of tissue by pathologists
American Joint Committee (AJCC): divides tumors into stages 0-IV-factors similar to TMN

21
Q

What is cervical intraepithelial neoplasia (CIN) aka Cervical dysplasia?

A

-Potentially pre-malignant transformation and abnormal growth (dysplasia) of squamous cells on surface of cervix

22
Q

What is the etiology of CIN?

A

HPV infection

23
Q

What is the pathogenesis for CIN?

A

Squamous dysplasia from HPV 16 and 18 strains incorporating in host genomes –> express E6 and E7; E6 inactivates p53 and E7 inactivates Rb

24
Q

There are three stages of CIN –all of which are asymptomatic. Each card will go through one. First –>

A 
CIN I (mild/flat condyloma) -lower 1/3 of epithelium is dysplastic and upper 2/3 has koilocytic change
-Koilocytic change=perinuclear halo and nuclear hyperchromasia
25
Q

What is the second stage of CIN ?

A

CIN II (moderate) -lower 2/3 is dysplastic and upper 1/3 has koilocytic change

26
Q

What is the third stage of CIN?

A

CIN III (severe dysplasia/carcinoma in situ) - entire epithelium is dysplastic –> no koilocytic change, basement membrane is intact ( not carcinoma yet)

27
Q

For screening it is recommended to do a yearly pap smear, what does a normal pap smear look like?

A
  • Superficial cells located at the top of the stratified squamous epithelium; very small nucleus –> non-mitotically active; mature cells
  • Intermediate cells: are in b/t the parabasal and superficial layers
  • Parabasal cells: near the BM; will show expanded nucleus –mitotically active
28
Q

What does an abnormal pap smear look like?

A
  • Increased nuclear/cytoplasmic ratio; disproportionately large nuclei (not round); deep basophilic nuclei (mitotically active), disorganized cellular arrangement
  • occurs at squamo-column junction (transformation zone)
29
Q

What is Schillers Test?

A

test for non-glycogen containing areas of the cervix, which may be a site of early carcinoma; uses iodine

  • Mitotic cells = glycogen absent (Being used) =fails to stain
  • Non-mitotic cells=glycogen =stains brown
30
Q

What are the 5 features of dysplasia/atypica?

A
  1. Increased nucleus to cytoplasmic ratio
  2. Nuclear hyperchromasia (blue/basophilic)
  3. Nuclear Pleomorphism (different sizes and shapes)
  4. Cellular pleomorphism
  5. Enlargement, irregularity and loss of polarity (orientation of cells doesnt make sense)
31
Q

Naturally in the cervix, squamous cells mature from bottom to top as they accumulate what?

A

glycogen

32
Q

What cells do you want to do a pap smear on?

A

Superficial cells

33
Q

What two HPV strains do not incorporate in the host genome –> do not cause dysplasia or carcinoma

A

6 and 11

34
Q

What do HPV 6 and 11 strains lead to?

A

Genital Warts (totally benign) -> but can still do koilocytic change (indicates the presence of HPV)

35
Q

When does CIN become cancer?

A

Invades the BM

36
Q

What is the most important predisposing factor for cervical cancer?

A

History of multiple sexual partners

37
Q

What is the most common symptom of cervical carcinoma?

A

Post-coital bleeding (also have dyspyrunia which is painful intercourse), white vaginal discharge (leukorrhea)

38
Q

How do the malignant cells present on histological slide?

A

Malignant squamous cells with keratin pearls = well differentiated in function b/c making keratin pearls

39
Q

What is Anaplasia?

A

De-differentiated or lack of differentiation in structure and function
Rapid cell growth and hallmark of malignancy

40
Q

How does Anaplasia appear on histological image?

A

Epithelial Origin -Carcinoma- cytokeratin stain (disseminate via lymphatics)
Mesenchymal origin-sarcoma-vimentin stain
(disseminate hematogenously via venous drainage) (liver and lungs frequent sties)
Muscle Origin - desmin stain

41
Q

What are the black areas of anaplasia on histological image?

A

Tumor giant cells (multinucleated) b/c anaplastic tumors divide at a very fast rate
-K167 is the stain for rapidly dividing tumor cells

42
Q

What age do women start getting pap smears?

A

21

43
Q

A pap smear is a screening test for cervical cancer, what are other screening tests commonly used?

A

Mammogram (breast cancer)
Digital Rectal Exam (prostate cancer)
Colonoscopy (colon cancer)

44
Q

PSH is considered a tumor marker, what is the role of a tumor marker enzyme?

A

To monitor response to treatment not

to diagnosis

45
Q

If a patient has an abnormal pap smear, what is the next recommended investigation?

A

Colposcopy and then biopsy (these will allow you to see the basement membrane)

Pathology Pre-Midterm (35 decks)

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