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MCC > Wk 5 Tumor Pathology > Flashcards

Wk 5 Tumor Pathology Flashcards

1
Q

What 3 processes are involved in hypertrophy?

A
  1. gene activation
  2. protein synthesis
  3. production of organelles
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2
Q

What occurs w/ hyperplasia?

A

Cell production from stem cells

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3
Q

Can permanent tissues undergo hypertrophy and hyperplasia?

A

Only hypertrophy b/c they cannot make new cells

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4
Q

What are permanent tissues in the human body?

A
  1. cardiac myocytes
  2. skeletal muscle
  3. nerve

*cannot make new cells so cannot undergo hyperplasia

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5
Q

What is an exception to hyperplasia being pathlogic?

A

Benign prostatic hyperplasia
-it is pathologic, but no increased risk of cancer

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6
Q

What is the role of atrophy?

A

Decrease in stress leads to decrease in organ size via decreased size and number of cells

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7
Q

How does a decrease in cell number occur?

A

apoptosis

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8
Q

What are two pathways to decrease cell size?

A
  1. ubiquitin-proteosome degradation of the cytoskeleton
  2. autophagy of cellular components
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9
Q

3 growth adaptations

A
  1. growth via hypertrophy and hyperplasia
  2. atrophy
  3. metaplasia
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10
Q

What causes metaplasia?

A

change in stress on organ -> change in cell type (metaplastic cells can handle new stress better)
-most often involves surface epithelium (squamous k or non, columnar, transitional/urothelium)

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11
Q

What is the mechanism of metaplasia?

A

reprogramming of stem cells
-reversible w/ removal of the driving stressor

ex. tx of GERD

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12
Q

What can occur w/ metaplasia?
Give an example and exception

A

Can progress to dysplasia and cancer

ex. Barrett esophagus
exception = apocrine metaplasia - a change seen in fibrocystic changes of the breast

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13
Q

What deficiency can result in metaplasia?

A

Vitamin A deficiency ->:
1. can go blind
2. -t(15;17) APL involves vitamin A receptor (RAR), causing cells to stay trapped in blast state, accum, -> leukemia
-tx = ATRA (vit A derivative) - binds to mutated receptor and allows cells to mature to neutrophils
3. metaplasia -> thickening of conjunctiva called keratomalacia
-vit A nec to maintain conjunctiva of eye (highly specialized squamous epithelium)

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14
Q

What process can mesenchymal tissues undergo?

A

metaplasia
bone, BV, fat, cartilage (CTs)
ex. myositis ossificans = inflam of skeletal muscle (usually due to trauma) which then converts to bone. Would be located close to a bone but not touching it b/c in skeletal muscle (diff from osteosarcoma)

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15
Q

Dysplasia

A

=disordered cellular growth
-refers to proliferation of precancerous cells (ex CIN=cervical intraepithelial neoplasia)
-arises from longstanding pathologic hyperplasia or metaplasia
-can see mitosis high up from basement membrane

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15
Q

Dysplasia

A

=disordered cellular growth
-refers to proliferation of precancerous cells (ex CIN=cervical intraepithelial neoplasia)
-arises from longstanding pathologic hyperplasia or metaplasia

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16
Q

Mechanism of dysplasia

A

Stress on cells
-reversible by alleviating stressor
-if stress persists, will progress to carcinoma (irreversible)

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17
Q

What is aplasia?

A

failure of cell production during embryogenesis
ex. unilateral renal agenesis

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18
Q

Hypoplasia

A

=decrease in cell production during emobryogenesis
-> small organ
ex. streak ovary in Turner syndrome

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19
Q

What are 4 steps that occur in a tumor in order for it to spread?

A
  1. down regulation of E-cadherin
  2. cells attach to laminin and destroy BM
  3. cells attach to fibronectin in ECM and spread locally
  4. entrance into vascular or lymphatic spaces allows for metastasis
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20
Q

What is the role of cadherins?

A

Keep epithelial cells attached to each other
-gets downregulated by tumor cells in order to detach and spread

21
Q

What happens to a cancerous cell after it detaches from the neighboring epithelial cell?

A

it attaches to the laminin in the basement membrane

22
Q

What happens to a cancerous cell after it detaches from the neighboring epithelial cell?

A

it attaches to the laminin in the basement membrane

23
Q

What happens to cancerous cells after it attaches to laminin?

A

Develops ability to make collagenase that destroys collagen type IV. Destroys basement membrane and then can travel to ECM where it attaches to fibronectin to spread locally to a BV or lymphatics

24
Q

How do carcinomas tend to spread?

A

Via lymphatics, so expect to see them at regional draining lymph nodes

25
Q

How do sarcomas tend to spread?

A

Hematogenously

26
Q

what carcinomas tend to spread hematogenously?

A
  1. Renal cell carcinoma (renal vein)
  2. hepatocellular carcinoma (hepatic vein)
  3. follicular carcinoma of thyroid
  4. choriocarcinoma = malignancy of placental tissue (trophoblasts)
27
Q

What are 3 ways carcinomas can spread?

A
  1. lymphatics (primary way)
  2. hematogenoulsy
  3. seeding (breaking into) of body cavities = omental caking
27
Q

What are 3 ways carcinomas can spread?

A
  1. lymphatics (primary way)
  2. hematogenoulsy
  3. seeding of body cavities = omental caking
28
Q

What is seeding of body cavities?

A

Classically seen in ovarian carcinoma -> omental caking

29
Q

Compare benign and malignant tumors

A
30
Q

Histological comparison of benign tumors and malignant tumors

A
31
Q

What distinguishes between bengin and malignant?

A

Benign tumors never metastasize and do not have metastatic potential

Malignant tumors have metastatic potential

32
Q

What is the role of immunohistochemistry in cancer?

A

-used to characterize malignant tumors that are difficult to classify on histology
- add antibodies to bind diff filaments or proteins
- certain intermediate filaments in particular cell types

33
Q

How are serum tumor markers useful?

A
  1. screening (PSA for prostate)
  2. monitoring response to tx (after surgery or chemo)

-elevated levels in screening always requires a tissue biopsy for diagnosis

34
Q

What questions does tumor grading take into account?

A
  1. architectural and nuclear features
  2. is it well differentiated and resemble the parent tissue?
  3. Is it poorly differentiated and not resemble the parent tissue?
34
Q

What questions does tumor grading take into account?

A
  1. architectural and nuclear features
  2. is it well differentiated and resemble the parent tissue?
  3. Is it poorly differentiated and not resemble the parent tissue?
35
Q

Is staging or grade more important?

A

Staging is more important than grade and is the key prognostic factor
-determined after final resection of tumor

36
Q

Is staging or grade more important?

A

Staging is more important than grade and is the key prognostic factor
-determined after final resection of tumor

37
Q

What is TNM staging?

A

T = tumor size or depth of invasion
N = spread to regional lymph nodes (second most important prognostic factor)
M = metastasis (single most important prognostic factor)

38
Q

Cancer that looks like it’s forming glands

A

=adenocarcinoma

39
Q

Liposarcoma

A

Cancer

40
Q

Lipoma

A

benign tumor of fat

41
Q

leiomyoma

A

benign tumor of smooth muscle
=fibroids

42
Q

leiomyosarcoma

A

malignant tumor of smooth muscle

43
Q

melanoma

A

malignant - tumor of pigment forming cells (melanocytes)

44
Q

seminoma

A

tumor of germ cells (in testis)
-malignant

45
Q

hepatocellular carcinoma

A

benign

46
Q

Differentiation

A

How much tissues looks like its norm counterpart

ex w/ lieosarcomas

47
Q

anaplasia

A

Something that looks more primitive
-defined by pleomorphism and hyperchromatic (dark staining nuclei)

48
Q

Severe dysplasia vs carcinoma in situ

A

in situ - malignancy is contained and hasn’t invaded
-the two terms are the same but applied to diff organs

MCC (44 decks)

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