Cell growth and neoplasia Flashcards

1
Q

What is development?

A

From the perspective of the cell: dramatic changes in …

  • Cell proliferation
  • Cell death (apoptosis)
  • Cell differentiation
  • Cell migration
  • Cell-cell interactions
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2
Q

For an adult organism with normal homeostasis:

A

From the perspective of the organism:

•Cell regulation is a highly orchestrated, more static program resulting in optimal function of specialized tissues/ organs/ organ systems.

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3
Q

What are some examples of tissues constantly dividing?

What are quienscent tissues/cells?

What are examples of non-dividing cells?

A

Continuously dividing tissues/cells

**Mostly in S phase of cell cycle

–eg: skin, gut epithelium, hematopoietic system

–Constant turnover

Quiescent tissues/cells (normaly don’t proliferate but can under certain stimuli?

-Can be in S phase (dividing) or G<u>0</u> phase (non-dividing)

–eg: hepatocytes

–Normally little to no turnover

–Capacity for proliferation if needed

Non-dividing tissues/ cells

**mostly in GO (not dividing)

–eg: CNS neurons

–Little to no capacity for proliferation

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4
Q

Hypertrophy and hyperplasia:

What are they?

A
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5
Q

What are some physiologic examples of hypertrophy?

What are some pathologic examples of hypertrophy?

A

Examples:

–Physiologic: uterus in pregnancy (actually combination of hypertrophy AND hyperplasia)

–Pathologic: heart in hypertension (high blood pressure)

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6
Q

What is hyperplasia?

It may be associated with what?

What are some physiologic examples?

What are some pathologic examples?

A

-Increase in cell number

–Often driven by hormones/ growth factors

–May be associated with an increased risk of neoplasia

–Physiologic

–>mammary gland during puberty and pregnancy

–Pathologic:

–>endometrium (since it is constantly renewing itself).

•known risk factor for endometrial neoplasia

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7
Q

What is metaplasia?

What are some examples?

Give an example from columnar to squamous epithelium change?

A

Metaplasia

–Change from one benign, differentiated cell type to another, usually in response to injury (eg: inflammation)

–May be associated with an increased risk of neoplasia

•Examples:

–Bronchus

–>Columnar (Pseudostratified) of the mainsteam bronchus epithelium changes to squamous metaplasia in response to smoking.

  • cause: smoking
  • known risk factor for bronchopulmonary neoplasia (or squamous cancer cancer in the mainstem bronchus).

–Esophagus

  • squamous to columnar (glandular) metaplasia (“Barrett esophagus”)
  • cause: acid reflux (from the stomach into the distal esophagus)
  • known risk factor for esophageal neoplasia
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8
Q

Neoplasia

What is it?

What is it origin usually?

How is it different from tumor?

A
  • “new formation”
  • Progressive, unchecked increase in cell number (-/+ invasion/metastasis)
  • Clonal process
  • Generally pathologic and irreversible

“tumor”

Original meaning (latin) = swelling

In current usage, generally synonymous with neoplasm

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9
Q

Neoplasia, what are some global mechanistic hallmarks:

What cell’s autonomous mechanism are disrupted?

What non-autonomous mechanisms are altered?

A

Disruption of normal homeostatic mechanisms

Altered cell-autonomous mechanisms

  • Activation of oncogenes (induce cell proliferation)
  • inactivation of tumor suppressors (which normaly suppress cell division)

Cell-nonautonomous mechanisms

•Altered microenvironment

–surrounding tissue, including stroma, blood vessels, immune cells

•Altered macroenvironment

–Circulating cells (eg: immune cells) and factors (eg: hormones, cytokines)

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10
Q

Benign neoplasms

Malignant neoplasm, how is it different than benign neoplasms?

A

Do not invade or metastasize (unregulated proliferation of cells that does not invade or spread to other sites)

–Cause injury largely by compression/ interference in function of adjacent structures

Malignant neoplasms

Invade and metastasize to other sites

“CANCER”

–Cause injury both by local tissue destruction and distant dissemination and tissue destruction

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11
Q

What are some pathologic differences between benign and malignant neoplasia?

Which one is circumscrived or encapsulated?

Necrosis is common in which one?

A
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12
Q

Microscopic pathologic features

which one is well differentiated?

Which one has a high rate of cell turnover?

Which one show cytologic pleomorphism?

in which one is the boundary between tumor and adjacent tissue is maintained?

A
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13
Q

General classification: *don’t pay too much attention

A
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14
Q
A
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15
Q

For benign neoplasms:

What is a way to treat?

Does it reccur?

Does it progress to malignant neoplasm?

A
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16
Q

What are some non-genetic factors that may lead to cancer?

A

What are some genetic factors that may lead to cancer?

17
Q

Dysplasia

What are some histologic characteristics?

A
  • Disordered growth”
  • In epithelia, hallmark of early premalignant neoplasia
  • Characteristic histologic features

Loss of cytologic uniformity

Loss of normal histologic maturation

Loss of architectural orientation

•Usually assigned histologic “grade” (low versus high; marked/extensive dysplasia = “carcinoma in-situ”)

18
Q

Histologic grade:

Low grade means more or less resemblance to normal tissue?

What about high grade?

A

Degree of tumor histologic differentiation (ie: resemblance of normal tissue counterpart).

Low grade: more differentiation/ greater resemblance to normal

High grade: less differentiation/ resemblance to normal (poorly differentiated)

  • Grading schemes vary by tumor type
  • Some schemes also take into account mitotic activity and tumor architectural features (eg: extent of gland formation in an adenocarcinoma)
  • Can be predictive of biologic behavior (tumor dependent), but overall less reliable than disease stage
19
Q

Multistep pathway to breat cancer:

A

Colon cancer

20
Q

Most important parameter is disease STAGE

A
21
Q

What is special about pediatric neoplasms?

A