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Pathophysiology > Chapter 7: Neoplasia > Flashcards

Chapter 7: Neoplasia Flashcards

1
Q

Benign Tumor Histology

A

Typical of tissue of origin and few mitoses

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2
Q

Benign Tumor Growth Rate

A

Slow

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3
Q

Benign Tumor Localization

A

Strictly local, often encapsulated/ no metasis

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4
Q

Benign Tumor Necrosis

A

Rare

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5
Q

Benign Tumor Recurrence after treatment

A

Rare

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6
Q

Benign Tumor Prognosis

A

Good, unless in critical area

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7
Q

Malignant Tumor Histology

A

Anaplastic, with abnormal cell size and shape mitoses, many mitoses

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8
Q

Malignant Tumor Growth Rate

A

Rapid

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9
Q

Malignant Tumor Localization/Metasis

A

Infiltrative/ frequent metases

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10
Q

Malignant Tumor Necrosis

A

Common

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11
Q

Malignant Tumor Reccurence after treatment

A

common

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12
Q

Malignant Tumor Prognosis

A

Poor if untreated

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13
Q

What is the purpose of grading and staging Tumors?

A

To predict clinical behavior of malignant tumor and guide therapeutic management

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14
Q

Grading (histological evaluation)

A

Anaplasia - lack of the degree of cell differentiation
Grade: 0-4

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15
Q

What is the grade of a benign tumor?

A

Grade 1-2

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16
Q

What is the grade for malignant tumors?

A

Grade 3-4

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17
Q

Staging (Clinical evaluation)

A

T (tumor size): 0-5
N (lymph node): 0-2
M (Metasis): 0-2

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18
Q

Examples of tumors that use different staging systems

A

Leukemia and Kidney tumor

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19
Q

Degree of Anaplasia

A

Greater degree of anaplasia, greater degree of grade, low degree of differentiation, and greater degree of aggressive malignancy = greater degree of malignant potential

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20
Q

What terminology indicates malignant tumors?

A

-carcinoma, and -sarcoma

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21
Q

Carcinoma

A

epithelial origin (adenocarcinoma)

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22
Q

Sarcoma

A

Mesenchymal (nerve, bone, muscle) origin

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23
Q

Leukemia

A

White blood cells

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24
Q

Carcinogen (external factors)

A

Potential cancer-causing agent

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25
Q

Oncogene (internal factors)

A

Proto-oncogene which enhances growth-producing pathways

26
Q

Tumor Suppressor Gene (Internal Factors)

A

Inhibits Cell Proliferation. Cancers may arise when tumor suppressor gene function is lost or abnormally inhibited

27
Q

Proto-Oncogenes

A

Normal Cellular genes that can be transformed into oncogenes by activating (gain of function) mutations
- Overactivation
- Overpdocution

28
Q

Gain of function mutations code for

A

Growth factors, receptors, cytoplasmic signaling molecules, and nuclear transcription factors

29
Q

When do proto-oncogenes become activated oncogenes?

A

When mutations alter their activity so that proliferation-promoting signals are generated inappropriately

30
Q

Retrovirus

A

One of the mechanisms to turn proto-oncogene to oncogene with overactivity

31
Q

Examples of retroviruses

A

HIV (Kaposi’s sarcoma)
Epstein-Barr Virus (Burkitt Lymphoma)
Human T-lymphocyte virus type 1 (Adult T-cell leukemia/lymphoma)
Hepatitis B (DNA virus, but not retrovirus)
Hepatitis C

32
Q

Tumor-Suppressor Genes

A

Contribute to cancer only when not present (Loss of functions). It also stops cell cycle for reparment.

33
Q

Autosomal Recessive

A

Both copies of tumor suppressor genes are inactivated when cancer develops

34
Q

What happens where there is a defective copy of tumor suppressor gene?

A

There’s a much higher risk for cancer development

35
Q

Rb Gene

A

“Master Brake” for the cell cycle. It blocks/stops cell division. It binds to transcription factors to inhibit cell entering cell cycle. Inhibits these factors from transcribing genes that initiate cell cycle (before entering cell cycle).

36
Q

p53 Gene

A

Most common tumor-suppressor gene defect identified in cancer cells. More than 1/2 of all types of human tumors lack functional p53. Normally, inhibits cell cycling and accumulates only after cellular damage, binds to damaged DNA and stalls division to allow DNA to repair itself. May direct cell to initiate apoptosis.

37
Q

BRCA1 and BRCA2 Genes

A

Associated with breast cancer

38
Q

Tumor Metastasis

A

Process by which cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites. Cancer cells generally spread via circulatory or lymphatic systems.

39
Q

Effects of Cancer on the Body

A

Pain, Cachexia, Immune System Deficits, and other effects

40
Q

Cachexia

A

Overall weight loss and generalized weakness due to the fact that rapidly growing cancer cells demand o2 and nutrients, loss of appetite, increased metabolic rate, and nausea

41
Q

Immune system Deficits

A

Suppressed by cancer cell secretions, cancers can also elude detection, and bone marrow suppression

42
Q

Bone Marrow Suppression

A

Contributes to anemia, leukopenia, and thombocytopenia. Due to invasion and destruction of bone marrow cells, poor nutrition, and chemotherapy. Can all be managed by blood replacement theraphy.

43
Q

Anemia

A

Deficiency in circulating red blood cells( Male: HGB<13 mg/dl; female: <12 mg/dl)

44
Q

What are the clinical manifestations of Anemia?

A

Pallor, fatigue, malaise, shortness of breath, and decreased activity tolerance

45
Q

Leukopenia

A

Deficiency in circulating white blood cells due to malignant invasion of bone marrow, malnutrition, and chemotherapy

46
Q

Clinical Manifestations of Leukopenia

A

Lymphadenopathy, joint swelling and pain, weight loss, anorexia, hepatomegaly, splenomegaly

47
Q

Neutropenia

A

Definitive diagnosis is made after bone marrow aspiration or lymph node biopsy. Absolute neutrophil count <500 cells/microL(normal range is 1,500-8,000).

48
Q

Thrombocytopenia

A

Deficiency in circulating platelets. Predispose to life-threatening hemorrhage if count is below 200,000.

49
Q

Clinical Manifestations of Thrombocytopenia

A

Petechiae, easy bruising, bleeding gums, occult hematuria, and retinal hemorrhages

50
Q

Hair Loss and Sloughing of mucosal membranes

A

Complications of chemotherapy and radiation therapy

51
Q

Paraneoplastic Syndromes

A

Tumor production of hormones or cytokines

52
Q

Examples of Paraneoplastic Syndromes

A

Hypercalcemia, Cushing syndrome secondary to ACTH secretion, Hyponatremia and water overload secondary to excess ADH secretion

53
Q

Types of Cancer Therapy

A

Surgical procedure, radiation therapy, drug therapy/chemotherapy, immunotherapy, targeted molecular therapy, stem cell transplantation and bone marrow transplantation

54
Q

Radiation Therapy

A

Kills tumor cells by damaging nuclear DNA(radiolysis). Initiates Apoptosis for the cells. Side effects are bone necrosis and bone marrow suppression.

55
Q

Drug Therapy/Chemotherapy

A

Systemic administration of anticancer chemicals to treat cancers known or suspected to be disseminated in the body. Most drugs are cytotoxic. Most effective on rapidly dividing cells. A side effect is bone marrow suppression.

56
Q

What are used in Immunotherapy?

A

Interferons, interleukins, and monoclonal antibodies

57
Q

Interferons

A

Glycoproteins produced by immune cells in response to viral infection

58
Q

Interleukins

A

Peptides produced and secreted by white blood cells. Also called lymphokines and cyotkines.

59
Q

Monoclonal Antibodies

A

Antibodies with identical structure that bind with specific target antigens

60
Q

Stem Cell Transplantation

A

Provides a method to restore bone marrow function after high-dose irradiation or chemotherapy. Used in malignant and nonmalignant disorders. Used to manage life-threatening disorders in which patient’s bone marrow cannot manufacture WBC, RBC, or platelets.

Pathophysiology (4 decks)

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