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Pathophysiology > cancer notes-- patho > Flashcards

cancer notes-- patho Flashcards

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1
Q

malignant growth

A

cancer cells invades adjacent tissues and travels in lymphatic system and bloodstream

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2
Q

benign growth

A

do not invade other tissues, more closely resemble cell of origin

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3
Q

etiology of cancer: genetic basis

A

cancer is a disease caused by a small number of mutations in a single cell

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4
Q

minimum number of mutations is ___ for cancer

A

2

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5
Q

carcinomas

A

tumors of epithelial origin

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6
Q

sarcomas

A

malignant cancers of bones, nerves, muscles

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7
Q

leukemias

A

malignant growths of WBC’s, only in blood

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8
Q

lymphomas

A

cancer of WBC’s and lymph tissue, usually start in lymph

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9
Q

adenocarcinomas

A

cancers of ductal or glandular tissue

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10
Q

tumor suppressor genes

A

inhibit tumor formation and cell proliferation, usually function to switch off cell division

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11
Q

there are ___ genes in each pair of tumor suppressor genes

A

2

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12
Q

one gene in each pair of tumor suppressor genes can be absent or damaged, loss of the second gene leads to ________ division.

A

uncontrollable

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13
Q

BRCA 1

A

chromosome 17; tumor suppressor gene that is autosomal dominant inheritance , 85% of women with mutation will develop breast cancer, also increased risk for ovarian cancer

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14
Q

BRCA 2

A

chromosome 13, accounts for 10-15% of all breast cancer cases

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15
Q

proto-oncogenes

A

normally act to turn on or maintain cell division

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15
Q

oncogenes

A

tumor causing genes that increase rate of cell proliferation

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16
Q

how do oncogenes increase the rate of cell proliferation?

A

they become permanently active or overproduce their products with mutations and disrupt intracellular communication pathways that regulate cell proliferation.

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17
Q

oncogene activation

A

virus or retirovirus, has a mutagenic effect= changes structure and function

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18
Q

cellular effects of oncogene

A

promote cell proliferation, growth factor, second messengers, abnormal gene transcription begins

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19
Q

caretaker genes

A

genes responsible for dna repair, mutation does not directly lead to tumor formation, increases mutation rate of all genes, does not lead directly to formation of cancer

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20
Q

pathogenesis of cancer

A

initiation– genetic mutation, carcinogen applied to cell. If no repair before cell division= cells are damaged

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21
Q

promotion

A

mutant cell induced to proliferate, reversible proliferation of altered initiated cells, promoting factors in proliferation

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22
Q

progression

A

cells acquire properties that allow mallignant behavior

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23
Q

progression properties

A

-increased growth rate and invasiveness of tumor
-tumors produce own growth factor
-lack contact inhibition
-able to metastasize

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24
metastasis
ability to spread to distant parts of the body, spread through blood or lymph pathways. Seeding is needed to kill all cells. Characteristics of primary site are retained
25
grading of cancer
microscopic anatomy (what cell looks like), number system is used
26
staging
location and pattern of spread
27
TNM classification
T describes the size of the tumor and any spread of cancer into nearby tissue; N describes spread of cancer to nearby lymph nodes; and M describes metastasis (spread of cancer to other parts of the body).
28
anatomical site classification--skin and glands
carcinomas
29
anatomical site classification-- connective tissue, muscle, bone, fat
sarcomas
30
warning signs of effect of cancer on host
change in bowel or bladder habits, a sore throat that does not heal, unusual bleeding or discharge from any body orifice, thickening or lump in breast or elsewhere, indigestion or difficulty swallowing, obvious change in a wart or mole, nagging cough or hoarseness
31
late signs of effect of cancer on host
pain, weight loss and weakness, bone marrow suppression (anemia, thrombocytopenia, leukopenia), loss of function of involved organ, obstruction, deficits in immune system competence
32
tumor markers are
produced by cancer cells, presence may indicate possibility of cancer
33
Carcinoembryonic antigen
CEA, colorectal or breast cancer
34
alpha-fetoprotein
testicular, liver cancer
35
human chorionic gonadotropin
HCG, testicular
36
prostatic specific antigen
PSA, prostate cancer
37
CA125
ovarian cancer
38
other tests used to diagnose cancer
X-ray, CT, ultrasound, MRI, PET, nuclear medicine studies, endoscopic exams
39
biopsy
definitive diagnosis test for cancer, only way to truly diagnose
40
surgery treatment for cancer
used to remove solid tumors
41
radiation treatment for cancer
kills cells that are not resectable due to location or that have escaped after surgery
42
immunotherapy treatment for cancer
boost immune system's ability to locate and destroy cancer cells
43
gene and molecular therapy
enhance tumor suppressor genes
44
risk factors for cancer
smoking, sunlight, alcohol, smokeless tobacco, estrogen, radiation, occupational hazards, high fat diet, obesity
45
common neoplastic disorders of bone marrow and lymphoid tissues
Lymphoma, plasma cell myeloma, leukemia
46
where is lymphoma located?
lymph nodes
47
where is plasma cell myeloma located, what is it?
malignant transformation of B-cell plasma cells, likes to form tumors on bony structures
48
where is leukemia located?
blood and bone marrow
49
Myeloid Neoplasms properties
myoproliferative (bone marrow makes too many RBC's)
50
Myeloid Neoplasms Cancers
Chronic Myeloid Leukemia, Acute Myeloid Leukemia, Polycythemia Vera, Essential Thrombocytopenia
51
Lymphoid Neoplasm properties
B cell neoplasm
52
Lymphoid Neoplasm Cancers
Chronic Lymphoid Leukemia, Acute Lymphoblastic Leukemia, Plasma Cell Myeloma, Hodgkin's Disease
53
Non-Hodgkin's Lymphoma properties
lymphomas of B cell, T cell and NK cell origin. Includes a large and diverse group of mallignancies
54
etiology of hematologic (myeloid and lymphoid) neoplasms
Exact cause of hematologic neoplasms is unknown. Basic mechanisms involve cell mutation that disrupts growth control & differentiation pathways.
55
Malignant Disorders of WBC's typical signs and symptoms
Malaise, weakness, Unexplained fever, night sweats, Recurrent infections, Lymphadenopathy with lymphoma & some leukemias, Very high total WBC count or the presence of abnormal cell types
56
leukopenia common clinical manifestations
lymphadenopathy, joint swelling and pain, weight loss, anorexia, hepatomegaly, splenomegaly
57
anemia common clinical manifestations
pallor, fatigue, malaise, shortness of breath, decreased activity tolerance
58
thrombocytopenia common clinical manifestations
platelet count below 20,000 cells/microliter, petechiae, easy bruising, bleeding gums, occult hematuria, retinal hemorrhages
59
neutropenia common clinical manifestations
absolute neutrophil count less than 500 cells per microliter, evaluation of peripheral blood sample is a key aspect of diagnosis. Definitive diagnosis is made after bone marrow aspiration or lymph node biopsy
60
Prevention and management of mallignant WBC disorders
bone marrow transplantation, peripheral stem cell transplantation, autologous transplantation, allogenic transplantation, graft vs. leukemia
61
bone marrow transplantation
transplantation of multipotent hematopoietic stem cells, usually derived from bone marrow, peripheral blood, or umbilical cord blood in order to replicate inside of a patient
62
peripheral stem cell transplantation
allows stem cells to be harvested from circulating bloodstream
63
autologous transplantation
stem cells from patient's own blood to be reinfused
64
allogenic transplantation
stem cells from closely matched relative
65
graft v. leukemia
transplanted cells in allograft that detect & kill leukemic cells.
66
myeloid neoplasms result from..
proliferation of an abnormal cell in bone marrow and overproduction of more than 1 cell type, offspring of abnormal cells build up and are released into bloodstream. Results in myoproliferative disease
67
chronic myeloid leukemia
myeloid neoplasm-- malignant granulocytes carrying Philadelphia chromosome
68
cml clinical presentation
high granulocyte count on CBC, splenomegaly
69
cml symptoms
fatigue, weight loss, sweats, bleeding, abdominal discomfort (enlarged spleen)
70
cml prognosis and treatment
does not respond well to chemo; poor overall survival time. untreated= median survival is 2 years, blast stage cml prognosis= 4 months
71
Acute Myeloid Leukemia
associated with transformation of myeloid stem cell, bone marrow aspirate must have greater than 20% blasts.
72
AML symptoms
bone pain, anemia, thrombocytopenia, increased infection succeptibility
73
AML common infection sites
skin, GI, GU, respiratory
74
AML prognosis
less than 50% and less than 30% of adults survive long term
75
chronic lymphoid leukemia symptoms
fatigue, weight loss, anorexia, increased susceptibility to infections
76
cll progression of cells
Malignant lymphocytes invade lymph tissues & bone marrow; disrupt function and cause enlarged, painless lymph nodes (lymphadenopathy) Enlarged spleen
77
cll prognosis and treatment
Certain genetic mutations present better/worse diagnosis. Chemotherapy used to induce remission. Stem cell transplantation to prolong remission.
78
acute lymphoblastic leukemia/lymphoma
Malignant transformation of lymphoblasts, 80% B-cells; 20%-T cells Lymphoblastic neoplasms: leukemia lymphoblastic lymphomas: same disease at a different stage
79
acute lymphoblastic leukemia/lymphoma symptom onset
abrupt; bone pain, bruising, fever, infection, loss of appetite, fatigue, abdominal pain, enlarged spleen, enlarged liver, enlarged lymph nodes
80
Plasma Cell Myeloma (multiple myeloma)
malignancy of mature, antibody-secreting b lymphocytes
81
plasma cell myeloma progression of cells
Malignant plasma cells invade bone & form multiple tumor sites; Bone destruction releases Ca+ into bloodstream (hypercalcemia). Pathologic fractures common.Excessive identical monoclonal antibodies made up of Bence Jones Proteins, accumulate in blood and urine.
82
diagnosis of plasma cell myeloma is based on:
Presence of Bence Jones protein Hypercalcemia Evidence of bone lesions. Bone marrow biopsy confirms diagnosis.
83
Hodgkin Disease
Malignant disorder of the lymph nodes
84
Hodgkin Disease cell progression
Malignant transformation of B cells in lymph nodes called Reed- Sternberg cells Grow/spread predictable, usually metastasizes along lymphatic pathways. Sets HD apart from other lymphomas
85
Hodgkin Disease (Hodgkin's Lymphoma) clinical manifestations
Early stages: often asymptomatic Painless lymphadenopathy; possibly with fever, night sweats, pruritus, weight loss, malaise. Lymph node enlargement above diaphragm, cervical nodes most common site.
86
hodgkin's disease prognosis and treatment
Localized tumors: radiation therapy (most common) Disseminated disease: chemotherapy
87
Non-Hodgkin's Lymphomqa (B cell, T cell and NK cell lymphoma)
DO NOT HAVE REED STERNBERG CELLS, majority arise in lymph nodes, tumor cells derived from one single mutant precursor cell
88
non-hodgkins lymphoma symptoms
Painless lymphadenopathy, fever, night sweats, weight loss, malaise, pruritus
89
combination therapy type of treatment
primary
90
stem cell transplant type of treatment
primary

Pathophysiology (6 decks)

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