N339 Exam 1 Flashcards
(128 cards)
1
Q
Neoplasia
A
new growth (tumor)
2
Q
Neoplasm
A
malignant growth (cancer)
3
Q
______ is the 2nd leading cause of death in the US
A
Cancer
4
Q
What are the top 3 new cancer types and leading causes of death (cancer types) in men and women?
A
Men: Protstate, lung/bronchus, colon/rectal
Women: Breast, lung/bronchus, colon/rectal
5
Q
Anaplasia
A
cells don’t differentiate
6
Q
Do daughter cells normally become more or less differentiated with each division?
A
daughter cells have less potential for differentiation
Each division of daughter cells becomes more specialized to that of adult tissue.
7
Q
Do benign cells have an increased or decreased rate of division (mitosis)?
A
Benign cells have few mitosis (low rate of cell div, ie grow slower.
8
Q
Do malignant cells have an increased or decreased rate of division?
A
increased rate, grow quickly.
9
Q
What characteristic allows malignant cells to metasticize?
A
lack of cell adhesion
10
Q
What is the difference b/w metastasis and infiltration?
A
metastasis-tumor sheds cells that leave originating organ and travel via lymph or vasc and invade new site.
infiltration-crablike extensions that indicate cancer w/in primary site of origin.
11
Q
Are benign tumors are strictly localized. How do they remain at their primary site of origin?
A
The body is able to wall off benign tumors by activating fibroblasts that encapusulate the tumor.
12
Q
Would you expect benign tissue/tumors to become necrotic? why or why not?
A
benign tissues grow so slowly that they become vascularized so don’t become necrotic vs malig grow so quick that they have necrotic core.
13
Q
Angiogenesis
A
New blood vessels form from pre-existing vessels.
14
Q
Is recurrence common after focalized treatment with benign tumors? with malignant?
A
Rare with benign
comml with malignant
15
Q
Compare the histology of benign vs malignant tumors.
A
benign: typical of tissue of origin, few mitoses
malignant: anaplastic with abnormal cell size and shape, many mitoses
16
Q
Compare the growth rate of benign vs malignant tumors.
A
benign: slow
malignant: rapid
17
Q
Compare the localization/metastasis of benign vs. malignant tumors
A
benign: striclty local, often encapsulated, no metastases
malignant: infiltrative/ frequent metastases
18
Q
Is tumor necrosis common or rare with benign vs maliganant tumors?
A
benign: rare
malignant: common
19
Q
If tumor type ends in “oma” is it benign or malignant? what are the exceptions?
A
Oma: benign with exceptions:
carcinoma and sarcoma = cancer
Melanoma, lymphoma, hepatoma, leukemia, myeloma
20
Q
What does the word “blast” indicate?
A
Daughter cell mutation
21
Q
“1/3 of all cancer deaths are related to ______”
A
environment
22
Q
Do the following increase or decrease cancer risk: and how?
- Tobacco Use
- Nutrition (fat, fiber, alcohol, antioxidants)
- Age
A
- tobacco bad: tars and nicotine cause genetic damage, 2nd hand smoke kills
- nutrition: Obese people have greater risk for cancer. Corr b/w obesity and cancer risk.
- Fiber is good. Enhances peristalsis and removal of toxins.
- Fat bad. assoc w/ lipoproteins, cholesterol etc.
- alcohol bad. Corr w/ hepatoma.
- antioxidants good. Limit amount of DNA damage by free radicals. spinach & blueberries!
- Age: longer we live, greater chance for mutation. Repair mechanisms and self destruction mechs slow. Ex. white cells decrease w/age (NK and leukocytes).
23
Q
The risk of developing cancer increases with age. It is estimated that ___ have almost a 1 in 2 lifetime chance of developing cancer, whereas ____ have a little more than a 1 in 3 chance
A
men, women
24
Q
Oncogenesis
A
process of tumor formation
25
Proto-oncogenes
normal genes that can mutate to form oncogenes Examples: Growth factors, cytoplasmic signaling pathways that govern cellular metabolism; transcription factors;
26
When proto-onc mutates it becomes an _______ or ______ gene.
oncogene or cancerous
27
Why factors contribute to proto -oncogene mutation?
1: oncogenic viruses
2: mutagenic event (Ex radiation exposure, cigarette smoke, UV light)
3: mutation of regulatory pathways
4: amplification of proto-oncogenes
28
What do Tumor suppressor genes do?
either repair DNA mutation or if can’t repair, then trigger apoptosis (programmed cell death).
29
What are angiogenic factors?
cytokines that flow thru interstit fluid to Blood vessels causing endothelial cells to undergo growth. Endothelial cells then grow new vessels that follow path of cytokine back to tumor to supply blood/nutrients.
30
If a mutation occurs in a daughter cell that has differentiated close to the normal functioning parent cell, what type of neoplasm has occurred?
well differentiatied, low malignancy
| termed "low degree of malignancy"
31
If a mutation occurs in a daughter cell that hasnt differentiated close to that of the normal functioning parent cell, what type of neoplasm has occurred?
moderatley differentiated, moderate malignancy
32
If a mutation occurs in a daughter cell very early in differentiation or lacks differentiation, what type of neoplasm has occurred?
poorly differentiated, highly malig neoplasm
33
what is the relationship between differentiation, mutational and malignancy?
Inverse relationship: mutation occuring earlier in differentiation results in the highest the degree of malignancy
34
If a cell with normal P53 gene has DNA damage, what function does P53 perform?
P53 is a tumor suppressor gene. P53 will initiate cell cycle arrest, repair of the gene and if repair doesn't work, P53 will activate genes responsible for celluar apoptosis.
35
In a cell lacking P53 or damaged P53 gene, what happens when gene mutation occurs?
no cell cycle arrest or repair, and no activation of apoptotic genes results in malignant tumor growth.
36
What are the 3 steps of Carcinogenesis?
Initiation
Promotion
Progression
37
What occurs during the initiation phase of carcinogenesis?
initiation: where the mutation occurs.
| genetic mutations that inappropriately activate proto oncogens and inactivate tumor suppressor genes.
38
What occurs during the Promotion phase of carcinogenesis?
Mutant cells proliferate, possibly due to activation of another oncogene or inactivation of a tumor suppressor gene
39
What occurs during the Progression phase of Carcinogenesis?
Mutant, proliferating cells begin to exhibit malignant behavior (ie development of the cancerous phenotype)
40
Cancer is thought to develop when _______ become inappropriately activated in a cell or when ________ become inactivated. This change in gene function is usually due to _______ in the cell’s DNA.
proto-oncogenes
tumor suppressor gene
mutations
41
Mutant proto-oncogenes disrupt the intercellular communication pathway that normally regulates cell proliferation. This disruption may occur through abnormal production of what? (4)
growth factors
receptors
cytoplasmic signaling molecules
nuclear transcription factors.
42
Both copies of a tumor suppressor gene usually must be _______ to eliminate its function. ____________ inhibit cellular proliferation in various ways. The _____ serves as a “master brake” on cell proliferation by inhibiting transcription factors. ____ inhibits cell cycling when the cell is damaged to allow time for DNA repair. P53 is also important in initiating _______ (programmed cell death) of damaged or unwanted cells.
```
inactivated
Tumor suppressor genes
Rb protein
P53
apoptosis
```
43
What are two types of carcinogenic agents?
Radiation and Oncogenic Viruses
44
What are two types of Radiation? provide examples.
```
Ionizing: contact w/ atomic bomb; assoc with leukemia; people that survived hiroshima had 30 fold increase in leukemia
UV radiation (sunlight): tanning
```
45
Name 5 types of oncogenic viruses
1. HPV- cervical carcinoma
2. EBV- mono; in Africa EBV gives rise to Burkitts lymph (kids disease)
3. HEP C and HBV: cause loss of hepatocytes, regenerate and more mitotic divisions lead to mutation
4. HTLV-1 causes adult T cell leuk-lymph leuk occurs in blood system; lymphoma in lymph organs
5. HIV causes Kaposi sarcoma; malignant
46
Name 5 chemical and/or environmental agents known to be carcinogenic to people (include what organ they affect).
1. Cigarette smoke- polycyclic hydrocarbons (lungs)
2. Asbestos- carcinogen causes mesothelioma in lungs; huge time lapse can occur b/w initiation and progression.
3. Carbon tetrachloride- Mothballs
4. insecticides, fungicides
5. Smoked Foods- gastro and intestines
47
Full expression of cancer in a host is a multistep process. These steps have been described as ____, _____ and _______. The initiating event is usually from genetic _____ . Promotion refers to the stage in which the mutant cell is induced to ______. Progression is the stage during which the mutant, proliferating cells acquire properties that allow malignant ______.
initiation, promotion, and progression
mutations
proliferate
behavior
48
Identify 4 tumor markers.
PSA: rapid rise in PSA may be flag for prostate cancer
Thyroglobulin: hormone assoc w/ thyroid carcinoma increase in TG red flag for thyroid carcinoma.
Neuron-specific enolase: assoc with small cell carcinoma of lungs or neuroblastoma.
Monoclonal Ig- indicative of M. myeloma (cancer of B cells causes holes in bones)
49
Malignant cells produce specialized enzymes and receptors to enable them to escape their tissue of origin and ______ . The spread of tumors generally occurs by way of the ______ or ______.
metastasize
bloodstream
lymphatic vessels.
50
Tumor cells often lodge in the ________ of the organs that drain them, such as liver and lung. Some tumors appear to be directed to certain tissues.
capillary beds
51
___________ is the process by which tumors stimulate the growth of ________ to support the growth of the tumor. Tumors cannot grow larger than __ mm in diameter unless they grow blood vessels into the tumor to provide __________.
```
angiogenesis
Angiogenesis
blood vessels
2
oxygen and nutrients.
```
52
Chemotaxis
chemical giving cell direction in which to move. when cancer cells leave vasculature, form antigen bond, triggers digestive enzymes which allow release and exit of cells to vasculature and other tissue. Ex. Breast ca secondary metastasis to spine
53
What are the 6 main effects on the body from Cancer?
```
Pain
Cachexia
Deficits in Immune System Competence.
Bone marrow suppression
Paraneoplastic syndromes
Hair loss due to radiation and chemotherapy
```
54
Cachexia (w/ cancer)
overall weight loss and general weakness. Loss of appetite causes weight loss, also feeding rapidly growing tumor w/ high caloric intake.
55
what is bone marrow suppression with regard to cancer?
cancer cells crowd out normal cells in BM killing normal marrow cells. Chemo also kills BM cells (highly mitotic). Leucopenia, thrombocytopenia (decrease in platelets), anemia occur.
56
Define Parandeoplastic syndromes.
inappropriate secretion of hormone-like substances by tumor
57
What are the 3 types of cells killed by Chemo treatment?
hair follicles, Bone Marrow cells, epithelial cells.
58
Name 5 types of cancer therapy and indicate whether they are local/focal or systemic treatments.
Surgery (local/focal). Ex: removal of tumor or biopsy of mass
Chemotherapy (systemic) or Radiation Therapy (focal/local or systemic with TBI)
Immunotherapy
Gene and Molecular Therapy
Stem Cell Transplantation
59
What does radiation therapy target?
rapidly growing or cycling cells.
60
Name 3 types of immunotherapy.
interferons: inhibit cell proliferation
interleukins: stimulate production of immune cells “leuk= white”
monoclonal Ab- target cancer cells for treatment and identify target cells for attack of immune defense cells.
61
What is Gene or Molecular Therapy?
Genetic alteration of tumor cells to make them more susceptible to cytotoxic agents or immune recognition ie
inserting specific type of gene into tumor cell DNA. Offspring of cells will have the gene. #1 gene for inserting is P53 (repair gene or apoptosis)
or
alteration of immune cells to make them more efficient killers of tumor cells.
62
When are stem cell transplants needed?
Often used when bone marrow function has been impaired by high-dose chemotherapy or whole-body irradiation
63
_____ of cancer while it remains localized is associated with the best prognosis for cure. The overall 5-year survival rate for patients with cancer is about __%.
Early detection
| 66%
64
The mainstays of cancer therapy are _____, ______ and ____ . Surgery and radiation therapy are effective for cancers that are ______. Chemotherapy is usually the treatment of choice for cancers known or suspected to be ________ in the body.
surgery, radiation therapy, and chemotherapy
localized
disseminated
65
Cells that _____ are the most susceptible to damage from radiation therapy or chemotherapy. However, in addition to cancer cells, ______ may be killed. Cells of the bone marrow,______ and _______ are particularly susceptible.
divide rapidly
rapidly dividing normal cells
hair follicles, and gastrointestinal mucosa
66
______ has the potential to specifically target cancer cells. At present, _______, _______ and ______ are being used to boost the immune system’s ability to locate and destroy cancer cells.
Immunotherapy
| interferon, IL-2, and monoclonal antibodies
67
________ may be used to alter cancer cells to suppress oncogenes, enhance tumor suppressor genes, make tumor cells more susceptible to cytotoxic agents, or interfere with the function of cancer gene products.
Gene and molecular therapy
68
Transplantation of _______ is an important adjunct to cancer therapy that provides a method to restore bone marrow function after ________.
hematopoietic stem cells
| high-dose irradiation or chemotherapy
69
1. What are the major organs and cellular components of the body’s defense against foreign antigens?
Skin and mucous membranes—monocytes and macrophages
Bone marrow—B lymphocytes and leukocytes
Thymus—T lymphocytes
Tonsils, spleen, and lymph nodes—B and T lymphocytes
Peyer patches – primarily B lymphocytes
70
How do immune cells communicate through cell-to-cell interactions and through secreted cytokines?
Antigen-presenting cells bind to T cells which stimulate intracellular signaling pathways in the B cell and helper T cell that promote clonal expansion and differentiation. Activation of the helper T cell causes release of cytokines, which is required for B cells to proliferate and begin antibody synthesis.
71
How do innate and adaptive immune mechanisms differ?
Innate immune mechanisms do not require any previous exposure to mount an effective response against an antigen, and a wide variety of different antigens are recognized.
Adaptive, or specific, immune mechanisms respond more effectively on second exposure to an antigen, and are highly restricted in the ability to recognize antigens
72
How do macrophages, granulocytes, and lymphocytes work together to locate, recognize, and eliminate pathogens?
Macrophages and dendritic cells are commonly the first immune cells to encounter the antigen; they engulf and display the antigen on their cell surface; macrophages secrete cytokines that stimulate white blood cell (WBC) production and help WBCs locate the area. T helper cells are activated by these antigen-presenting cells and secrete cytokines that stimulate the production of WBCs in the marrow, initiate proliferation of mature B and T cells, and stimulate the phagocytic potential of macrophages and neutrophils. T cells also assist in B cell proliferation and antibody secretion
73
How do noncellular immune system components, including antibodies, complement, and clotting factors, aid the immune response?
Antibodies bind to particular antigens and function in precipitation, agglutination, neutralization, opsonization, and complement activation. Complement activation results in inflammation and formation of membrane attack complexes that directly lyse cellular antigens. Tissue injury from the infectious process activates the coagulation cascade which forms a fibrin meshwork to help entrap and localize the agent. The kinin system is also activated, which promotes vasodilation to increase blood flow to the area
74
Name two type of inflammation.
Acute
| Chronic
75
What are 3 activities that occur during acute inflammation?
1. Increased Vascular Permeability
2. Emigration of Leukocytes, principally neutrophils
3. Phagocytosis
76
What are 3 activities that occur during chronic inflammation?
1. Macrophages and lymphocytes predominate
2. Granulomatous Inflammation (formation of granulomas)
Ex. Mycobacterium tuberculosis
77
Which leukocyte is the 1st to appear with acute inflammation? what is this cells role?
Neutrophil; phagocytosis
78
Is a monocyte found in blood or tissues? same for macrophage? What is the purpose of these two cell types?
monocyte: found in blood. becomes a
macrophage when in tissues.
Phagocytosis
79
Does a macrophage found in tissue indicate acute or chronic inflammation?
chronic
80
What type of leukocyte is associated with parasitic infections?
eosinophils, allergic reaction
81
Which leukocyte contains histamine granules and is associated with allergic response?
Basophils
82
What role do lymphocytes play in inflammation?
immune reponse
83
What are the two stages of inflammation?
1. Vascular
| 2. Cellular
84
What two key events occur during the vascular stage (1st stage) of inflammation?
1. dilation of vessels (vasc dilation) and
| 2. permeability
85
How do fenestrations play a role in the vascular stage of inflammation?
all vessels w/ exception of cerebral have fenestrated arteries (slit-like pores) in vessels, facilitate:
1. immigration of leukocytes
2. WBC mvmt and exudate out of vessels.
When fenestrations enlarge (as with vasodilation) increased permeability results. increased dilation and permeability = stage 1.
86
What are the key events that occur during the cellular stage of inflammation?
1. primarily neutrophil immigration.
2. If neutrophils dont recognize pathogen, macrophages or lymphocytes predominate.
Ex. Tb bacteria: surrounds itself w/ waxy coating that prevents dehydration of the bact. Also hides receptors preventing phagocytosis. waxy coat attracts macrophages which ISOLATE the bact. Lymphocytes then surround macroph. Bact isn’t dead at this step, just dormant b/c of surrounding macroph/lymphocyte combo called a GRANULOMA (path surrounded by concentric layers of macroph and lymphocytes).
87
What happens if a pathogens antigens aren't identified by neutrophils during the primary neutrophil immigration step of the cellular stage?
phagocytosis can't occur and infection.
88
If infection takes hold for weeks, months or years is it acute or chronic?
chronic
89
What are the 3 key steps of inflammation?
1. protective response (neutralizes and destroys invading and harmful pathogens by neutrophils).
2. Limits the spread of harmful agents to other areas.
3. Activate the healing process
90
What is the duration of an Acute Inflammatory Response?
depends on frame of reference, has a short duration < two wks.
91
What are 3 types of Alterations in Immune Function?
1. Autoimmunity
2. Hypersensitivity Reactions
3. Immunodeficiency Disorders
92
What are the cardinal signs of inflammation?
Pain
Heat
Redness
Swelling
93
Describe the pathway from tissue damage to cardinal signs of inflammation.
1. tissue damage
2. triggers release of vasoactive and chemotactic factors which trigger
3. PAIN, Vasodilation, increased permeabliity and neutrophil emigration
4 causing: heat, redness and swelling
94
how does increased permeability cause swelling?
allows outflow of exudate
95
What are the 3 chemical mediators of inflammation? what does each one cause?
1. Endothelial binding of neutrophils and macrophages causes emigration of neutrophils & macrophages to tissue (RECRUITMENT)
2. Vasoactive Chemicals causes vasodilation
3. Chemokines causes vasodilation.
All contribute to phagocytosis
96
What is a chemokine?
chemicals that communicate from cell-cell, also can be chemotactic substances.
97
What action can chemical mediators of acute inflammation produce?
1. Vasodilation
2. Increased Permeability (immediate or sustained)
3. Chemotaxis
4. Opsonin
5. Pain
98
How do histamine and Serotonin act as chemical mediators?
Both cause:
vasodilation
increased permeability (immediate)
bronchial constriction (smooth muscle contraction)
99
What cells produce histamine and serotonin?
Mast cells and Basophils
100
How does bradykinin act as a chemical mediator?
Same as histamine and serotonin:
1. very potent vasodilator
2. increases permeability (immediate)
3. bronchial constriction (smooth muscle constriction only difference: bradykinin are plasma proteins that is synthesized in the liver. So w/ inflamm response, liver is triggered to increase production of bradykinin.
101
How is the liver involved in inflammatory response?
1. liver increases synthesis of bradykinin (plasma proteins)
| 2. Complement is also synthesized in the liver
102
What function does complement have as a chemical mediator?
1. facilitates phagocytosis
| 2. involved in chemotaxis
103
what function do prostaglandins provide as chemical mediators?
1. induce vasodilation and
2. bronchoconstriction
3. inhibits inflammatory cell function
104
How do lysosomal proeases contribute as chemical mediators during inflammatin?
enzyme break down cell walls and along with free radicals are released by neutrophils to destroy pathogen.
105
Why are lysosoamal enzymes considered a double edge sword?
Double edged sword: if crazy inflamm response, lysosomal protease isn’t tissue specific (will destroy surrounding normal tissues).
106
How do leukotrienes act as chemical mediators?
increased permeability (immediate)
bronchial constriction (smooth muscle
contraction)
chemotaxis
107
When tissue is injured, a number of cell membranes are destroyed and inflammatory mediators including ________ and _______ are released (also released by neutrophils and endothelial cells).
leukotrienes and protoglandins
108
In the arachidonic acid pathway following tissue damage, what two pathways are triggered?
Lipoxygenase and Cyclooxygenase
109
What chemical mediator is triggered in the lipoxygenase pathway and what function does the mediator perform?
leukotrienes
increase microvascular permeability
induce smooth muscle contraction
constrict pulmonary airways
110
What chemical mediators are triggered in the cyclooxygenase pathway and what fxn to they perform?
1. Prostaglandins: induce vasodilation, bronchole constriction and inhibit inflammatory cell fxn.
2. Thromboxane: vasoconstriction, bronchoconstriction, promotes platelet fxn.
111
When prostaglandins are producted in the cycloxygenase pathway, they induce _____, inhibit ______ cell function to restrict _______.
vasodilation
inflammatory
swelling
112
When thromboxane is produced in the cyclooxygenase pathway, it causes vasoconstrcition, _______ and promotion of _________ function to repair _______ tisssue and stop _________.
bronchoconst,
platelet
damaged
bleeding
113
What would corticosteroids do to the arachidonic acid pathway?
Shut down the whole system: Lipoxygenase and cyclooxygenase pathway would not occur. No leukotrienes, prostoglandins or thrombaxanes would be triggered).
114
What would Aspirin or NSAIDs do to the arachidonic acid pathway?
shut down the cyclooxygenase pathway (ie. no prostoglandins or thromboxanes will be triggered).
115
What are the 4 steps of inflammation at the cellular stage?
0. Bacterial infection elicits response from endothelium. Endothelial cells release chemokines to communicate with neutrophils.
1. margination
2. emigration
3. chemotaxis
4. phagocytosis
116
Describe margination (part of cellular stage of inflammation).
neutrophils draw to wall of vessel or margin (pavementing) b/c of chemokines expression from endothelial cells. Vasodilation and increased permeability
117
Describe emigration (part of cellular stage of inflammation)
2. Emigration: pseudopodia move Neutrophil thru fenestration, pull themselves thru vessel wall
118
Describe chemotaxis (part of cellular stage of inflammation)
3. once neutrophil in tissue, have to find bacteria; bact give off surface mlcls during mvmt that are chemotactic. Mlcls from bact flow thru interstit fluid away from source. Neutrophil receptors stick to bact mlcl, triggers pseudopodia to pull toward mlcls and keep moving toward the bacteria. Eventually, get to bact. and phagocytize it.
119
Describe phagocytosis (stage of cellular stage of inflammation)
4. Phagocytosis: once neutrophils binds w/ bacteria
120
Name 4 types of inflammatory exudate
1. Serous
2. Fibrinous
3. Purulent
4. Hemorrhagic
121
What are 3 functions of exudate with the inflammatory response?
1. Promotes flow of Antibodies into tissue and helps emigration of leukocytes out of vessels and into tissue
2. Causes dilution of toxins and irritating substances (chemicals released from inflammatory cells and toxins from bacteria).
3. Transport of nutrients for repair
122
What is Serous exudate and at what stage of inflammation does it occur?
small amt of clear fluid that occurs with mild inflammation
123
What type of exudate is serosanguineous drainage and what does it indicate?
serous exudate tinged w/ blood due to capillary injury.
124
What is fibrinous exudate and what stage of inflammation does it occur at? What can it lead to?
-associated with a greater amount of inflammation
| Increased permeability leads to leakage of large protein molecules.
125
What can happen when fibrinogen leaks in to tissues from blood vessels with inflammation?
scar formation from fibrous build-up
126
What is purulent exudate and what stage of inflammation does it occur at?
Pus associated with severe inflammation possibly from a bacterial infection.
127
What color is purulent discharge?
yellow
128
What is hemorrhagic exudate and what stage of inflammation does it occur at?
occurs with severe leakage from the blood do to tissue damage that causes vessel necrosis. Associated with the most severe stage of inflammation.
