Unit 2 Flashcards

1
Q

What is the sequence from DNA to Protein?

A

Replication, transcription, and translation

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2
Q

What is DNA replication?

A

DNA is separated (unzipped) and two new strands are formed using each previous strand to create 2 exact copies

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3
Q

What is transcription?

A

DNA to RNA; mRNA

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4
Q

What is translation?

A

RNA to a protein; tRNA

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5
Q

Define retrovirus

A

Viruses that use RNA as their genetic material and carry code for enzyme reverse transcriptase; converts RNA to DNA

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6
Q

Define gene polymorphism

A

Change in the sequence of DNA which then results in a change in the sequence of mRNA

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7
Q

What is a silent mutation?

A

A mutation that doesn’t change the primary protein sequence

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8
Q

Define Mutations

A

Any inherited alteration of genetic material; noticeable changes in the organism

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9
Q

What is an example of a favorable mutation?

A

Sickle Cell Anemia in Africa; protects against malaria

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10
Q

List the 3 types

A

Point mutations, frameshift mutations, and base-pair substitution

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11
Q

What is a point mutation?

A

A mutation that doesn’t change the reading frame; change only one single base

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12
Q

Can point mutations be silent?

A

Yes they don’t always change the protein sequence; silent mutation

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13
Q

What happens when the protein sequence is changed in a point mutation?

A

Missense mutation or nonsense mutation

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14
Q

What is a missense mutation?

A

Changing of one base changes one amino acid to another

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15
Q

What is nonsense mutation?

A

Changing of one base changes the codon from an amino acid to a stop codon resulting in a short protein

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16
Q

What is a frameshift mutation?

A

Insert or delete one or more base pairs in the reading frame shifting everything

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17
Q

Can frameshift mutations be silent?

A

No

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18
Q

What is a base-pair substitution?

A

One base pair is replaced by another

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19
Q

Can a base-pair substation be silent?

A

Yes if the substitution does not change the amino acid; silent substitution

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20
Q

What is a mutagen?

A

Agents that are known to increase the frequency of mutations

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21
Q

Give some examples of mutagens

A

Ionizing radiation, chemical agents, UV radiation, viruses

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22
Q

What is a mutational hot spot?

A

Some regions of the DNA that are weak and often mutated

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23
Q

What is a karyotype?

A

An ordered display of chromosomes from largest to smallest; best done during metaphase of Mitosis

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24
Q

Define homologous chromosomes

A

Nearly identical chromosomes; the same number 5 and 5

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25
Q

Define non-homologous chromosomes

A

Non-identical chromosomes; different number 9 and 22

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26
Q

How can we detect chromosomal abnormalities in the fetus?

A

Amniocentesis and Chorionic villus sampling

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27
Q

Define euploid

A

Cells that have a multiple of the normal number set (23) chromosomes; 23 x ____

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28
Q

Define haploid

A

One set of 23 chromosomes (sex cell)

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29
Q

Define diploid

A

Two sets of 23 chromosomes; 46 total (somatic cell)

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30
Q

Define polyploid

A

When a euploid has more than the diploid number of chromosomes; still contain a multiple of 23 chromosomes

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31
Q

Define triploid

A

Three sets of 23 chromosomes; 69 total - fetus will not survive

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32
Q

Define tetraploid

A

Four sets of 23 chromosomes; 92 total - fetus will not survive

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33
Q

Define aneuploidy

A

Cell that does not contain an exact multiple of 23 chromosomes; 45 or 47 total

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34
Q

Define trisomy

A

Cell containing three copies of one of the chromosome “pairs”; 47 total

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35
Q

Define monosomy

A

Presence of only one of any of the chromosomes “pairs”; 45 total

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36
Q

What is disjunction?

A

The process of splitting chromosomes into equal amounts of genetic material to each gamete

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37
Q

What is nondisjunction?

A

An error in which homologous chromosomes or sister chromatids fail to separate normally during meiosis or mitosis; gives rise to aneuploidy

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38
Q

Give an example of autosomal aneuploidy

A

Down Syndrome (trisomy 21)

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39
Q

Name characteristics of Down Syndrome

A

Low nasal bridge, round face, long and flat tongue, low set ears, short stature, heart defects, and respiratory defects

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40
Q

Give examples of sex aneuploidy

A

Turner’s Syndrome (monosomy X), Triplo-X (trisomy XXX), and Klinefelter’s Syndrome (trisomy XXY)

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41
Q

Name characteristics of Turner’s syndrome

A

Sterile, short, webbed neck, widely spaced nipples, little body hair, and underdeveloped breasts

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42
Q

Name characteristics of Triplo-X

A

Sterile, menstrual irregularity, and mental retardation (gets worse with more X’s)

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43
Q

Name characteristics of Klinefelter’s syndrome

A

Male appearance, female-like breasts, small testes, sparse body hair, and long limbs (gets worse with more X’s)

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44
Q

List chromosomal structure abnormalities

A

Breakage, deletions, inversions, duplications, and translocations

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45
Q

Define chromosomal breakage

A

If a chromosome breaks, physiological mechanisms will usually repair it; breaks can heal in a way that alters the structure of the chromosome

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46
Q

What is a clastogen?

A

Agents of chromosomes breakage

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47
Q

Give some examples of clastogens

A

Ionizing radiation, chemicals, and certain viruses

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48
Q

Define deletions

A

A breakage resulting in loss of DNA

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49
Q

Give an example of a deletion

A

Cri du chat (cry of the cat)

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50
Q

What is Cri du chat?

A

Deletion of short arm (p) of chromosome 5

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51
Q

Name characteristics of Cri du chat

A

Low birth weight, mental retardation, microcephaly (small head), and shrieking cry

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52
Q

Define inversions

A

Breakage followed by a reversal of the fragment during re-insertion (putting piece in backwards)

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53
Q

Define duplications

A

Replication of a gene sequence resulting in an amino acid sequence being repeated multiple times

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54
Q

What happens if duplication occurs in the same region as Cri du chat?

A

Mental retardation occurs, but no physical abnormalities

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55
Q

Define translocation

A

Interchange of material between non-homologous chromosomes (13-4, 2-5); from one place to another

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56
Q

When does translocation occur?

A

When two chromosomes break and the segments are rejoined in an abnormal arrangement

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57
Q

Define gene

A

Segment of DNA that codes for a protein or regulatory molecule

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58
Q

Define locus

A

The physical (geographic) location of a gene along a chromosome

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59
Q

Define allele

A

Different form (copy) of a particular gene

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60
Q

Define homozygous

A

Two alleles of a particular gene on a pair of homologous chromosomes are identical

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61
Q

Define heterozygous

A

Two alleles of a particular gene on a pair of homologous chromosomes are not identical

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62
Q

Define genotype

A

Genetic make-up of an organism; what they have

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63
Q

Define phenotype

A

Visible observation or tested for; what they show

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64
Q

Define carrier

A

can pass “bad” gene to their offspring but are not affected themselves

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65
Q

Define proband

A

The first in the family to be seen in a health care facility and diagnosed with the disease

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66
Q

What is recurrence risk?

A

The probability (%) of a family with a specific genotype having a child with an expected phenotype

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67
Q

Define penetrance

A

The proportion of individuals of a particular genotype that expresses its phenotype in a specific environment; how many people with the disease actually show it

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68
Q

Define Expressivity

A

Relative capacity of a gene to affect the phenotype of the organism of which it is part; how much of the disease an individual shows

69
Q

What is a polygenic trait?

A

Trait that involves multiple genes

70
Q

Give an example of a polygenic trait

A

Hair color, height, and eye color

71
Q

Other than genetic alterations what else has influence over disease and disorders?

A

Diets, habits, and exposures (environment)

72
Q

Give an example of diseases due to environment

A

Colon cancer is more common in the US and Stomach cancer is more common in Japan

73
Q

What is multifactorial inheritance?

A

Responsible for the greatest number of people that will need special care because of a genetic disease

74
Q

Give some examples of multifactorial diseases?

A

Atopic reactions, diabetes, cancer, spina bifida/anencephaly, pyloric stenosis, cleft lip, cleft palate, congenital hip dysplasia, club food, and more

75
Q

Define multifactorial trait

A

Traits follow a bell-shaped curve because they are influenced by both the environment and genetics

76
Q

Give some examples of multifactorial traits

A

Blood pressure, serum cholesterol, or all the values reported in a blood chemistry panel

77
Q

What is the Threshold model?

A

Model used to describe multifactorial traits/ you either have them or you don’t

78
Q

Define liability in the Threshold model

A

As the number of genetic and/or environmental risk factors increase, so does the liability for that disease; when it is so great that it reaches a threshold, an abnormality disease results

79
Q

How are liability and threshold related?

A

They are inversely proportional; as liability increases your threshold decreases

80
Q

How does the recurrence risk increase?

A

More than one family member is affected (sibling risk), expression of disease in proband is more severe, and proband is less common than affected sex

81
Q

How does the recurrence risk decrease?

A

If the disease is expressed in more remotely-related relatives

82
Q

Define tumor

A

Growth of tissues caused by the uncontrolled replication of cells

83
Q

Define neoplasm

A

New and abnormal development of cells that are unresponsive to normal growth control mechanisms; may be benign or malignant

84
Q

Define cancer

A

Invasion of surrounding tissues that have the ability to travel to, and proliferate at distant sites (metastasis)

85
Q

Benign vs Malignant

A

Benign: slow growth, encapsulated, non-invasive, well differentiated, low mitotic rate, and does not metastasize

Malignant: rapid growth, non-encapsulated, invade local structures and tissues, poorly differentiated, high mitotic rate, and metastasize

86
Q

How are tumors named?

A

According to their tissue of origin with the suffix “-oma”; benign tumors have simpler names than malignant ones

87
Q

Give examples of benign tumor names

A

Lipoma (fatty), fibroma (fibrous), osteoma (bone), and chondroma (cartilage)

88
Q

Give examples of malignant tumor names

A

Fibrosarcoma (fibrous connective), Chondrosarcoma (cartilage), Hemangiosarcoma, Squamous carcinoma (epithelial), glioblastoma (glial cells), and retinoblastoma (retina)

89
Q

What is Carcinoma in situ (CIS)?

A

Pre-malignant or pre-invasive epithelial malignant tumor that is localized in the epithelium and hasn’t broken through the basement membrane

90
Q

Define transformation

A

Process by which a normal cell becomes a cancer cell; not a single event

91
Q

Define anaplasia

A

Loss of differentiation and organization; doesn’t look like a cell anymore

92
Q

List histological features of cancer cells

A

Bizarre nuclei, cell shape, and sizes due to rapid cell division, invasion of the basement membrane, de-differentiation (more like embryonic cells), cellular or extracellular accumulations; build up (“mucus lakes” in lung cancer), and necrotic debris

93
Q

Lis abnormal gene expression in cancer cells

A

Turn on genes that: guide the cell through the cell cycle (violate check points), bring blood vessels to the cell (angiogenesis), and helps the cancer cell move to places it doesn’t belong (dissolve connective tissue barriers and move in and out of blood vessels)

94
Q

Define oncogenes

A

Cancer genes

95
Q

Explain the multi-hit model of carcinogenesis

A

Carcinogenesis is a multi-step process characterized by age and exposure to environmental agents/carcinogens that results in inactivation of tumor suppressor genes and amplification of oncogenes

96
Q

Step 1 of multi-hit model

A

Inactivation of APC tumor suppressor gene resulting in dysplastic epithelium and then early adenoma

97
Q

Step 2 of multi-hit model

A

Activation of K-ras oncogenes (growth factor) resulting in intermediate adenoma

98
Q

Step 3 of multi-hit model

A

Inactivation of tumor suppressor gene 18q resulting in late adenoma

99
Q

Step 4 of multi-hit model

A

Inactivation of TP53 tumor suppressor gene (tells cells to do apoptosis) resulting in carcinoma

100
Q

Step 5 of multi-hit model

A

Inactivation of other tumor suppressor genes resulting in metastatic cancer

101
Q

Where does cancer usually occur?

A

In body cells that are constantly dividing through out life (skin, bone marrow, intestinal lining, etc.)

102
Q

What is the Philadelphia chromosome?

A

Occurs in Chronic myelogenous leukemia (CML) there is translocation between chromosome 9 and 22; doesn’t make normal proteins

103
Q

Define tumor markers

A

Biological markers (tags) produced by cancer cells: cellular products, antigens, or alteration of the genes or chromosomes

104
Q

Give examples of tumor markers of cellular products

A

Hormones, antibodies, and enzymes

105
Q

Give an example of tumor markers that are antigens

A

Tumor-Specific Antigen (TSA)

106
Q

How do we indicate the presence of cancer?

A

If a tumor marker leaks into the blood, CSF, or urine, or if we get a sample of the cells from the cancerous tissue

107
Q

What else can we use tumor markers for?

A

To screen and identify people at a high risk of cancer, diagnose specific types of tumors, follow the clinical course of cancer

108
Q

What do tumor markers often lack?

A

Specificity, sensitivity, predictability, and feasibility

109
Q

Tumor marker example: Hormones

A

“Ectopic” (out of place) hormone production is the production of hormones by tumors of non-endocrine origin; ACTH, HCG, HGH, ADH, TSH, epinephrine, and norepinephrine

110
Q

Tumor marker example: Enzymes

A

Cancers don’t produce new enzymes; instead we find abnormal levels of normal enzymes. These are usually only detected in the blood when the tumor is large or metastasis has occured

111
Q

Tumor marker example: Antibodies

A

Produced by some cancers; multiple myeloma

112
Q

Tumor marker example: Tumor-specific Antigens

A

Cancer cells express “non-self” flags; HER2/neu

113
Q

Tumor marker example: Viral tumor-specific antigens

A

Produced and expressed by virally-transformed cells

114
Q

Tumor marker example: Oncofetal tumor-specific antigens

A

Expressed by cells during embryonic development but are absent or low in normal adult cells; fetoprotein in hepatic, pancreatic, and epithelium cancers, and carcinoembryonic antigen (CEA) in colonic, pancreatic and breast tumors

115
Q

Tumor marker example: Protein tumor-specific antigens

A

Function in proliferation, enzymatic processes, as receptors, and cellular structures; Prostate-specific antigen (PSA)

116
Q

What is PSA?

A

Glycoprotein produced by the prostate whose values are related to prostate mass; a tumor cell marker (TCM) used as a screening test for prostate cancer; blood test

117
Q

Define paraneoplastic syndrome

A

Signs and symptoms unrelated to the local effects/presence of the neoplasm caused by substances released from the tumor to an immune response to the tumor

118
Q

Examples of paraneoplastic syndrome

A

Hypercalcemia in breast and renal carcinomas from PTH-related protein, Polycythemia in cerebellar hemangioma and hepatocellular carcinoma from erythropoietin, and Hypoglycemia in hepatocelluar carcinoma from insulin like substance

119
Q

Define anchorage-indpendence

A

Continued growth even when unattached from the original tissue; free moving

120
Q

Define autonomy

A

Cancer cell’s independence from normal cellular controls; grow on their own without regards to other cells

121
Q

What are proto-oncogenes?

A

Unaltered, normal health alleles of genes that control/regulate cellular growth and differentiation

122
Q

What are oncogenes?

A

Is a proto-oncogene that has been altered (mutate) by carcinogenic agent; cancer gene

123
Q

What are tumor-suppressor genes?

A

Encode for proteins that inhibit cell division; anti-oncogenese, fight cancer

124
Q

How can can occur?

A

Either by the activation of oncogenes or the inactivation of tumor-suppressor genes

125
Q

Define loss of heterozygousity

A

Patient is born a carrier; has one mutated gene that is recessive, the second copy (normal) of gene mutates and now you have two bad genes –> cancer

126
Q

Give an example of genetic alterations in cancer

A

p53 (tumor-suppressor) gene mutations; hypoxic environments will activate p53 TS with activates p53 protein to activate apoptosis, but in cancer p53 gene is mutated so abnormal cells can proliferate

127
Q

List contributors to cancer growth

A

Autocrine stimulation, immortality, angiogenesis and angiogenesis

128
Q

What is autocrine stimulation?

A

Cancers have the ability to secrete and respond to their own growth factors; increased expression of growth factor receptors, cancer cells create numerous copies of genes and expression of gene products (HER2/neu - breast cancer and bcr/abl - tyrosine kinase in CML)

129
Q

What is immortality?

A

The only cells in the body that are immortal are stem cells; telomeres are protective end-caps of chromosomes that are maintained by telomerase, as telomeres are lost cell loses ability to divide, but cancer cells can activate telomerase which keeps the cells in place and keeps them growing

130
Q

What is angiogenesis?

A

Process that results in new blood vessels which allow cancers to enlarge

131
Q

List genetic alterations

A

Point mutations, translocation, and gene amplification

132
Q

What is a point mutation?

A

A small base-pair change can result in a normal proto-oncogene becoming an unregulated oncogene; translocated either increases synthesis or fusion of a gene

133
Q

What is translocation?

A

Part of chromosome is replaced by a part of a different chromosome; 8 and 14 - burkitt’s lymphoma and 9 and 22 - CML (philadelphia)

134
Q

What is gene amplification?

A

Instead of two copies of a given gene there may be hundreds of copies; over expression of an oncogene

135
Q

What are cancer stem cells?

A

Cells that divide to give rise to more cancer cells; parent cancer cell that are often based on cell surface markers “CD”

136
Q

What does CD stand for?

A

Cluster of differentiation

137
Q

What do we do with cancer stem cells?

A

We tag them with a florescent light to mark each one

138
Q

Define stroma

A

Original tissue cancer started in; house

139
Q

What are the interactions between cancer cells and stoma?

A

Normally growth factors and adhesive proteins in the surrounding connective tissue and blood vessels keep cells from going “off the reservation”, but in cancer cells begin to express genes that allow them to divide uncontrollably and move freely in stroma = carcinoma in situ, next step eats through basement membrane = carcinoma

140
Q

How does chronic inflammation increase cancer?

A

Inflammatory cells release cytokines to stimulate cellular proliferation, angiogenesis, and promote healing so they are easily mutated by cancer cells

141
Q

Give some examples of cancers associated with chronic inflammation

A

Colon cancer, liver cancer, and lung cancer

142
Q

What is an oncogenic virus?

A

Viruses that change the genetic makeup of the cell, which results in the alteration of the daughter cell

143
Q

Give examples of oncogenic viruses

A

Epstein-barr virus (EBV) - hodgkin lymphoma, burkitt lymphoma, Human Papilloma virus (HPV) - cervical cancer, HIV - kaposi sarcoma, and hepatitis B virus (HBV) - hepatocellular carcinoma

144
Q

What are oncogenic bacterium?

A

Bacteria that can cause cancer

145
Q

Give an example of an oncogenic bacterium

A

Helicobacter pylori - bacteria that infects stomach; common causes are peptic ulcer disease, gastric lymphomas, and gastric carcinomas; think chronic inflammation

146
Q

Define metastasis

A

Spread of cancer from the initial site of neoplasm development to distance tissues of the body; sequence of events

147
Q

Step 1 of metastasis: detachment

A

Cells break loose from their original location

148
Q

Step 2 of metastasis: invasion

A

Cellular proliferation, barrier destruction, secretion of proteases and protease activations - degrades basement membrane, increased motility

149
Q

Step 3 of metastasis: intravasation

A

passage into vessels (blood or lymph)

150
Q

Step 4 of metastasis: adherence in favorable sites

A

certain types of cancerous cells have a preference for specific organs; organ tropism - encouraged by growth factors, hormones, presence of tumor receptors, and route

151
Q

Step 5 of metastasis: extravasation

A

Leaves blood or lymph and invades secondary tissue

152
Q

Step 6 of metastasis: colonization

A

establishment in new tissue

153
Q

Sequence of metastasis

A

Local transformation and extension, motility, angiogenesis, invasion, intravasation, adherence at favorable site, extravasation, and colonization

154
Q

Stage 1 cancer

A

Neoplastic cells in original site, well differentiated cells

155
Q

Stage 2 cancer

A

Metastatic cell in original site and local lymphatics, moderately-differentiated cells

156
Q

Stage 3 cancer

A

Cells in original site and distant lymphatics, poorly differentiated cells

157
Q

Stage 4 cancer

A

Metastatic cells are found in many body areas, very poorly differentiated cells

158
Q

List systemic effects of neoplasms

A

Vessel invasion (bleeding), lymphatic invasion (lymphedema), nerve invasion (pain, numbness, tingling), bone cortex invasion (pain and fracture), bone marrow invasion (pancytopenia, infection, bleeding), and liver invasion (hepatic insufficiency)

159
Q

List clinical manifest ions of cancer

A

Pain, fatigue, anemia, infections, and cachexia syndrome

160
Q

Pain

A

little or no pain = early malignancy, influenced greatly by fear, anxiety, sleep loss, and psychological responses. Pressure on sensitive structures, obstruction, severe stretching of tissues, terminal cancer = severe pain

161
Q

Fatigue

A

Sleep disturbance, biochemical changes to treatment, diminished activity level, nutritional status, and necrosis factors

162
Q

Anemia

A

Reduction in red blood cell numbers caused be chronic bleeding, malnutrition, therapies, malignancy in blood-forming organs; also leukopenia and thromboycytopenia from malignancy in bone marrow

163
Q

Infection

A

Most common event leading to demise of patient with malignancy - reduction in immunologic functions due to treatment regimens, poor wound care, and compromised patient care

164
Q

Cachexia syndrome

A

Ill health, wasting, emaciation and decreased quality of life. Symptoms = reduced sweet, sour, salty sensations, decreased appetite, weight loss, altered metabolism

165
Q

Treatments for cancer

A

Chemotherapy, radiation, and surgical therapy

166
Q

Chemotherapy

A

Destroy cells that are in stage of vulnerability, eliminates enough cells for the immune system to take care of the rest (cocktail of drugs), targeted therapy - enzyme inhibitors, monoclonal antibodies which direct at a specific tumor antigen

167
Q

Radiation

A

Damages DNA of the rapidly dividing neoplastic cells

168
Q

Surgical therapy

A

Excisional, debulking, palliative - useful when tumor has not passed beyond stage 3, tumor and anything infected lymph node must be removed