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Pathophysiology > Week 1 Cell Review, Genetcis, Cancer > Flashcards

Week 1 Cell Review, Genetcis, Cancer Flashcards

1
Q

What is the most basic unit of life

A

Cells

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2
Q

Size of a cell

A

1 micrometer

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3
Q

What does a cell membrane do

A

Defines cell

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4
Q

What do all living organisms have

A

Cells

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5
Q

What is cytoplasm

A

Things inside a cell

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6
Q

What is cytosol

A

The fluid alone in the cell membrane

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7
Q

What do Eukaryotes have in their nucleus

A

They have nucleoplasm (Cytoplasm in the nucleus)

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8
Q

Complex RNA and protein structure

A

Ribosomes

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9
Q

What is genetic information stored as

A

DNA

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10
Q

Matured RBC don’t have what?

A

DNA

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11
Q

Eukaryotes have what?

A

Membrane bound nucleus

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12
Q

Prokaryotic DNA is where

A

The cytoplasm

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13
Q

Eukaryotic DNA is where

A

In the nucleus

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14
Q

Specialized cell structure that preforms a specific function

A

Organelle

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15
Q

Pseudopod

A

Used to moved around or attack

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16
Q

Cilia(hair-like)

A

Used to move around or move other things

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17
Q

Where is cilia found

A

Only in unicellular organisms

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18
Q

What is the cilia in our lungs used for

A

To move around saliva

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19
Q

Flagella (Tail-Like)

A

Helps move the cell forward

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20
Q

Flagella (Tail-Like)

A

Helps move the cell forward

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21
Q

What is Oxytricha Trifallax

A

It is a unicellular organisms
It can have two nuclei
Mates and mingles DNA

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22
Q

What is found in all cells

A

Membranes
Cytoplasm
Ribosomes

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23
Q

Purpose of Celluar respiration

A

Break down glucose into carbon dioxide and water to produce ATP

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24
Q

What are the major steps of cellular respiration

A
  1. Glycolysis
  2. Pyruvate Oxiudation
  3. Citric Acid cycle
  4. Oxidative phosphorylation
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25
Q

What are the electron carriers in cellular respiration

A

NAD+ and FAD

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26
Q

What do NAD+ and FAD become and when

A

NAD+ turns to NADH
FAD turns to FADH2
When they gain electrons

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27
Q

NAD⁺ + 2e⁻ + 2H⁺ → NADH + H⁺

A

Celluar respiration reaction

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28
Q

FAD + 2e⁻ + 2H⁺ → FADH₂

A

Celluar respiration reaction

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29
Q

Location of glycolysis

A

Cytoplasm

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30
Q

What’s the process of glycolysis

A
  • Glucose (6-carbon) → 2 Pyruvate (3-carbon each)
    • ATP produced
    • NAD⁺ converted to NADH
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31
Q

What’s the oxygen requirement for Glycolysis

A

Can occur WITHOUT oxygen (Anaerobic)

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32
Q

Location of Pyruvate Oxidation

A

Mitochondrial Matrix

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33
Q

Process of pyruvate oxidation

A
  • Pyruvate → Acetyl CoA (2-carbon molecule)
    • CO₂ released
    • NADH generated
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34
Q

Pyruvate oxidation oxygen requirement

A

Requires oxygen Indirectly.

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35
Q

Citric Acid cycle location

A

Mitochrondial matrix

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36
Q

Process of Citric acid cycle

A

Acetyl CoA combines with a 4-carbon molecule
- Cycle regenerates the 4-carbon molecule
- Produces ATP, NADH, and FADH₂
- CO₂ released

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37
Q

Oxygen requirement for Citric Acid cycle

A

Require oxygen indirectly

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38
Q

Location for Oxidative Phosphirylation

A

Innner mitochondrial membrane

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39
Q

Process of Oxidative Phosphorylation

A

NADH and FADH₂ deposit electrons into the electron transport chain (ETC)
- Electrons move through ETC, releasing energy to pump protons (H⁺) out of the mitochondrial matrix
- Creates a proton gradient
- Protons flow back into the matrix via ATP synthase, producing ATP
- Oxygen accepts electrons and protons to form water (H₂O)

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40
Q

Location for oxidative phosphorylation

A

Requires oxygen DIRECTLY

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41
Q

Location for fermentation

A

Cytoplasm

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42
Q

Process of Fermenation

A

Glycolysis can occur without oxygen by using fermentation.

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43
Q

The conversion of co enzymes of electron transport chain is where

A

across the membrane of the Krista

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44
Q

Glycolysis Produced (Net)

A

2 ATP
2NADH

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45
Q

Pyruvate———->Acetyl-COa Produced(net)

A

2NADH

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46
Q

Krebs Cycle Produced (Net)

A

6NADH
2ATP
2QH2

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47
Q

How many ATP’s does NADH produce

A

2-3

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48
Q

How many ATP’s does QH2 produce

A

1.5- 2 ATPS

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49
Q

Maximum amount of ATP that can be produced in Celluar respiration

A

27-30

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50
Q

The study of inherited traits and patterns

A

Genetics

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51
Q

Who is known for the study of gene inheritance

A

Mendel

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52
Q

Who is know for the study of DNA structure

A

Watson & Crick

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53
Q

What is know for the study of sequencing human genes

A

The Human Genome Project

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54
Q

What does genetics and genomic healthcare have implications for

A

Health promotion
Illness prevention
Health maintenance
Health Treatment

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55
Q

Emerging healthcare discipline, applies genetic information as part of clinical care

A

Genomics

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56
Q

What are the types of genetic disorders

A

Congenital and Accquired

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57
Q

Congenital Disorder

A

Present at birth due to inherited gene alterations

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58
Q

Acquired Disorder

A

Gene altered by external factors
(Oncology, rare diseases)

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59
Q

Nurses must understand and use genomic information in healthcare

A

Genomic literacy

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60
Q

Nurses must understand and use genomic information in healthcare

A

Genomic literacy

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61
Q

How can a nurse use genomic literacy in healthcare?

A

-Incorporate, utilize advances in genomic healthcare
-Identify hereditary risk, make connections to genetic consultation, testing

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62
Q

How can a nurse use genomic literacy in healthcare?

A

-Incorporate, utilize advances in genomic healthcare
-Identify hereditary risk, make connections to genetic consultation, testing

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63
Q

Specializes in care of patients with genetic diseases, including risk assessments and education.

A

Genetic Nurse

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64
Q

Specializes in care of patients with genetic diseases, including risk assessments and education.

A

Genetic Nurse

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65
Q

The study of gene expression changes without altering DNA sequence

A

Epigenetics

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66
Q

What does gene expression do

A

-Biologic mechanisms that turn genes off/on
-Chemical mediators modify cell activity, expression, function
-Not part of DNA code (attached to DNA)

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67
Q

Influences for Gene expression

A

Environmental factors (Diet)

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68
Q

Influences for Gene expression

A

Environmental factors (Diet)

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69
Q

Gene expression is linked to

A

Cancers, cognitive behavior, CV, respiratory, autoimmune, reproductive disorders

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70
Q

The complete set of genes or genetic material present in a cell or organism

A

Genome

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71
Q

Understanding gene roles in health, disease, and drug response (Pharmacogenomics)

A

Gene Function Research

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72
Q

Maple sand sequenced the entire human genome, identifying approximately 20,000-25,000 genes

A

Human Genome Project

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73
Q

Maple sand sequenced the entire human genome, identifying approximately 20,000-25,000 genes

A

Human Genome Project

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74
Q

Developed a map of human genetic variations(haplotypes), focusing on the 0.1 of genes that differ among individuals

A

HAPMAP

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75
Q

The molecule that carries genetic information used for growth, development, functioning, and reproduction.

A

DNA

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76
Q

Genetic basis for human characteristics, dictate protein synthesis

A

DNA (Deoxyribonucleic Acid)

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77
Q

Repository of hereditary characteristics carried through cell division (mitosis)

A

DNA

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78
Q

Responsible for most Celluar functions

A

Proteins

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79
Q

DNA determines what

A

Which proteins are produced and how they function.

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80
Q

Segments of DNA that act as a blueprint for protein synthesis. on/off switch” for individual protein

A

Genes

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81
Q

Basic unit of heredity, paired segment(s) make-up DNA helix
-Encodes functional products/specific protein

A

Genes

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82
Q

A sequence of three nucleotides in a gene that corresponds to a specific amino acid or stop signal during protein synthesis.

A

Codon

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83
Q

Organized bundles of DNA within the nucleus of cells.

A

Chromosome Structure

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84
Q

arrangement of chromosomes within cell

A

Karyotype

85
Q

23 pairs of chromosomes (22 autosome pairs and 1 pair of sex chromosomes).
-Sex Chromosomes: XX for females, XY for males.

A

Human Karyotype

86
Q

Cell division process that duplicates chromosomes for each new cell.

A

Mitosis

87
Q

Different forms of the same gene located at the same position (locus) on a chromosome. Each individual inherits one allele from each parent.

A

Allele

88
Q

genetic inheritance from parent to child (described by Gregor Mendel)

A

Mendelian Inheritance

89
Q

Dominant and recessive Genes

A

Dominant alleles mask the effect of recessive alleles

90
Q

An individual has two different alleles for a gene.

A

Heterozygous

91
Q

An individual has identical alleles for a gene.

A

Homozygous

92
Q

The genetic information (gene)

A

Genotype

93
Q

expressed traits (dominant allele)

A

Phenotype

94
Q

% of individuals with a specific genotype that express phenotype.

A

Penetrance

95
Q

Example of Penetrance?

A

-BRCA1 gene: 85% penetrance for breast cancer.
-BRCA2 gene: 20% penetrance for breast cancer.

96
Q

Diseases caused by single gene mutations
-typically inherited in autosomal dominant or recessive patterns

A

Mendelian Disorders (inherited):

97
Q

Diseases caused by single gene mutations
-typically inherited in autosomal dominant or recessive patterns

A

Mendelian Disorders (inherited):

98
Q

Only one mutated copy of the gene is necessary for the condition to develop.

A

-Autosomal Dominant Disorders:

99
Q

Two copies of the mutated gene are necessary for the condition to develop.

A

Autosomal Recessive Disorders:

100
Q

-Sex-Linked Disorders:

A

Disorders associated with genes located on the sex chromosomes (X or Y).

101
Q

-Result from the interaction of multiple genes and environmental factors.
-More common and include conditions like heart disease and diabetes

A

Multifactorial (Complex) Disorders:

102
Q

-Often multiple genes on multiple chromosomes
-Changes in number/structure of chromosomes
-often resulting from errors during meiosis.

A

Chromosomal Disorders:

103
Q

-Congenital Disorders:

A

Genetic disorders present at birth

104
Q
  • Genetic Disorder
A

due to gene expression issues during developmen

105
Q

a genetic disorder caused by a mutation in the hemoglobin gene, abnormal hemoglobin (Hbs)
Red blood cells become sickle shaped
Global Impact: Apporioxiametly 100 million carriers worldwide

A

Sickle Cell Disease

106
Q

What recessive type is sickle cell?

A

-Autosomal Recessive: The disease manifests when an individual has two copies of (homozygous SS)

107
Q

Sickle Cell Trait

A

Heterozygous individuals (AS) are carriers and may pass the gene to offspring.

108
Q

Inheritance pattern for Sickle Cell

A

-Inheritance patterns depend on parents genotype
-Parents heterozygous (both have trait)
-25% of children – no SSD gene
-50% of children – SSD gene, carrier
-25% of children – SSD disease

109
Q

Hemophilia Inheritance Pattern

A

Father, no gene; Mother heterozygous (carrier)
-The Male offspring will have a 50% chance of having hemophilia XY
(XY son won’t have hemophilia XHY son will have hemophilia)
-The female offspring will have a 50% chance of being a carrier of hemophilia XX
(XX daughter will not have hemophilia gene/XXH daughter is a carrier of hemophilia)

110
Q

-A visual tool used to document family history and identify patterns of inherited diseases.
-This helps in assessing health risks influenced by genetics, culture, and social factors.
-Impacted by ethnic, cultural, social practices

A

Genogram

111
Q

provide holistic picture for health promotion, disease prevention

A

Nursing Implications

112
Q

Genes,when mutated or overexpressed, promote the development of cancer

A

Oncogenes

113
Q

Normal genes that code for proliferation
(When mutated, they become oncogenes, leading to uncontrolled cell proliferation)

A

Porto-Oncogenes

114
Q

Results in chromosomal translocation or gene overexpression (gene “stuck on”)

A

Activation of Oncogenes

115
Q

-Growth factors stay “turned on”, grow out of control (cancer), lack of apoptosis

A

Activation of Oncogenes:

116
Q

-Genes that regulate cell division (mitosis)
-repair DNA mistakes (proliferation)
-Control apoptosis

A

Tumor-Suppressor Genes:

117
Q

-unregulated cell proliferation, tumor growth
-Removes the checks on cell proliferation
-Mutations recessive until anomaly or deletion removes dominant growth control

A

Inactivation of tumor suppression:

118
Q

Mutation Causes

A

Typically triggered by carcinogens or environmental factors
(leading to unregulated cell growth and cancer)

119
Q

____ are a natural part of DNA/ cell replication

A

Errors

120
Q

Where are mistsakes fixed during DNA and cell replication

A

DNA repair process(repair enzymes)

121
Q

Where are mistsakes fixed during DNA and cell replication

A

DNA repair process(repair enzymes)

122
Q

Cells have mechanisms to correct most replication errors: uncorrected errors become permanent mutation

A

DNA repair

123
Q

Permneanet changes in the DNa that can occur during genetic code

A

Mutations

124
Q

Changes in a single nucleotide, which can lead to changes to protein function

A

Point Mutations

125
Q

changes in multiple nucleotides within one or more genes. Can affect larger sections of DNA, impacting the function of multiple proteins.

A

Multi-point mutations

126
Q

Mutations can lead to what

A

various diseases, including cancer (when they affect critical genes)

127
Q

Hereditary disorder resulting in severe elevations in cholesterol (LDL & total)
in the blood.
-Absent/dysfunctional LDL receptor gene, liver can’t uptake LDL cholesterol
-LDL cholesterol builds up in blood stream

A

Familial Hypercholesterolemia (FH):

128
Q

Prevalence of Familial Hypercholesterolemia (FH

A

1 in 500 in US (heterozygous); half normal, half defective

129
Q

Homozygous FH:

A

1 in 1 million (more severe)

130
Q

Etiology of Familial Hypercholesterolemia (FH):

A

Autosomal dominant disorder resulting from mutations in the LDL receptor gene.

131
Q

Assessment of Familial Hypercholesterolemia (FH):

A

-atherosclerosis (plaque in arteries)
-CV: coronary artery disease (CAD) early in life
-Xanthelasma: cholesterol deposits in skin

132
Q

Marfan’s Syndrome

A

Hereditary disorder of connective tissue (mutation in protein production)

133
Q

What mutation is Marfan’s syndrome

A

of FBN1 gene (codes for fibrillin/body structure)

134
Q

Prevalence of Marfan’s syndrome

A

1 in 10,000 births, 75% of cases familial
-Fatal if untreated, average age death 30 – 40 y/o

135
Q

Autosomal dominant disorder caused by mutations in the FBN1 gene.

A

Etiology of Marfan’s Syndrome

136
Q

Assessment of Marfan’s Syndrome

A

Expression, manifestation varies (mild to severe)
-CV: heart and blood vessel structure, most critical symptoms
-Mitral valve prolapse, weakness of aorta & arteries (rupture)
-Skeletal: tall; abnormally long, thin digits; hyperflexible joints
-Vision problems

137
Q

Cystic fibrosis(CF)

A

Inefficient chloride transport over cell membrane, thick/sticky mucus

138
Q

Etiology Cystic fibrosis(CF)

A

Autosomal recessive disorder caused by mutations in the CFTR gene.

139
Q

Cystic fibrosis mutation

A

CFTR gene (chloride regulation)

140
Q

Clinical Manifestations of Cystic fibrosis

A

Respiratory infections
pancreatic dysfunction
malabsorption.

141
Q

Prevalence of cystic fibrosis

A

1,000 cases/year; 30,000 living cases in U.S.
-Most common lethal inherited disease w/European ancestry
-Fatal if untreated, typically diagnosed by age 1

142
Q

Down Syndrome

A

A chromosomal disorder characterized by an extra copy (3 total) of chromosome 21 (trisomy 21)
-Most common chromosomal d/o in humans

143
Q

Prevelance of Down Syndrome

A

1 per 800 births (6,000 cases/year)
-Error in meiosis, trisomy 21 (95% of cases)

144
Q

Error in meiosis Increased maternal age (aging oocyte); 1/50 births, mother 45+ y/o

A

Etiology of Down Syndrome

145
Q

Assessment for Down Syndrome

A

-Physical: distinct facial characteristics (flat facial profile, small/square head, upward eye slant)
-Cognitive delay; varies, 20% near-normal cognitive function

146
Q

“New growth” characterized by disorganized, uncoordinated, and uncontrolled cell proliferation, resulting in a neoplasm (tumor).
-Greek, neos = new + plasis = molding

A

Neoplasia

147
Q

Benign Tumor

A

-Non-cancerous
-cells are well-differentiated
-limited proliferation
-typically retain some normal function
-do not invade neighboring tissues.

148
Q

Malignant Tumor

A

-Cancerous
-Less differentiated, uncontrolled proliferation
-less differentiated cells w/uncontrolled growth
-tendency to invade other tissues and metastasize
-Does not retain “Normal function”

149
Q

Oncology:
-The Study of Tumors
-Study of neoplasms (neoplastic disorders)
-particularly malignant
-Greek, onkos = swelling + logos = study of

A

Oncology

150
Q

Benign tumor of glandular origin

A

Adenoma

151
Q

Malignant tumor of epithelial origin

A

Carcinoma

152
Q

Malignant tumor originating in glandular tissue

A

Adenocarcinoma

153
Q

Malignant tumor originating in connective tissue

A

Sarcoma

154
Q

Genetic mutations occur (Stages of Carcinogenesis)

A

Initiation

155
Q

Pre-neoplastic cells proliferate, accumulating further mutations (Stages of Carcinogenesis)

A

Promotion

156
Q

Pre-malignant cells/lesions transition to cancer cells w/rapid proliferation (Stages of Carcinogenesis)

A

Progession

157
Q

Genetic Instability:

A

-This instability is a hallmark of cancer
-Uncorrected mutations typically rare (cell checkpoints, cyclins prevent)
-Do not maintain “normal” function, typically more primitive (embryonic)

158
Q

Goal of cancer cells

A

-survival, proliferation
-“Normal” cells require complex growth process, environment, etc.
-CA cells immortal; infinite divisions possible & always dividing
-CA cells secrete their own growth factors
-Loss of contact inhibition (auto stop): grow regardless of density/crowding
-Non-encapsulated, invade/destroy neighboring tissue
-Metastasis to body
-Loss of anchorage dependence: CA cells grow not attached to anything
-cancer cells can divide indefinitely due to the activation of telomerase enzyme that maintains telomere length.

159
Q

Cancer cells can detach from the primary tumor and spread to distant sites via the bloodstream or lymphatic system, forming secondary tumors.

A

-Metastasis:

160
Q

-Proto-Oncogenes:

A

Normal genes that promote cell growth and division.
(When mutated, they become oncogenes, driving uncontrolled cell proliferation.)

161
Q

increase risk of cancer

A

Oncogene

162
Q

Part of a chromosome breaks off and attaches to another, leading to abnormal gene activation.

A

Chromosomal Translocation:

163
Q

An oncogene becomes overactive, leading to excessive cell division

A

Gene Overexpression:

164
Q

Function to inhibit cell growth, repair DNA, and apoptosis (cell death)
Inactivation of tumor suppression: cells proliferate unchecked, contributing to tumor growth.

A

Tumor-Suppressor Genes:

165
Q

Cancer Growth/Proliferation Influences:

A

-Amount of cells actively dividing at any given time compared to normal cells.
-CA cells: more cells in active division than “normal” cells
-CA cells: same length of cell cycle, just more cells in division so multiply faster

166
Q

Direct Invasion:

A

-Cancer cells invade adjacent tissues
-Secrete enzymes that break down surrounding structures
-Difficult to define margins/edges (no capsule)

167
Q

-Tumor cells can shed into nearby body cavities causing formation of new tumors in those spaces.

A

Seeding:

168
Q

Metastasis Spread:

A

-Spread from primary/origin tissue to secondary site/tissue
-Cancer cells break away from primary site, travel to other tissue
-Lymphatic spread: lymph nodes typically first site of spread
-CA gains access to bloodstream via lymph & lymph nodes

169
Q

Cancer cells enter blood stream, carried through the body via blood (& lymph)
-Metastasis depends on: cancer type, speed of cancer growth, behaviors/environment

A

Metastasis

170
Q

Bone (access via bloodstream), Brain (cross blood brain barrier)

A

Lung Cancer

171
Q

Liver (most common site of metastasis, filters blood via portal circulation

A

Colon Cancer

172
Q

Bone (50+% of cases), brain, liver, lung (direct seeding d/t location)

A

Breast Cancer

173
Q

Commonly spreads to the vertebrae. (direct invasion d/t location)

A

Prostate Cancer

174
Q

Bone, brain (50% of cases), liver, lung

A

Melanoma

175
Q

Risk of cancer for men

A

40.9% risk of developing cancer; 20.2% risk of cancer-related death.

176
Q

Risk of cancer for women

A

39.1% risk of developing cancer; 17.7% risk of cancer-related death.

177
Q

Racial Disparties in Cancer

A

White individuals have higher rates of cancer diagnosis, while Black individuals have higher rates of cancer mortality.

178
Q

Greatest risk factor for cancer

A

Age is the greatest risk factor, with cancer risk increasing significantly in individuals over 55 years old.

179
Q

Exposure to chemicals like tobacco smoke, asbestos, and certain dyes can lead to mutations that trigger cancer. Approximately 90% of cancer cases are linked to chemical exposure.

A

Chemical Carcinogens

180
Q

Both ionizing radiation (e.g., X-rays, gamma rays) and non-ionizing radiation (e.g., UV light) can cause DNA mutations leading to cancer.

A

Radiation

181
Q

Persistent inflammation can promote mutations and cancer development.

A

Chronic Inflammation

182
Q

Oncogenic viruses such as HPV (linked to cervical cancer) and Hepatitis B (linked to liver cancer) integrate into the host genome and trigger cancer.

A

Viruses

183
Q

Genetic predispositions can significantly increase cancer risk, with over 50 types of cancer having a familial component.

A

Heredity

184
Q

Hormonal imbalances can contribute to the development of certain cancers, though the exact mechanisms remain unclear.

A

Hormones

185
Q

Linked to several cancers due to metabolic, hormonal, and immune system changes.

A

Obesity

186
Q

Examples of Chemical Carcinogens

A

Lifestyle-Cigarettes
Environmental/Occuptial- Asbestos, benzene (Inhalation & absorption), insecticides
Dietary- Nitrosamines (Smoked Meat), Hydrocarbons (Charcoal), high fat, low fiber diet

187
Q

-Tumors disrupt normal tissue architecture, leading to ulceration, bleeding, and non-healing wounds. Compression of nearby structures can cause pain.

A

Impaired Tissue Integrity:

188
Q

Reduced red blood cell (RBC) count due to bone marrow suppression, cytotoxic effects of cancer treatments, or blood loss from tissue destruction.

A

Anemia

189
Q

Characterized by severe weight loss, muscle wasting, and loss of appetite, driven by a hypermetabolic state and chronic inflammation.

A

Cancer Anorexia-Cachexia Syndrome:

190
Q

Persistent fatigue not relieved by sleep, often a direct result of cancer or its treatment. This can persist for months or even years after treatment.

A

Fatigue and Sleep Disorders:

191
Q

Cancer Satge 0

A

Abnormal cells are present but have not spread.

192
Q

Cancer Stage 1

A

Cancer is present; tumor is small but invasive.

193
Q

Cancer Stage 2

A

Primary tumor is larger but has not metastasized.

194
Q

Cancer stage 3

A

Tumor has spread to lymph nodes.

195
Q

Cancer stage 3

A

Tumor has spread to lymph nodes.

196
Q

Cancer Stage 4

A

Cancer has spread to distant parts of the body.

197
Q

TNM Staging System: T

A

T (Tumor): Size and extent of the primary tumor.

198
Q

TNM Staging System: T

A

T (Tumor): Size and extent of the primary tumor.

199
Q

TMN: Staging System N

A

N (Nodes): Number of nearby lymph nodes involved.

200
Q

TMN Staging System: M

A

M (Metastasis): Presence of distant metastasis.

201
Q

T1 tumor size

A

Less than 2cm

202
Q

T1 tumor size

A

Less than 2cm

203
Q

T2 tumor size

A

2-5cm

204
Q

T3 tumor size

A

5 or greater

205
Q

T4 tumor size

A

Tumor extends to skin or chest wall

206
Q

-Focus on educating patients about reducing exposure to cancer risk factors
-Environmental hazards (sunlight, second hand tobacco, etc.)
-Smoking prevention
-Alcohol abuse prevention
-Increasing activity, decreasing obesity

A

Cancer Education (Primary Prevention):

207
Q

-Early detection through screening tests can significantly improve outcomes by identifying cancer at an earlier, more treatable stage.
-Pap smear (cervical cancer)
-colonoscopy (colon cancer)
-mammography (breast cancer)
Tumor Markers (serum): antigens indicating presence of tumor
-PSA: prostate-specific antigen
-CEA (carcinoembryonic antigen), CA 125 (cancer antigen 125)

A

Cancer Screening (Secondary Prevention):

208
Q

-Early detection through screening tests can significantly improve outcomes by identifying cancer at an earlier, more treatable stage.
-Pap smear (cervical cancer)
-colonoscopy (colon cancer)
-mammography (breast cancer)
Tumor Markers (serum): antigens indicating presence of tumor
-PSA: prostate-specific antigen
-CEA (carcinoembryonic antigen), CA 125 (cancer antigen 125)

A

Cancer Screening (Secondary Prevention):

Pathophysiology (1 decks)

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