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132 Cards in this Set

  • Front
  • Back
Protoplasm
*living substance inside the cell
*also called bioplasm
Ergastic Substances
*non-living cell components
Divisions of Protoplasm
*cytoplasm
*nucleoplasm
Tonoplast
*large water-filled vacuole enclosed by a membrane
*occupies most of the volume of many plant cells
Major Classes of Organic Compounds
*hydrogen
*carbon
Mitochondria
*energy production through formation of ATP
*involved in apoptosis through release of cytochrome C
Endoplasmic Reticulum
*outer membrane contains ribosomes
Ribosomes
*translate mRNA into proteins
Golgi Complex
*modifies and transports proteins made in RER
*contains processing enzymes
Lysosomes
*trash compactors of the cell
*single membrane structure
*contains acid hydrolases for breaking down macromolecules
Structure of DNA
*double helix of sugar phosphate groups held together by hydrogen bonds between the bases
*sequence of bases specifies genetic code
Bases of DNA
*thymine-cytosine
*adenine-guanine
Width of Strand of DNA
2 nM wide
Chromatin
*unit of DNA packaged into a chromosome
*genes are on chromosome
Telomeres
*long arrays of bases of varying lengths that protect the terminal ends of chromosomes
Result of Cell Division
some telomeric DNA is lost, initiating senescence
Telemorase
the rebuilding of telomeric DNA in stem and cancer cells
Phases of Mitosis
*prophase
*metaphase
*anaphase
*telophase
*interphase
Prophase
*cell getting ready to divide
*duplicates DNA
*gets centrioles in the right position
Metaphase
*DNA lines up along a central axis
*centrioles send out specialized tubules that connect to the DNA
*chromatin has now condensed into chromosomes
*two strands of the chromosome are connected at the center with a centromere
*tubules connect to the centromere, not the DNA
Anaphase
half of the chromosomes are pulled to each side of the cell
Telophase
*cell membranes close in and split into two separate cells with half of the original DNA for each cell
Interphase
*resting state of the cell
*performing general life functions
*duplicating nucleic acids to prepare for prophase again
Cell Cycle
G1 - S - G2 - M
Production of X-Rays
from liberated electrons
Production of Gamma Rays
liberated from the nucleus
Mass and Charge of Electrons
*negative charge
*small mass
Mass and Charge of Protons
*positive charge
*larger mass
Mass and Charge of Neutrons
*no charge
*large mass
Mass and Charge of Alpha Particles
*positive charge
*very large mass
Direct Ionization
liberated electron interacts directly with the DNA, causing a strand break
Indirect Ionization
liberated electron reacts with water, producing free radicals, which damage DNA
Primary Mechanism X-Rays Use
Indirect Radiation
Linear Energy Transfer
rate at which energy is deposited in matter
Units of Linear Energy Transfer
KeV per micron
High LET Particles
*alpha particles
*neutrons
Mechanism of Action for High LET Radiation
*greater likelihood of producing double strand DNA breaks, which kills cell
*less likelihood of producing single strand breaks, which can be repaired
Type of Ionization that High LET Radiation Uses
direct ionization
Effect on the Survival Curve of High LET Radiation
direct ionization results in the straight initial slope of the survival curve
Relative Biologic Effectiveness
quantity used to compare doses of radiation needed to produce the same biologic effect
Standard of Relative Biologic Effectiveness
*250 kV
*D250/D
Units of Relative Biologic Effectiveness
no units, just ratio
Factors Used to Determine Relative Biologic Effectiveness
*linear energy transfer
*dose of radiation
*number of fractions
*dose rate
*biologic endpoint
How Linear Energy Transfer Influences Relative Biologic Effectiveness
high linear energy transfer beams result in greater relative biologic effectiveness
Shoulder for High Linear Energy Transfer Beams
small shoulder
How Dose Fractionation Influences Relative Biologic Effectiveness
increased dose fractionation results in greater relative biologic effectiveness
How Dose Rate Influences Relative Biologic Effectiveness
lower dose rate results in greater biologic effectiveness
How Relative Biologic Effectiveness Influences Repair of Radiation Damage
tissues with higher relative biologic effectiveness show repair of radiation damage
Type of Radiation with High Relative Biologic Effectiveness
neutrons
Interaction Between RBE and LET
relative biologic effectiveness increases as linear energy transfer increases until it reaches a max of 6 at 100 keV per micron
Effect of Linear Energy Transfer of 6 at 100 keV per micron
separation between ionizations is almost equal to the diameter of the DNA, increasing the likelihood of double strand breaks
Effect of Linear Energy Transfer of Greater Than 6 at 100 keV per micron
no increase in effectiveness as additional ionizations are overkill, as the DNA has already been fatally damaged
Effects of Radiation on Chromosomes
*repair is attempted for DNA breaks
*errors result
Types of Errors Resulting from Attempts at DNA Repair
*deletions
*translocation
*abnormal chromosomal formations
Lethal Structural Changes As A Result of Radiation
*dicentrics
*anaphase bridges
*rings
Ways Ionizations are Deposited
*spurs
*blobs
Differences Between Spurs and Blobs
*blobs larger than spurs
Width of DNA
2 nM
Size of Spurs
3 ion pairs that cover 4nM
Division Delay
non-lethal event where temporary block exists between G2 and M phases of cell cycle
Factors That Effect the Length of the Division Delay
the higher the radiation dose, the longer the division delay
Effect of the Division Delay on Cell Cycle
synchronizes cell population by putting more cells into G2 phase at the same time
Apoptosis
*mechanism of programmed cell death for some cells including lymphocytes, oocytes, and spermatogonia
*cell dies before undergoing mitosis
How Apoptosis Occurs
*cell condenses
*produces blebs of cytoplasm
Gene Involved in Apoptosis
P53 gene
Reproductive Failure
inability to divide indefinitely or produce a clone
Most Common Response of Tumors and Normal Tissue to Radiation
reproductive failure (clonogenic death)
When Reproductive Failure Occurs
*when cell attempts mitosis
*cell often maintains other functions until death
Most Effective Response to Radiation
reproductive failure
Why Different Tumors Have Different Responses to Radiation
reproductive failure in fast and slow growing tumors
How Reproductive Failure Influences Tumor Status
*some tumors don't shrink, just stop growing
*why we wait six months to evaluate treatment
X Axis of Survival Curve
*dose
*exhibited linearly
Y Axis of Survival Curve
*percent survival
*exhibited as a logarithm
N on Survival Curve
*extrapolation number
*defines size of the shoulder
*where dotted line crosses the y axis
Do on Survival Curve
*terminal slope
*where survival curve goes from .01 to .0037
Dq on Survival Curve
description of the size of the shoulder
Alpha and Beta on Survival Curve
*used in linear quadratic model
*assumes some killing
*linearly proportional to dose
*quadratically proportional to the square of the dose
*constants when used in an alpha/beta ratio to describe the shape of the curve
Sublethal Damage
can be repaired unless additional damage occurs
Experiments that Demonstrate Sublethal Damage
split dose experiments where survival of cells exposed to specific dose of radiation increases if dose is delivered in two fractions seperated by time
Result of More Time Between Fractions
survival increases as a result of sublethal damage
How Sublethal Damage Influences the Survival Curve
more sublethal damage results in a wider shoulder
Potentially Lethal Damage
damage that may be expressed depending on the environment
Conditions That Result in Increased Survival Following Radiation Exposure
conditions that are poor for growth
Clinical Relevance of Potentially Lethal Damage
of little clinical relevance, but may effect some tumors
Law of Bergonie and Tribondeau
*poorly differentiated cells are more sensitive to radiation
*rapidly dividing cells are more sensitive to radiation
Effect of Dose Rate on Survival Curve
*decreased dose rate allows more repair of sublethal damage
*cells with large shoulders on the survival curve have a greater dose rate effect, and thus will benefit from a higher dose rate
Oxygen Enhancement Ratio
measure of increase radiosensitivity with addition of oxygen
Type of Radiation Most Likely to Exhibit Oxygen Enhancement
x-rays
Effect of Hypoxia on Radiation
hypoxia increases a cells resistance to radiation, resulting in increased survival compared to aerated cells
Effect of Increased Oxygen on Radiation
increased radiosensitivity
Way the Cell Cycle Influences the Oxygen Enhancement Ratio
*increased oxygen enhancement ratio in S phase
*decreased oxygen enhancement ratio in G2 phase
Oxygen Effect with High LET Beams
no oxygen effect as there is no shoulder
Oxygen Effect with Large Tumors
*large tumors outgrow blood supply and are hypoxic
*more cell survival with large tumors
Effect of Mitosis on Radiosensitivity
highly mitotic cells are very radiosensitive, as mitosis is the most radiosensitive phase
Least Sensitive Phase of Cell Cycle
G2
TD 5/5
dose where 5% of the population irradiated will develop the complication at 5 years
TD 50/5
dose where 50% of the population irradiated will develop the complication at 5 years
Systemic Response of Hematopoietic System
-bone marrow stem cells
-very sensitive
-acute anemia and thrombocytopenia
-no chronic effects
Systemic Response of Skin System
-epithelial cells
-very sensitive
-acute erythema and desquammation
-chronic ulceration, fibrosis, and telangietasis
Systemic Response of Digestive Tract
-crypt cells of jejunum
-very sensitive
-acute shortening of villi and diarrhea
-chronic small bowel obstruction and hematochezia in rectum
Systemic Response of Reproductive System
-spermatogonia and oocytes
-very sensitive
-acute azospermia
-chronic infertility
Systemic Response of Respiratory System
-type II pneumocytes
-sensitive
-acute pneumonitis
-chronic fibrosis
Systemic Response of Urinary System
-tubule cells
-very sensitive
-acute nephritis, hypertension, proteinuria, and uremia
-chronic hypertension and nephropathy
Systemic Response of Nervous System
-oligodendrocytes and possibly neurons
-sensitive
-acute Lhermitte's sign
-chronic myelopathy
Examples of Early Responding Tissues
-skin
-hair
Examples of Late Responding Tissues
-spinal cord
-muscle
Shoulder on Survival Curve for Early Responding Tissues
smaller shoulder than late responding tissues
Alpha/beta ratio for Early Responding Tissues
higher alpha/beta ratio
Tolerance Dose for Spinal Cord
4500 cGy
Tolerance Dose for Small Bowel
4500 cGy
Tolerance Dose for Lens
500-1000 cGy
Tolerance Dose for Lung
1500-2000 cGy
Tolerance Dose for Partial Brain
6000 cGy
Tolerance Dose for Whole Brain
4500-5000 cGy
Somatic Effects
-seen in exposed individual
-acute or late
Genetic Effects
-seen in progeny of exposed individual
-result of mutation that occurred that was not lethal to cell
-also called hereditary effects
Stochastic Effects
-no threshold dose (except zero)
-dose will not predict severity, but will predict likelihood of occurence
Example of Stochastic Effect
secondary malignancy
Deterministic Effects
-threshold dose
-severity is determined by dose of radiation
Example of Deterministic Effects
cataracts
Defining Characteristics of Radiation Induced Malignancy
-not a recurrence of original tumor
-within the radiation field
-occurs after a latent period of years, usually 8-10 years
-all types of tumors may be seen
Exposure Required to Induce Hematopoietic Syndrome
2.5-10 Gy
Prodromal Stage of Hematopoietic Syndrome
nausea and vomiting
Latent Stage of Hematopoietic Syndrome
no overt symptoms, but decline of hematologic indicators
Illness Stage of Hematopoietic Syndrome
-begins about 3 weeks after exposure
-fever, chills, sweats, epilation, hemorrhage, bleeding, infection
LD50 for Hematopoietic Syndrome
4 Gy
Supportive Measures for Hematopoietic Syndrome
-fluids, transfusions, and antibiotics for doses below 5 Gy
-bone marrow transplant may be attempted for doses between 8-10 Gy
-GI syndrome will be fatal at doses above 10 Gy
Four Rs of Radiobiology
-repair
-reoxygenation
-repopulation
-redistribution
Repair
-sublethal damage is repaired
-fractionation takes advantage of repair in normal tissues
Reoxygenation
-hypoxic cells are aerated
-fractionation takes advantage of reoxygenation of the tumor cells, as hypoxic parts of the tumor are oxygenated and become more radiosensitive
Redistribution
-cells are synced into more radiosensitive part of the cell cycle
-fractionation takes advantage of tumor cells being redistributed so they are more radiosensitive
Regeneration
-repopulation with new cells
-fractionation takes advantage of regeneration of healthy tissue