Term
|
Definition
| Ganglion in the sympathetic trunk (inferior cervical/T1) for heart and lungs. |
|
|
Term
|
Definition
| These nerves head to the splanchnic compartment (viscera) |
|
|
Term
| Collateral (prevertebral) ganglia |
|
Definition
| These ganglia contain cell bodies for sympathetic nerves going to the abdominal and pelvic viscera. The pre-synaptic nerves pass through the sympathetic trunk without synapsing. |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Parasympathetic nerves come from: |
|
Definition
| Parasympathetics have "craniosacral outflow." They come from the vagus nerve and pelvic splanchnic nerves (spinal ventral rami S2,3,4) |
|
|
Term
At what levels do sympathetic nerves leave the spinal cord?
At what levels do they return? |
|
Definition
Leave: T1-L2
Return: All levels. Through the communicating rami and the dorsal root. |
|
|
Term
The somatic nervous system invades:
The autonomic invades:
The exception is: |
|
Definition
Somatic - somatopleure (body wall)
Autonomic - splanchnopleure (viscera)
Exception - Sympathetics. They're everywhere (arteries) |
|
|
Term
|
Definition
| Ribosomes in a neuron. Look like black sprinkles in the cell body. |
|
|
Term
|
Definition
| Support cells in the CNS. Line ventricles and central canal. |
|
|
Term
|
Definition
| A scaffolding in brain tissue. Processes surround small vessels, neurons and CSF spaces. Most common source of brain tumors. |
|
|
Term
|
Definition
| Phagocytotic. Proliferate as needed. From the monocyte cell line, not the neural crest. |
|
|
Term
| Multiple sclerosis targets which part of the nervous system? |
|
Definition
| It is an autoimmune disorder affecting myelination. |
|
|
Term
|
Definition
| Areas of cytoplasm that allow for cytoplasmic continuity from the outside to the inside of the schwann cell. |
|
|
Term
| How is a nerve signal sent? |
|
Definition
| Depolarization causes Calcium channels to open. The influx causes synaptic vesicles to fuse to the cell wall and release their neurotransmitter. This attaches to postsynaptic receptors, causing a change in conformation that opens ion channels. Depolarization and propagation or hyperpolarization are both possible. |
|
|
Term
| Why is perinerium different from perimyseum? |
|
Definition
| It has tight junctions (blood nerve barrier), dense bodies (actin), can act like smooth muscle and produce collagen like fibroblasts. |
|
|
Term
| Internal Vertebral Plexus |
|
Definition
| Veins lining the epidural space. How prostate cancer metastasizes to the brain. |
|
|
Term
|
Definition
| These are like post-synaptic sympathetic cells for the whole body. They are innervated by pre-synaptic sympathetic neurons. |
|
|
Term
|
Definition
| AKA Sheath of Schwann. The outermost layer of Schwann cell that surrounds the axon. |
|
|
Term
|
Definition
| Thin part between the axon hillock and the myelin sheath. Where an axon potential is generated. |
|
|
Term
| Slow transport (in a neuron) |
|
Definition
| Only anterograde (body to terminal). For structural elements. |
|
|
Term
| Fast transport (in a neuron) |
|
Definition
| Both directions. Anterograde is for many cell organelles and elements (including small molecules like AAs, sugars, etc). Retrograde is for the same, plus things endocytosed at the terminal. |
|
|
Term
|
Definition
| Button like dilation at the terminal of the axon. Filled w/ synaptic vesicles. |
|
|
Term
|
Definition
| conical dense inward projections of the neural membrane at the axon terminal. |
|
|
Term
| Myelin Basic Protein (MBP) |
|
Definition
| Protein that is part of the myelin sheath that aids in compaction. MS is an autoimmune attack on MBP. |
|
|
Term
|
Definition
| A transmembrane glycoprotein that connects adjacent layers of myelin sheath. A major structural component of myelin. |
|
|
Term
|
Definition
| Intermediate filaments that, along with microtubules, are important components of axons and dendrites. |
|
|
Term
| Where does the phrenic nerve come from? |
|
Definition
| C3,4,5 keeps the diaphragm alive. It comes from the ventral rami of these 3 vertebrae. |
|
|
Term
|
Definition
| When the abdominal wall doesn't entirely form and the intestines are outside the body. |
|
|
Term
| Follow the developmental chain of paraxial mesoderm |
|
Definition
| Turns into somites. These divide into deramyotome, and sclerotome. Deramyotome divides into dermatome and myotome. Myotome divides into hypo mere and epimere. |
|
|
Term
| Intermediate mesoderm develops into: |
|
Definition
|
|
Term
| Lateral plate mesoderm turns into: |
|
Definition
| Splanchnic mesoderm and somatic mesoderm. These along with endoderm and ectoderm respectively form splanchnopleure and somatopleure. |
|
|
Term
|
Definition
| Non-nervous tissue that comes from the neural crest. |
|
|
Term
|
Definition
| The aponeuroses that cover the rectus abdominous. |
|
|
Term
| In the lower 1/4 of the abdomen what are the layers and their order? |
|
Definition
| X Oblique, I Oblique, Transversus abdominous, rectus abdominous, transversalis fascia, parietal peritoneum. |
|
|
Term
|
Definition
| AKA Cooper's ligaments. Attach the breast to deep fascia. |
|
|
Term
| Intercostal nerves run between which two layers? |
|
Definition
| It runs between the internal innercostal muscles and the innermost intercostal muscles. |
|
|
Term
|
Definition
| Bowed outward. Thoracic region of the spine. |
|
|
Term
|
Definition
| Inward curvature. As in the cervical and lumbar regions of the spine. |
|
|
Term
|
Definition
|
|
Term
| What are the 3 intrinsic muscle layers of the back? |
|
Definition
| Splenius, Erector spinae, and Transversospinalis. |
|
|
Term
|
Definition
| The facia right above the parietal pleura in the thorax. |
|
|
Term
|
Definition
| The layer right above the parietal peritoneum in the abdomen. |
|
|
Term
|
Definition
| Protein rich fluid (from thoracentesis or pericardiocentesis). |
|
|
Term
|
Definition
| Water fluid from thoracentesis or pericardiocentesis. |
|
|
Term
|
Definition
| Embryologic precursor for the central tendon of the diaphragm. |
|
|
Term
|
Definition
| Embryonic precursors that eventually combine to separate the pleural and pericaridal cavities. It turns into the fibrous pericardium. |
|
|
Term
| Layers of the pericardium |
|
Definition
| Fibrous (connective tissue anchoring the heart), then two serous layers: parietal pericardium (fused to the fibrous pericardium) and the visceral pericardium (aka epicardium on the heart muscle itself). |
|
|
Term
|
Definition
| Plural space, pericardial space, peritoneal space. |
|
|
Term
|
Definition
| For respiration. Increased volume leads to decreased pressure. |
|
|
Term
|
Definition
| Diaphragm, External Intercostals, Pectoralis Maj. and min., Serratus anterior. |
|
|
Term
| Forced Expiration Muscles |
|
Definition
| Internal intercostals, rectus abdominous. |
|
|
Term
|
Definition
| Where the trachea splits. |
|
|
Term
|
Definition
| 1. Drain fluids 2. Absorb emulsified fat 3. Immune system 4. Re-circulate proteins from blood capillaries. |
|
|
Term
| What are the 3 main lymphatic trunks? |
|
Definition
| 1. Jugular trunk (drains head/neck) 2. Subclavian trunk (drains axillary nodes) 3. Bronchomediastinal trunk (drains heart and lungs). All dump in at the junction of the internal jugular vein and the left subclavian vein. |
|
|
Term
| What part of the body's lymph empties in the right side? |
|
Definition
| Above the umbilicus and right of center. The only exception being the deep body wall which drains into the thoracic duct. |
|
|
Term
| Where does lymph cross the superficial fascia from the superficial body wall to go to deeper lymphatic vessels? |
|
Definition
| The axillary or superficial inguinal nodes. |
|
|
Term
|
Definition
| Where the lymph drains from the superficial inguinal nodes to the deeper lymphatics. LVAN - nerve is outside the sheath. |
|
|
Term
|
Definition
| The line separating the gut from the body wall. (anus) Lymph will not penetrate this. |
|
|
Term
|
Definition
| Receive lymph in the abdomen. Dumps into the cisterna chyli. Collects everything from lower half of the body (superficial and deep - including the abdominal organs) |
|
|
Term
| Where does deep lymph in the arm go? |
|
Definition
| The axillary lymph nodes. |
|
|
Term
| Where does lymph from the heart and lungs drain? |
|
Definition
| To the bronchomediastinal trunk. (lymph can pass to opposite sides here). |
|
|
Term
| Where does lymph from the breast drain? |
|
Definition
| Upper lateral - axillary nodes. Medial - can drain to the parasternal nodes. Some can drain to the opposite breast. Possibly the superficial inguinal nodes as well (rare). |
|
|
Term
| What and to where do the deep parasternal lymph nodes drain? |
|
Definition
| They drain anterior intercostal lymph, upper liver lymph, and some breast lymph to the bronchomediastinal trunk. |
|
|
Term
| Where does esophageal lymph go? |
|
Definition
| To the thoracic trunk and/or the bronchomediastinal trunk. |
|
|
Term
| What are the 6 imaging modalities? |
|
Definition
| X-ray, Ultrasound, MRI, CT Scan, Nuclear medicine, PET scan |
|
|
Term
| What does effective radiation does account for? |
|
Definition
| Dose, harm, sensitivity of organs. |
|
|
Term
| What is the ALARA principle? |
|
Definition
| For radiation exposure: As Low As Reasonably Achievable. Think: is there an alternative? |
|
|
Term
|
Definition
| 1. Air 2. Fat 3. Soft tissue or water 4. Bone 5. Metal/contrast |
|
|
Term
| Types of X-ray imaging (7) |
|
Definition
| X-ray, Mamography, Fluoroscopy (GI contrast studies), Angiography (blood vessel studies), Myelography (spinal subarachnoid space), Arthrography (joint space), CT |
|
|
Term
| What material can ultrasound not penetrate? |
|
Definition
| Air. Therefore it can only be used on certain structures. (Black you see is fluid) |
|
|
Term
| What is duplex dopler used for? |
|
Definition
| Echocardiography. To see blood flow. |
|
|
Term
| What is nuclear medicine? |
|
Definition
| Imaging where an image is generated by a radioactive agent tagged to a specific tissue. Tests for function rather than anatomy. Eg: bone scan |
|
|
Term
| What allows for specificity in pharmacology (and biology)? |
|
Definition
| Receptors. The body has many unique chemical receptors that are incredibly specific. |
|
|
Term
| What is a receptor (pharmacology)? |
|
Definition
| Anything that can be a drug target, including: 1. Cell surface or intracellular regulatory proteins 2. Enzymes 3. Structural Proteins 4. Nucleic Acids (ATP) |
|
|
Term
| What two features does a receptor need? |
|
Definition
| A recognition site and a transduction mechanism. |
|
|
Term
| What determines the quantitative relationship between a drug and its pharmacological effects? |
|
Definition
|
|
Term
| What does an antagonist do? |
|
Definition
|
|
Term
|
Definition
| Binds and eliminates the constitutive activity of a receptor, something an antagonist cannot do. Has negative efficacy. |
|
|
Term
|
Definition
| Inactivation of one drug by the direct binding of another drug. Bind the drug before it can act. |
|
|
Term
|
Definition
| Using a drug targeting a physiological response that will counteract the actions of another drug. Eg: Insulin |
|
|
Term
| Pharmacological antagonism |
|
Definition
| Ligands that bind to, but do not activate, receptors. What you normally think of. |
|
|
Term
|
Definition
|
|
Term
| Why are some antagonists irreversible? |
|
Definition
| They form covalent bonds with the receptor. |
|
|
Term
| What is an uncompetitive allosteric site? |
|
Definition
| A site that requires receptor activation before it becomes accessible. |
|
|
Term
| What is a noncompetitive allosteric site? |
|
Definition
| An allosteric site where the antagonist can bind regardless of the presence or absence of agonist. |
|
|
Term
| Agonist independent negative allosterism |
|
Definition
| Inverse agonist. Reduces activity regardless of the presence of the agonist. |
|
|
Term
| Partial Agonist vs. Full agonist |
|
Definition
| Full agonist can elicit a maximum effect. Partial can't no matter how much you use. |
|
|
Term
| Do competitive antagonists have to look like their agonist? |
|
Definition
| No. They may resemble the agonist, or they may be quite different. |
|
|
Term
| What is pharmacokinetics? |
|
Definition
| Quantitative relationship between drug concentration and response. Looking at drugs in vivo. What is its effect? Will it metabolize? Are the metabolites active? What is their effect? |
|
|
Term
|
Definition
|
|
Term
|
Definition
| The concentration/dose that yields 50% of the maximum response that drug can elicit. |
|
|
Term
|
Definition
| This is a measure of the drug effect. Seen by the equation. |
|
|
Term
|
Definition
| A & B are equally effective. A & C are equipotent. They are more potent then B. |
|
|
Term
| What has an efficacy of 0? (Pharm) |
|
Definition
| Antagonists. They never produce a response by themselves. |
|
|
Term
| Quantal Dose Response Curve |
|
Definition
| This is used when the response is binary (death or not, pregnant or not, etc.) ED50 is the dose where half of the people had the effect. |
|
|
Term
|
Definition
| Toxic ED50/Beneficial ED50. Measures the relative toxicity vs the therapeutic utility of a drug. The farther apart the two curves are the better. You want the Index to be a high number. |
|
|
Term
|
Definition
| Lethal Dose 50. The Toxic ED50 when death is the measure of toxicity. |
|
|
Term
|
Definition
| The study of how genetics affects variation in drug response. Often an enzyme variant can greatly affect drug response (metabolized faster or slower than normal). |
|
|
Term
|
Definition
| The important graph you see in pharmacology. |
|
|
Term
| How do competitive antagonists affect the DR curve? |
|
Definition
| Parallel shift to the right. Requires a higher concentration of agonist to have the same effect, but it can overcome it completely. Decreases potency, no effect on efficacy. |
|
|
Term
| How does a non-competitive antagonist affect the DR curve? |
|
Definition
|
|
Term
| Noncompetitive antagonist |
|
Definition
| An antagonist that binds covalently to the orthosteric site or an allosteric site. It takes certain receptors out of play. This decreases the efficacy of a drug, but doesn't affect its potency. |
|
|
Term
| What is an inhibition-response relationship? |
|
Definition
| Agonist dependent. Determines the potency of the antagonist at a given agonist concentration. |
|
|
Term
|
Definition
| Agonist independent. Determines the antagonist equilibrium constant. |
|
|
Term
| Inhibition Response Curves |
|
Definition
| These measure response at various antagonist concentrations. |
|
|
Term
|
Definition
| These measure antagonist concentration at which 50% of the effect is inhibited. This will change depending on the agonist concentration. |
|
|
Term
|
Definition
| The fold increase in agonist concentration needed to give the same % response in the presence of a given concentration of antagonist. |
|
|
Term
|
Definition
| The name for the transduction process between receptor binding and biological effect |
|
|
Term
|
Definition
| Not all receptors need to be bound to achieve 100% effect. This can make low doses of non-competitive antagonist seem like competitive antagonists. |
|
|
Term
| Monod-Wyman-Changeux model |
|
Definition
| Receptors are in two states, active or inactive. Agonists and antagonists shift the eqbm toward one or the other. |
|
|
Term
| Koshland-Nemethy-Filmer model |
|
Definition
| Receptors undergo sequential non-concerted changes to a multitude of possible conformations. |
|
|
Term
| Name the 5 major receptor families. |
|
Definition
| 1. Intracellular receptors 2. Receptors that act as an enzyme 3.Enzyme-Linked Receptors 4. Ligand/Voltage Gated Ion Channels 5. G Protein-coupled receptors |
|
|
Term
| List 3 characteristics of Intracellular receptors |
|
Definition
| 1. Ligands must be lipophilic (to cross the plasma membrane - often these are steroids) 2. Receptors often enter the nucleus after binding to alter gene transcription 3. This action usually takes time. |
|
|
Term
| List characteristics of Enzyme-Linked Receptors |
|
Definition
| Signaling response is slow (hours). Start a cascade that leads to changes in transcription. Kinases and kinase associated. |
|
|
Term
| Receptor Tyrosine Kinases (RTKs) |
|
Definition
| These are Enzymatic receptors (type 2). |
|
|
Term
| Tyrosine-Kinase associated receptors (type 3) |
|
Definition
| These kinases can float away and trigger other mechanisms in the cell once activated. Cytokine receptors are the largest family of these. |
|
|
Term
| Ion channels have 3 gating mechanisms. What are they? |
|
Definition
| 1. Voltage gated 2. Ligand gated 3. Mechanically gated |
|
|
Term
| Name 3 types of ligand gated ion channels. |
|
Definition
| 1. Cys-loop receptors (pentameric) 2. Ionotropic Glutamate Receptors (tetrameric) 3. Ionotropic ATP receptors (trimeric) |
|
|
Term
| What are two examples of channelopathies? |
|
Definition
| Cystic fibrosis, long QT syndrome |
|
|
Term
| What are 4 families of G protein coupled receptors? |
|
Definition
| A. Rhodopsin-like B. Secretin-like C. metabotropic 4. Frizzled family |
|
|
Term
| What are the relative time frames of the receptors? |
|
Definition
| Fastest to slowest - ion channels, GPCRs, Enzyme linked, Intracellular |
|
|
Term
|
Definition
|
|
Term
| What are the two types of tachyphylaxis? |
|
Definition
Receptor Mediated: only the activated receptor desensitizes (loss of receptor function or decrease in receptor number)
Non-receptor mediated: Decoupling of downstream elements required for signaling. |
|
|
Term
| What is Beta-arrestin an example of? |
|
Definition
| Receptor mediated tachyphlaxis. It prevents interaction between the receptor and the G-protein. It also promotes internalization of receptors (decreasing receptor #). |
|
|
Term
| What is the resting potential of a cell? |
|
Definition
|
|
Term
| What is the Vm (membrane potential) of cells used for? |
|
Definition
| 1. Potential Energy. It acts as a battery to power many cellular processes. 2. Communication (in excitable cells only). |
|
|
Term
| What is the ion permeability model? |
|
Definition
| The conceptual explanation for membrane potentials and how they work. They key is K+ is leaked out of the cell until the chemical force equals the electrical force (occurs w/ a net - inside the cell). |
|
|
Term
|
Definition
|
|
Term
| Goldman-Hodgkin-Katz Equation |
|
Definition
| This equation is used to find the membrane potential. It does this by evaluating the equilibrium potentials of all of the ions and adjusting for their permeability. Sort of a weighted average. |
|
|
Term
|
Definition
| Uses Ohm's Law to understand membrane potentials. Can be used experimentally. |
|
|
Term
| How does the cell compare to a circuit? |
|
Definition
| Ion channels are conductors, the membrane is a capacitor, the nernst potentials are batteries. Helps explain the time delay. |
|
|
Term
| What is G in the Equivalent Circuit model? |
|
Definition
| Conductance. You use that and their potentials to calculate the membrane potential. They are capacitors and conductors in series. |
|
|
Term
|
Definition
| It moves 3 Na out and 2 K in. Balances when the pump equals the flux due to leakage. This one complex uses ~30% of your energy. |
|
|
Term
| Name two types of action potentials that differ from each other. |
|
Definition
|
|
Term
| Why can't you have multiple action potentials in a row? |
|
Definition
| Absolute Refractory period. The Na and K channels are inactivated after they open. Afterward the hyper-polarization causes the relative refractory period. |
|
|
Term
| How does the NaKATPase work? |
|
Definition
Exposed Na+ sites inside the cell. ATP driven mech. (phophorylates the pump). The change in conformation
lowers the binding affinity for Na+. Potassium binding sites are exposed. Then the phosphate is hydrolyzed, which make it change conformation again. This lowers binding affinity for K+ and we start over. |
|
|
Term
|
Definition
| Have a binding site like an enzyme. Have conformational change. Slow flux rates. |
|
|
Term
|
Definition
| Discriminate based on size and charge. Open channels allow ions and H20 to pass. Fast flux. |
|
|
Term
| Voltage gated Na channels have many pores all part of the same polypeptide. |
|
Definition
| They are repeats of 6 subunits 4 repeats form the channel. |
|
|
Term
| How does a voltage sensor work? |
|
Definition
| It has to be packed with charges opposite the charge you want to sense. It will attract or repel. This tugging motion opens the gate. |
|
|
Term
| How many types of K+ channels are there? |
|
Definition
| Many. 6 TM and 2TM versions. Each repeat is its own peptide. Products of different genes form the pore. Functional heterogeneity. |
|
|
Term
| How do channels have ion selectivity? |
|
Definition
| They have built in hydrogen bonding that only works for the ion of the right size. |
|
|
Term
| List some unique characteristics of stem cells. |
|
Definition
| They retain DNA markers due to asymmetric DNA division, they replicate as needed, they are able to pump out drugs quickly (a protective mechanism). |
|
|
Term
| How does a stem cell know what to become? |
|
Definition
| The stroma! The microenvironment around the cell. |
|
|
Term
| Why does scar tissue form rather than replacement of healthy tissue by stem cells? |
|
Definition
| If the stroma/microenvironment is destroyed, stem cell formation is blocked, so scar tissue forms. |
|
|
Term
| Describe the difference between endocrine, paracrine, and autocrine signaling. |
|
Definition
| Endocrine - releases hormone into the bloodstream. Widespread affect. Paracrine - affects nearby cells. Autocrine - affects itself. |
|
|
Term
|
Definition
| Increase in the size of cells. Proliferation of organelles. Eg: muscle growth after weight lifting. |
|
|
Term
|
Definition
| Increase in the number of cells. Eg: a callus. |
|
|
Term
|
Definition
| Decrease in the size of cells |
|
|
Term
|
Definition
| Decrease in the number of cells. Eg: Post menopausal endometrium |
|
|
Term
|
Definition
| Change in differentiation from one cell type to another. Reversible. Eg: Barret's esophagus, Myositis ossificans, smokers lung (simple squamous). Can serve as a nidus for dysplasia. |
|
|
Term
|
Definition
| Abnormal hyperplasia with a propensity to malignant change. Sometimes reversible. Linked to DNA damage. Eg: HPV - 1/3 will go away, 1/3 won't do anything, 1/3 will cause cancer. |
|
|
Term
|
Definition
| Cellular autonomy and uncontrolled growth. Benign and malignant tumors. Irreversible. |
|
|
Term
|
Definition
| Causes cell division. Activates a receptor and starts a cascade that initiates the cell cycle. |
|
|
Term
|
Definition
| Causes cells to migrate or scatter. |
|
|
Term
|
Definition
| Differentiation-inducing factors (cause morphology to change) |
|
|
Term
|
Definition
| Cell releases signaling molecules intracellularly (within itself). Never leave the cell like autocrine signals. |
|
|
Term
| List the 4 ways a cell can respond to a stimulus or injury. |
|
Definition
| 1. Ignore (quiescence) 2. Adapt 3. Divide and differentiate 4. Die (Apoptosis or Necrosis) |
|
|
Term
|
Definition
| Death of groups of cells. Plasma membrane damage and activation of degradation enzymes in an uncontrolled manner. Leads to inflammatory response, and random breaks in DNA. Ghost like appearance - due to degradation of proteins/organelles. |
|
|
Term
| List the 5 types of necrosis |
|
Definition
| 1. Caseous 2. Coagulative 3. Liquefactive 4. Fat 5. Tumor |
|
|
Term
| Pathology: Pink means... Blue means... |
|
Definition
| Pink - Cell death. Blue - WBCs are infiltrating, or it's malignant. |
|
|
Term
|
Definition
| Cell death caused by ishemia (aka infarction) or by exposure to toxic agents. Early acute inflammation, later scar formation. |
|
|
Term
|
Definition
| A form of coagulative necrosis. Tissue dissolves and a cyst forms. No immune response is triggered. Eg: Brain after ischemic injury. |
|
|
Term
|
Definition
| A group of macrophages that are turned on and become large. Trying to wall off things the immune system can't remove. May be caseous in the center. If they are that's a sign of infection rather than genetic or foreign body disease. |
|
|
Term
|
Definition
| Occurs in a granuloma. Looks like cheese. Has characteristics of both coagulative and liquefaction necrosis (center slowly liquefies). |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Occurs w/ the pancreas. Damage causes it to auto digest. Yellowish to white. Accumulates calcium (saponification) which can cause physiologic problems. |
|
|
Term
|
Definition
| A term used for a type of coagulation necrosis in the soft tissues of the lower limbs. |
|
|
Term
|
Definition
| Cell death that occurs when a tumor's growth outstrips its blood supply. Therapy leads to necrosis of tumors. |
|
|
Term
| What are the 5 mechanisms that lead to necrosis? |
|
Definition
| 1. ATP Depletion 2. Loss of calcium homeostasis 3. Free radicals (as in re-perfusion injury) 4. Loss of membrane permeability 5. Damage to DNA and proteins. |
|
|
Term
|
Definition
| Yes. Certain storage diseases can cause necrosis. Once the cell accumulates too much of something it will die. |
|
|
Term
| How do you measure the degree of necrosis? |
|
Definition
| Serum enzymes. They're released into the blood when the cells die. |
|
|
Term
| What are two key differences between apoptosis and necrosis? |
|
Definition
| Apoptosis is the death of a single cell (not groups of cells). Also apoptosis does not trigger an immune response. |
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Term
| What is the ultimate cell executioner in apoptosis? What activates it in intrinsic apoptosis? |
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Definition
| Caspases (through proteolytic cleavage). Activated by cytochrome c. |
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Term
| How does extrinsic apoptosis work? |
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Definition
| Apoptotic receptors are activated. |
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Term
| What are 5 uses for apoptosis? |
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Definition
| 1. Tissue remodeling in embryo 2. Removal of activated T cells at the end of immune response 3. Removal of DNA damaged cells 4. Killing of inflammatory cells at immune privileged sites (eye) 5. Elimination of virus infected cells |
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Term
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Definition
| Fatty liver. Reversible. Eventually over accumulation leads to cell death which triggers an inflammatory response which leads to fibrosis (cirrhosis) which is not reversible. |
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Term
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Definition
| Liver accumulations. Tangled intermediate filaments. Reversible. |
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Term
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Definition
| Basically a pore that brings bad proteins back into the cell where they can be targeted by the ubiquitin-proteosome system. |
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Term
| List 4 things that accumulate in the cell. |
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Definition
| 1. Lipofuscin - The "sludge" of cells. Accumulates of the cell's life. Non-toxic to the cell. Clears when cells divide. 2. Melanin 3. Hemosiderin - accumulation of ferritin. 4. Uric acid - leads to gout |
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Term
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Definition
| Bruise. The body wants to recover the iron. |
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Term
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Definition
| Calcium deposition in damaged tissue due to negative charge in dead tissue. Also Psammoma bodies - tomb for cancer cell. |
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Term
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Definition
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Term
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Definition
| Limited replication of cells. They can only divide about 50 times. |
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Term
| What are the 7 Hallmarks of cancer? |
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Definition
| 1. Self-sufficiency in growth signals 2. Insensitivity to growth-inhibitory signals 3. Evasion of apoptosis 4. Limitless replicative potential 5. Sustained angiogenesis 6. Tissue invasion and metastasis 7. Defects in DNA repair |
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Term
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Definition
| Extreme disorganization. Lack of differentiation. As in neoplasia. |
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Term
| What are the two factors needed to cause cancer? |
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Definition
| Initiation and promotion. |
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Term
| What are some pro to-oncogene products? |
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Definition
| Growth Factors, Growth Factor Receptors, Signal transducers, Transcription factors. |
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Term
| What are the 4 ways a Proto-oncogene can become an oncogene? |
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Definition
| 1. Mutation 2. Abnormal activity (removal of the regulatory domain) 3. Gene translocation (anything to chrome 14) 4. Amplification (additional repeats). |
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Term
| What do oncogenes affect? |
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Definition
| 1. Cell proliferation or 2. Cell differentiation (keeps a cell in it's active proliferative state) 3. Cell survival (no apoptosis) |
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Term
| What are the 4 functions of tumor suppressor genes? |
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Definition
| 1. Antagonize an oncogene. 2. Transcription factors 3. Regulate the cell cycle (RB, p53) 4. Induce apoptosis. |
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Term
| Do malignancies come from dysplasia? |
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Definition
| Yes, but more commonly they arise de novo. |
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Term
| What are the 4 main categories for cancer? |
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Definition
| Carcinoma (epithelial), Lymphoma (lymphocytic), Melanoma (melanocytic), and Sarcomas (most everything else - mesoderm) |
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
| Variation in cell size and shape. |
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Term
| Malignant cells have what characteristics? |
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Definition
| Ugliness. Pleomorphism and Anaplasia. Loss of architecture. |
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Term
| What 3 factors determine tumor growth rate? |
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Definition
| What proportion of the cells divide, how fast they divide, and the ratio of cell division to cell death (turnover). |
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Term
| What are the 3 pathways of metastatic spread? |
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Definition
| 1. Lymphatic 2. Hematogenous (usually through small veins to other sites) 3. Seeding of body cavities (tumors in the peritoneum) |
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Term
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Definition
| T1-4 N0-3 M0-1 The combined measure is used to determine the stage of the cancer. |
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Term
| Why are people w/ cancer sick? |
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Definition
| Direct effect of the tumor, Cachexia, Paraneoplastic syndromes, infection, bleeding/thrombosis |
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Term
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Definition
| Wasting, lethargy, loss of appetite. Due to increased caloric consumption (some due to tumor, mostly metabolic). Etiology linked to cytokines. |
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Term
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Definition
| Remote effects of the tumor. Eg: Ectopic hormone production (parathyroid leads to hypercalcemia), Autoimmune (body trying to attack the tumor accidentally self attacks). |
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Term
| Hematologic effects of cancer |
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Definition
| Infection/immunosuppression, Thrombosis/bleeding, anemia. This is usually what actually kills people w/ cancer. |
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Term
| Are geographic risk factors for cancer environmental, or racial/cultural? |
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Definition
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Term
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Definition
| Stage - extent of the tumor spread (0-IV) Grade - degree of differentiation. |
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Term
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Definition
| Used to measure DNA synthesis and thus see tumor growth. |
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Term
| What are the 4 steps of tumor invasion? |
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Definition
| 1. Changes of tumor cell-cell interactions (cadherins) 2. Degradation of the ECM (using MMPs) 3. Changes in the attachment of tumor cells to ECM proteins (prepare for migration) 4. Locomotion - directed by tumor cell-derived cytokines. |
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Term
| What are the 7 steps of metastasis? |
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Definition
| 1 Invasion of the basement membrane 2 migration through the ECM 3 Penetration of the vessel wall 4 Survival and transport in vessels 5 Arrest in target organ 6 Extravasation in secondary sites (leave vessel) 7 Survival and growth at metastatic site |
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Term
| Dominant or Recessive? Tumor suppressor genes vs oncogenes. |
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Definition
| Oncogenes are dominant. Tumor suppressors are recessive. |
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Term
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Definition
| An oncogene in breast cancer. |
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Term
| What is the most commonly mutated oncogene? |
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Definition
| The RAS oncogene. RAS is a signal transducer used in a lot of pathways in the cell. A mutation here causes lots of problems. |
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Term
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Definition
| A commonly mutated oncogene, involved in apoptosis. |
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Term
| What does Cyclin D-CDK4 do? Why is it important? |
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Definition
| It phosphorylates RB. The on-off switch for the cell cycle. |
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Term
| Which checkpoints in the cell cycle check for DNA damage? |
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Definition
| The G1-S checkpoint (mediated by p21 and p53) and the G2-M checkpoint (mediated by p53). |
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Term
| What is the "guardian of the genome"? |
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Definition
| The P53 gene. It acts as a molecular policeman looking for DNA damage. It can arrest the cell cycle or initiate apoptosis if it finds problems. |
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Term
| What are the pro-apoptotic genes? |
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Definition
Intrinsic: p53, cytochrome-c, BAK, BAX, Caspases.
Extrinsic: TNFr and FAS are the receptors. They induce the assembly of DISC and recruitment of caspases through the FADD. |
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Term
| What are the anti-apoptotic genes? |
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Definition
| BCL2 (if this gets translocated to an active site it will suppress apoptosis and can lead to tumor formation), MCL1, IAP. |
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Term
| What is the APC/B-Catenin pathway? |
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Definition
| Two genes whose mutation leads to colon cancer. |
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Term
| BRCA-1,2 are what kind of genes? |
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Definition
| DNA recombination repair genes. |
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Term
| What are the 3 types of DNA repair that can be defective in cancer? |
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Definition
| 1. Mismatch repair 2. Nucleotide excision repair 3. Recombination repair. |
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Term
| What are "caretaker" genes? |
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Definition
| DNA repair genes. Defects here lead to a higher risk of malignancy vs defects in the "gatekeeper" genes (i.e. oncogenes and tumor suppressor genes). |
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Term
| Why are carcinogens electrophilic? |
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Definition
| They bind to nucleophilic DNA to form a carcinogen-DNA adduct. Direct acting are naturally electrophilic, indirect acting must first be activated by the body to become electrophilic. |
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Term
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Definition
| A test for carcinogenicity. |
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Term
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Definition
| Direct-acting carcinogens. Used as chemotherapy agents. |
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Term
| Aflotoxin is a fungus that tends to mutate what gene? |
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Definition
| P53. This is correlated w/ a specific mutation that is involved with hepatocellular carcinomas. |
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Term
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Definition
| UV light, radiation, asbestos |
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Term
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Definition
| The epithelium that lines the body cavities. |
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Term
| What is an infectious carcinogen? |
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Definition
| HPV. This has proteins that when they insert into the genome they block p53 and bind RB not allowing either to prevent proliferation. Also H. Pylori |
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Term
| Why may inflammation cause cancer? |
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Definition
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Term
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Definition
| Groups of cells in lacunae of cartilage. |
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Term
| Epithelial reticular cells |
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Definition
| Make up Hassal's (thymic) corpuscle |
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Term
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Definition
| A molecule activated by DNA damage. Involves p53 in it's cascade. |
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Term
| What does a high D0 indicate? |
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Definition
| Radiation resistance. Low D0 indicates radiation sensitivity. |
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Term
| When in the cell cycle are cells most radiosensitive? |
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Definition
| M>G2>G1>early S>late S G0 most resistant of all. Also all are more resistant in hypoxic conditions. |
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Term
| Differentiated and non dividing cells are radio resistant or radio susceptible? |
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Definition
| Radio resistant. Undifferentiated and dividing are the most radio susceptible. |
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Term
| What is the effect of hypoxia on cells? |
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Definition
| Make them more susceptible to mutation, but more resistant to radiation damage. |
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Term
| What are the 4 effects of fractionation of radiotherapy? |
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Definition
| 1. Repair/recovery (benefits normal cells) 2. Reassortment in the cell cycle (aids in killing tumor cells) 3. Repopulation of cells (benefits the tumor) 4. Reoxygenation (aids in killing tumor cells) |
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Term
| Acute effects of Total body radiation exposure (3) |
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Definition
| From highest does to lowest 1. Cerebrovascular syndrome 2. GI syndrome 3. Hematopoietic syndrome - Bone marrow transplant can be utilized. |
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Term
| Stochastic vs Deterministic events w/ radiation |
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Definition
Stochastic - can happen at any level. All radiation is bad.
Deterministic - there is a threshold that causes damage (usually to whole systems) |
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Term
| Late response vs early to radiation |
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Definition
| Early <90 days. Commonly dividing tissues (skin, jejunum, colon, testis). Late - .5-5yrs. (affects spinal cord, kidney lung bladder). Alpha-beta ratios tell about late effects. It is easier to effect division than function. That's why you see late effects. |
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Term
| List 3 types of Electron Beam Radiation Therapy (EBRT). |
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Definition
| 1. 3D Conformal (plan based on CT scan) 2. Conventional (based on body landmarks) 3. Intensity Modulated Radiation Therapy (planned w/ a computer) |
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Term
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Definition
| Close therapy. Inserting radiation emitting seeds into the target area. Used for prostate, Head and neck, Gynecologic, Intraoperative. |
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Term
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Definition
| High dose, very focused external beam RT. Gama knife (great for the brain - must completely immobilize the pt), linear accelerator, cyperknife (on robot arm - good for moving targets (lungs). |
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Term
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Definition
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Term
| Radiation considerations you should look at |
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Definition
| Time, Distance (1/R2) - 2 times the distance is 4 times less dose, shielding. |
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Term
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Definition
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Term
| Biologic Response Modifiers |
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Definition
| Using the immune system to fight cancer. |
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Term
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Definition
| The part of an antigen that is recognized by the immune system. |
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Term
| What are the 8 ways Biotherapy can be used (cancer)? |
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Definition
| 1. Promotion of apoptosis 2. Augmentation of the immune response 3. Differential/cellular maturation 4. Interfere w/ growth promoting factors 5. Inhibition of metastases 6. Amelioration of chemo/radiation toxicity 7. Targeting of cytotoxic molecules to tumors 8. Inhibition of angiogenesis. |
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Term
| What are 5 biotherapy treatments? |
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Definition
| 1. Interferons/Interleukin - Used for renal and melanoma malignancies. 2. Monoclonal Antibodies - _umab's, Creating antibodies specifically tailored to the disease. 3. Vaccines - Only vaccine like is where you ship white cells out 4. Recombinant Toxins - Targeted toxins 5. Adoptive Immunotherapy - Bone marrow transplant. Relied on donor cells to do the work. Getting better. For leukemias. |
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Term
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Definition
| A potent immunosuppressor. Used by tumors. |
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