Term
| 4 general ways the brain is sensitive to toxins |
|
Definition
| CNS functions depends on a delicate electrochemical balance that is easily disturbed ::: Passage of neurotoxins through the blood brain barrier or blood-csf barrier ::: Regressive CNS changes later in life (alzheimers) ::: minor alterations in the CNS can cause profound outcomes (unlike other parts of the body) |
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|
Term
| What are the two barriers in the brain to chemicals? |
|
Definition
| the blood brain barrier (BBB) and the blood-CSF barrier (BCB) |
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Term
|
Definition
| compartmental, functional, and structural |
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|
Term
| 3 compartments that make up the "compartmental design" of the brain |
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Definition
| CSF compartment: CSF in ventricles ::: ECF compartment: interstitial or extracellular fluid (ECF) between neurons and neuroglial cells ::: ISF compartment: intracellular fluid within neurons and neuroglial cells |
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Term
| structural design of the nervous system |
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Definition
| CNS (brain and spinal cord) and PNS (efferent and afferent systems) |
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|
Term
| The afferent/efferent system controls motor skills |
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Definition
|
|
Term
| The afferent/efferent system control sensory input |
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Definition
|
|
Term
| The autonomic/somatic nervous system conveys info to smooth muscles and glands. Whereas the autonomic/somatic nervous system conveys info to skeletal muscles. |
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Definition
|
|
Term
| Functional design of the brain |
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Definition
| divides the brain into sections based on function... see notecard |
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Term
| The ___ is the part of the CNS that is the "conductor" between the brain and effectors. It also controls reflexes |
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Definition
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|
Term
| The ___ level of the brain is in charge of subconscious activities and is made up of what 3 parts? |
|
Definition
| lower -- brain stem and diencephalon (thalamus and hypothalamus) |
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|
Term
| The ___ is the part of the CNS responsible for life support (hear beat, blood pressure, etc) |
|
Definition
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|
Term
| The ___ is the part of the CNS that is responsible for sending sensory info to the cerebral cortex (relay station) |
|
Definition
|
|
Term
| The ___ is the part of the CNS that controls the basic instincts and hormones |
|
Definition
|
|
Term
| The ___ is the part of the CNS that control cognitive functions, storage, and motor activity |
|
Definition
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|
Term
| The ___ is the part of the CNS that controls fine body movement |
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Definition
|
|
Term
| the ___ is the part of the CNS responsible for memory |
|
Definition
|
|
Term
| the ___ is the part of the CNS responsible for social behavior and emotion |
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Definition
|
|
Term
| the ___ is the part of the CNS responsible for morality |
|
Definition
| anterior cingulate cortex |
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|
Term
| How are the basal ganglia vulnerable to neurotoxicants? |
|
Definition
| Fe, Mn, and MPTP cause movement disorders like Parkinsons |
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|
Term
| How is the hippocampus sensitive to neurotoxicants? |
|
Definition
| PB, HB and PBB cause learning an dmemory disorders like Alzheimers |
|
|
Term
| how are the choroid plexuses sensitive to neurotoxicants? |
|
Definition
| Pb, Mn, Hg, Fe -- cause brain development and neuroendocrine disorders |
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|
Term
|
Definition
| globus pallidus, substantia nigra, and subthalamic nucleus |
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|
Term
| Hypokinetic disorders and Parkinson's -- how do they work? |
|
Definition
| Substantia Nigra is damaged, which leads to less dopamine released, so the striatum is not fully stimulated, so less GABA is released to the globus pallidus, so less glutamate is produced by the thalamus to modulate movements -- this causes damage to the direct path, so the indirect path dominates --- see handout |
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Term
| Parkinson's is an example of a hyper/hypokinetic disorder |
|
Definition
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|
Term
| Huntington's is an example of a hyper/hypokinetic disorder? |
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Definition
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|
Term
| Hypokinetic disorders are caused by damage to the direct/indirect pathway. Hyperkinetic disorders are the opposite. |
|
Definition
|
|
Term
| Alzheimer's disease may be caused by problems with what brain structure? |
|
Definition
| hippocampus -- due to memory, problem solving, language, and judgement problems |
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|
Term
| Alzheimer's disease may be caused by problems with what brain structure? |
|
Definition
| hippocampus -- due to memory, problem solving, language, and judgement problems |
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|
Term
| how do the choroid plexuses act like kidneys in the brain? |
|
Definition
| serve as a barrier between blood and csf and secrete, transport, and remove debris from csf |
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|
Term
| Why is it significant that neurons don't contain a mitotic apparatus? |
|
Definition
| because they cannot reproduce themselves -- once they're dead, they're dead |
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|
Term
| 4 ways neurons are vulnerable to neurotoxicants |
|
Definition
| peculiar architecture - long processes and large surface area ::: lack of ability to reproduce ::: high metabolic rate and little ability for anaerobic metabolism (13 gal/hr of blood flows through brain) ::: contain biotransformation enzymes |
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|
Term
| ___ are caleld Schwann cells when they formed the myelin sheath in the spinal cord |
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Definition
|
|
Term
| Why are neuroglial cells particularly vulnerable to neurotoxicants? (4 reasons) |
|
Definition
| are key structural components of the BBB and BCB , are the first cell types to be exposed to toxins ::: lipophilic toxins tend to accumulate in neuroglials ::: neuroglials are highly metabolically active, which results in a high incident of brain tumors :: activation of neuroglials cause inflammation, leading to Parkinsons and Alzheimers |
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|
Term
| types of synapses based on physical properties |
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Definition
| chemical (unidirectional) and electrical (uni- or bi-directional) |
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|
Term
| Classification of synapses based on morphology |
|
Definition
| type 1 - round synaptic vesicles, wide synaptic cleft, large active zone, usually excitatory ::: type 2 - flat synaptic vesicles, narrow synaptic cleft, small active zone, usually inhibitory |
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|
Term
| vulnerability of synapses to neurotoxicants (4 reasons) |
|
Definition
| synapses contain a variety of neurotransmitters and their specific receptors, which serve as sites for most drugs and toxins ::: the normal functions of synapses rely on the structural and functional integrity of neurons, chemical blanace in the synaptic cleft, and surrounding neuroglial cells ::: neurotoxicants entering the CSF or ISF can directly alter the signal transduction at synapses ::: disruption of synaptic communication results in the disorders of thought, learning and response |
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|
Term
| Vulnerability of brain barriers to neurotixcants (5 reasons) |
|
Definition
| the BBB and BCB maintain the chemical stability of the cerebral compartments ::: fast blood flow to the choroid plexus warrants an efficient influx of materials, some of which are toxic, to the CNS ::: The BBB and BCB are not well developed in immature brains ::: Some areas of the brain do not have a BBB ::: the BCB is critical to brain development |
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|
Term
| 2 types of disposition-sensitive neurotoxicities |
|
Definition
| Mn can accumulate in Fe-rich brain areas and cause oxidative stress in neurodegenerative disorders :: Pb can accumulate int he choroid plexus and cause implimations in learning defects |
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|
Term
| 2 types of biochemical machinery-sensitive neurotoxicities |
|
Definition
| Mn can act on Fe-regulatory processes to increase cellular overload of Fe :: MPTP can act on mitochnodrial respiratory chain to damage energy production |
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|
Term
| Cell type-sensitive neurotoxicities |
|
Definition
| neurons are more sensitive than astrocytes to Pb toxicity :: Neurons are more sensitive than astrocytes to Mn Toxicity |
|
|
Term
| Energy-sensitive neurotoxicities |
|
Definition
| aka Hypoxia -- lack of O2 supply to entire nervous system (global hypoxia), brain areas with high metabolic activity particularly susceptible |
|
|
Term
| Order of sensitivity to hypoxia: |
|
Definition
| neurons > oligodendrocytes > astrocytes > microglia > capillary endothelial cells |
|
|
Term
| Co, pb, Cd, Zn ... each of these involvement with hypoxia |
|
Definition
| Co: cardiac arrest :: Pb: hemorrahge of cerebral blood vessels :: Cd: hemorrahge in spinal sensory ganglia :: Zn: transient global ischemia |
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|
Term
| ___ hypoxia is characterized by inadequate O2 supply. Results? Causes? |
|
Definition
| Anoxic Hypoxia -- respiratory paralysis, interference with O2 carrying capacity of blood -- caused be CO and nitrite |
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|
Term
| ___ hypoxia is caused by inadequate blood supply. Results? Causes? |
|
Definition
| Ischemic hypoxia -- cardiac arrest, hypotension due to vasodilation, cerebral hemorrhage -- causes: cobalt, nitropruside, pb |
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|
Term
| __ hypoxia is characterized by an arrested cellular membrane. results? causes? |
|
Definition
| cytotoxic hypoxia -- cytochrome oxidase inhibitors and metabolic inhibitors -- causes: cyanide, azide, dinitrophenols |
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|
Term
| consequences of metal-induced toxicity on neuronal cell bodies |
|
Definition
| neuronopathy: loss of entire cell body and it's processes, degeneration of dendrites and axons, irreversible damage |
|
|
Term
|
Definition
| depletion of Nissi bodies by Trimethyl-Pb |
|
|
Term
| consequences of heavy metal toxicity on axons |
|
Definition
| axonopathy: injury occurs along the axons, so longer axons are more susceptible.. neuronal cell body stays intact... possible regeneration in the PNS -- caused by Aluminum toxicity |
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|
Term
| consequences of metal-induced toxicity on neuroglial cells |
|
Definition
| myelinopathy - injury occurs in the myelin sheath and results in a slow and aberrant conduction of impulses.. neuronal cell body intact.. possible remyelination in the PNS and CNS --- ex: triethyltin (TET) |
|
|
Term
| heavy metal-induced toxicity at synapses |
|
Definition
| alterations occur at synaptic junctions resulting in altered behavior or impaired performance on neurological tests. neuronal body intact, treatment is possible. |
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|
Term
| heavy metal-induced toxicity at synapses can act on what 7 mechanisms? |
|
Definition
| neurotransmitter synthesis, neurotransmitter release, neurotransmitter reuptake, neurotransmitter deactivation, neurotransmitter agonist or antagonist, ion channels, and membrane excitability |
|
|
Term
| How does cocaine work as a neurotoxicant? |
|
Definition
| acts on the CNS to induce a sense of enhanced physical strength and mental capacity but causes neuronal damage by chromatolysis.. results in psychosis and behavioral change.... mechanism: blocks reuptake (and therefore increases synaptic concentration of) catecholamines, activates dopaminergic neurons at medial prefrontal cortex, profound and long-lasting depeletion of dopamine in caudate nucleus |
|
|
Term
| heavy metal-induced toxicity on brain barriers |
|
Definition
| damage occurs at the endothelia of the BBB or the epithelia of the BCB and alters physical properties of the barreirs such as secretion and transport ::: examples - Pb on BBB, Pb in choroid plexus, Mn in choroid plexus |
|
|
Term
| How does Alzheimer's disease work? |
|
Definition
| formation of senile plaques consisting of insolbue B-amyloid proteins in the ISF space... causes nueronal cell death |
|
|
Term
| What heavy metal can cause parkinson-like symptoms? |
|
Definition
|
|
Term
| a heritably altered, relatively autonomous growth of tissue |
|
Definition
neoplasm
Carlson definition: genetic change in a cell that gives it a growth advantage |
|
|
Term
| literally means "without form" -- characterized by a marked change from a highly differentiated cell to one that is less differentiated and more embryo-like. less organized and functional than normal tissue. |
|
Definition
|
|
Term
| a term applied to neoplasms that are localized and encapsulated |
|
Definition
|
|
Term
| a reversible change in cells, that may include an altered size, shape, and or organizational relationship |
|
Definition
|
|
Term
| increased organ or tissue size due to increase in cell number... usually due to body necessity |
|
Definition
|
|
Term
| a term applied to neoplasms that are locally invasive. growth is rapid, disorderly, and progressive |
|
Definition
|
|
Term
| presence of a disease process at a site distant from the site of origin |
|
Definition
|
|
Term
| ___ is the hallmark of malignancy |
|
Definition
|
|
Term
| a mass or swelling, one of the cardinal signs of inflammation. |
|
Definition
|
|
Term
| When could a benign tumor be a big problem? |
|
Definition
| if it's in an area of the body (especially the brain) in which space is an issue. any mass that takes up space can cause problems |
|
|
Term
| a family of diseases having the common characteristic of uncontrolled cell growth.. used to indicate a process that has the characteristics of a malignant neoplasia |
|
Definition
|
|
Term
| an agent (chemicals, radiants, viruses, etc) that leads to a statistically significant increased incidence of neoplasms as compared with that in untreated animals |
|
Definition
|
|
Term
| Properties of Benign vs. malignant tumors |
|
Definition
|
|
Term
| What are the top 5 cells most likely to get cancer? |
|
Definition
| Epithelium, Connective tissue, hemopoietic and immune system, nervous system, multiple histogenetic cellular origin |
|
|
Term
| In general, what cells are at risk for cancer? |
|
Definition
| any cell capable of dividing |
|
|
Term
| Levels of spermatogenesis |
|
Definition
| spermatogonia, spermatocytes, spermatids, spermatozoa |
|
|
Term
| Cells involved in spermatogenesis |
|
Definition
| Leydig, Sertoli, myoepithelial |
|
|
Term
|
Definition
| various synthetic chemicals that interfere with normal functioning of the endocrine system and therefore with the action of hormones |
|
|
Term
| Factors that increase kidney susceptibility to toxins |
|
Definition
| high renal blood flow, concentrates tubular fluid and chemicals, transport of chemcials into tubular cells, biotransformation to toxic metabolites and possibly bioactivation, high energy demand and high concentration of sulfhydryl enzymes |
|
|
Term
| In general, what is bioactivation? |
|
Definition
| production of toxic metabolites |
|
|
Term
| __% of cardiac output goes through the kidneys |
|
Definition
|
|
Term
| Any chemical that restricts ___ or ___ production will cause renal damage.. why? |
|
Definition
| O2 or ATP -- because the kidneys have such a high energy demand |
|
|
Term
| ___ are the most potent nephrotoxins |
|
Definition
| heavy metals -- most will cause some amount of kidney damage |
|
|
Term
| How do heavy metals produce nephrotoxicity? |
|
Definition
| react with -SH enzymes in proximal tubules, inhibit enzyme function, denature proteins - causing necrosis |
|
|
Term
| Halogenated hydrocarbons target mainly the ___ in the kidney. ___ is an early sign of this toxicity |
|
Definition
| proximal tubules ... proteinuria |
|
|
Term
| Cadmium toxicity... ___ is most affected organ ... long/short half life ... indicator of toxicity ... most toxic form? |
|
Definition
| Kidney ... long (10 years) ... proteinuria (specifically B2-microglobulin) ... Cd2+ |
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|
Term
|
Definition
| ends up in liver first, SH groups on metallothionine bind up Cd and liver excretes it into kidney, Cd remains bound to MT for years in kidney until it eventually breaks off and kills cells |
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|
Term
| ___ is a classic nephrotoxin that causes ARF within 24 hrs and death within 48. |
|
Definition
|
|
Term
| Most toxic form of mercury? |
|
Definition
|
|
Term
| Why does Hg cause ARF and Cd causes delayed damage? |
|
Definition
| Cd is bound up by MT, Hg is not |
|
|
Term
| How does chloroform induce kidney damage? |
|
Definition
| is metabolized to reactive intermediate in the tubules |
|
|
Term
| how does carbon tetrachloride cause kidney damage? |
|
Definition
| is bioactivated by microsomal enzymes.. forms a free radical which causes lipid peroxidation |
|
|
Term
|
Definition
|
|
Term
| How can hemoglobin synthesis be inhibited? |
|
Definition
| by lead, for sure at 2 enzymatic steps in process and probably at 2 others |
|
|
Term
| 2 steps that lead for sure inhibits hematopoiesis |
|
Definition
|
|
Term
| ___ is a disease that decreases granulocyte production. due to? |
|
Definition
| leukopenia -- benzene, arsenic, TNT, chemotherapy agents |
|
|
Term
| ___ is a decrease in WBC (specifically neutrophil) production. due to? symptoms? |
|
Definition
| Neutropenia -- benzeme, tnt, arsenic, heavy metals -- infection, fever, sore throat, sores in mouth |
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|
Term
| __ are the cells that are the 1st line of defense against infection |
|
Definition
|
|
Term
| ___ are the most active cells in combating infection |
|
Definition
|
|
Term
| a low thrombocyte count can cause ___. symptoms, and causes? |
|
Definition
| thrombocytopenia -- bruising, porpura -- napthalene, DDT |
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|
Term
| ___ is a folic acid or vit B-12 deficiency. how is this characterized? |
|
Definition
| megaloblastic anemia -- w/o enough folic acid and B-12, cells can't produce DNA so instead of dividing, they just keep growing bigger into megaloblasts |
|
|
Term
| a condition where bone marrow does not produce sufficient new cells to replenish blood cells (RBCs, WBCs, and platelets) |
|
Definition
|
|
Term
|
Definition
| men: androgen production in the testes ::: women: surge of LH when follicle is mature, directs formation of the corpus luteum |
|
|
Term
| women: stimulates growth and maturation of graafian follicles ;;; men: stimulates spermatogenesis |
|
Definition
| FSH (Follicle Stimulating Hormone) |
|
|
Term
| category that encompasses LH and FSH |
|
Definition
|
|
Term
| 2 cells involved in menstruation and their purpose |
|
Definition
| granulosa - nourishment and endocrine ;;; theca - endocrine |
|
|
Term
| 2 cells involved in menstruation and their purpose |
|
Definition
| granulosa - nourishment and endocrine ;;; theca - endocrine |
|
|
Term
| Toxicity in female reproductive system |
|
Definition
| early stages (preovulatory) can cause failure of folliculogenesis, later can cause failure of corpus luteum maintenance |
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|
Term
|
Definition
| a piece of DNA covalently bonded to a (cancer-causing) chemical. This has shown to be the start of a cancerous cell, or carcinogenesis |
|
|
Term
| what occurs in oxidant-induced hemolysis? |
|
Definition
| Sulfhydryl groups are oxidized (see note card), which compromises membrane integrity... seems to be more common in G6PD-deficient RBCs... caused by primaquine, napthalene, arsine, and copper sulfate |
|
|
Term
| what is anemia, in general? |
|
Definition
| a decrease in the number of mature RBCs, or a decreased O2 carrying capacity in RBCs |
|
|
Term
| what disease involves red blood cells changing shape to get through the spleen bc they're too big... and if they don't get through, macrophages eat them? |
|
Definition
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|
Term
|
Definition
|
|
Term
| What is the function of erythropoeitin? |
|
Definition
| produced by kidneys, transferred to bone marrow, stimulates RBC production |
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|
Term
| Why might we look for increased number of reticulocytes in the blood? |
|
Definition
| if body is lacking mature RBCs, it will release reticulocytes before they're mature.. elevated levels of reticulocytes indicates this problem |
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|
Term
| __ is the chemical of choice to cause aplastic anemia |
|
Definition
|
|
Term
|
Definition
| when fat and collagen in the bone marrow causes decreased production of all types of blood cells |
|
|
Term
| 3 types of lab measurements |
|
Definition
| hematocrit - % of blood that is cells (usually 40-50%) ::: RBC count - 4.5-5.5M cells/uL ::: Hemoglobin - 13-16g/dL |
|
|
Term
| What are two problems that a RBC count could find? |
|
Definition
| decreased number of mature RBCs or increased number of reticulocytes |
|
|
Term
|
Definition
| fatigue, lethargy, increased heart rate (compensatory), maybe jaundice due to decreased ability of bilirubin disposal |
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|
Term
|
Definition
|
|
Term
| why does time to tumor matter? |
|
Definition
| if a tumor (or cancer) is detected soon after an exposure, it's easy to determine what caused it... if it happens 50 years later it's not |
|
|
Term
| Why are epithelial cells the #1 cancer cells? |
|
Definition
| because they divide constantly |
|
|
Term
| There are both ___ and ___ differences in cancer rates |
|
Definition
| genetic and environmental |
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|
Term
|
Definition
| international association for research on cancer |
|
|
Term
| irritant contact dermatitis accounts for __-__% of chemical-induced skin diseases |
|
Definition
|
|
Term
| a local, inflammatory skin reaction |
|
Definition
|
|
Term
| what is the difference between irritant and allergic contact dermatitis |
|
Definition
| irritant - caused by contact with chemicals ... allergic - caused by Type IV HS reaction |
|
|
Term
| Compounds associated with irritant contact dermatitis |
|
Definition
| solvents, cleaners, acids, bases, oxidizing agents, reducing agents |
|
|
Term
| ___ are a special class of corrosive agents that include mustard gases and produce a delayed response that usually results in blistering at the site of contact |
|
Definition
|
|
Term
|
Definition
hives - triggered by type I immune reaction (IgE)
ex: latex allergy |
|
|
Term
| ___ results in blistering and reddening of the skin after a chemical is activated by UV light |
|
Definition
|
|
Term
| ___ is a delayed type IV HS and involves a chemical being activated by light to form an antigen |
|
Definition
|
|
Term
| ___ resemble acne in appearance, primarily occur on the upper body after systemice exposure to iodides and bromides |
|
Definition
|
|
Term
| ___ is also known as oil acne and occurs at the site of exposure due to clogging of the sebaceous glands and hair follicles |
|
Definition
| local acneiform eruptions (regular acne) |
|
|
Term
| ____ is an occupational/environmental illness that occurs after systemic exposure and leaves a very disfiguring nad persistant acne. Chemicals react with Ah receptors in sebaceous gland and produce hyperplasia. Chemicals involved? |
|
Definition
| chloracne -- dioxin and PCBs |
|
|
Term
| 3 stages of carcinogenesis |
|
Definition
| initiation, promotion, and progression |
|
|
Term
| ___ is the stage of carcinogenesis that involves irreversible mutation in the DNA of a somatic cell |
|
Definition
|
|
Term
| ___ is the stage in carcinogenesis where clonal expansion of initiated cells occurs by providing a selective growth advantage |
|
Definition
|
|
Term
| promotion occurs by what two conditions |
|
Definition
| either increase in the number of tumors or decrease in the latency period of tumors (or both) |
|
|
Term
| ___ is the stage of carcinogenesis that involves the accumulation of further genetic alteration in a population of initiated cells that hae been provided a growth advantage through promotion |
|
Definition
|
|
Term
| Tumor heterogeneity occurs during which stage of carcinogenesis |
|
Definition
|
|
Term
| ___ are genes capable of producing cancer. how are they formed? |
|
Definition
| oncogenes -- formed from acute transforming retroviruses (viruses that can "transform" other cells into cancer cells) |
|
|
Term
| How do genes become oncogenes? |
|
Definition
| normal genes are transduced (stolen) by retroviruses, then they are activated (altered to make them oncogenic) |
|
|
Term
| normal, cellular counterparts of oncogenes that are shown to be activated in tumors |
|
Definition
|
|
Term
| 5 mechanisms of activation of protooncogenes |
|
Definition
| point mutations, gene rearrangement, gene amplification, chromosomal translocation, increased transcription |
|
|
Term
| What is the general function of oncogenes? |
|
Definition
| they are positive regulators of cell growth if the carcinogenic process is induced |
|
|
Term
| in normal cells, the ___ code for proteins that function as negative regulators of cell growth |
|
Definition
|
|
Term
| why are oncogenes easier to inactivate than tumor suppressor genes? |
|
Definition
| oncogenes only have 1 allele that needs to be inactivated, TS genes have 2 |
|
|
Term
| what gene is termed the 'guardian of the genome' because it detects DNA damage? |
|
Definition
|
|
Term
|
Definition
| nutrient homeostasis (blood sugar, cholesterol), particulate filtration, protein synthesis, bioactivation and detoxification, bile formation and biliary secretion |
|
|
Term
| 5 reasons why the liver is susceptible to toxins |
|
Definition
| its size (5% of body mass), filters blood first from GI tract and abdomen (hepatic first pass effect), eventually filters all blood, is primary organ responsible for biotransformation |
|
|
Term
| blood supply to liver comes from what two blood vessels? |
|
Definition
| hepatic arter and hepatic portal vein |
|
|
Term
| Components of the portal triad |
|
Definition
| portal vein (takes blood from gut to liver), hepatic artery (takes blood from heart to liver), bile duct |
|
|
Term
|
Definition
| near the portal triad (lost of O2 and nutrients), middle area, Central vein (high drug metabolism) |
|
|
Term
| what zone of the liver is targetted by ethanol? |
|
Definition
|
|
Term
| what zone of the liver is targeted by acetaminophen and halogenated solvents? |
|
Definition
|
|
Term
|
Definition
| fatty liver, cell death, cannilicular cholestasis, bile duct damage, sinusoid disorders, fibrosis, cirrhosis, hepatitis, immune-mediated response |
|
|
Term
|
Definition
| accumulation of fat in liver due to oversupply of fat, interference wiht triglyceride cycle, increase in ehtanol, decrease in metabolism of fats |
|
|
Term
|
Definition
|
|
Term
|
Definition
| liver peroxidation (CCl4 creates a free radical taht damages lipid membrane) and generation of metabolites (usually by acetaminophen) |
|
|
Term
| damage to caniliculi causes bile to collect in blood and jaundice occurs in what disease/ |
|
Definition
|
|
Term
| how would you diagnose bile duct damage? |
|
Definition
| look for increased bilirubin and serum enzymes in blood |
|
|
Term
| how would you diagnose cell death via necrosis? |
|
Definition
| look for serum enzymes like ALT and AST in the blood |
|
|
Term
|
Definition
| fibroblasts try to help repair liver damage, collagen builds up as scar tissue and interferes with the normal architecture of the liver |
|
|
Term
| 2 factors invovled in cirrhosis |
|
Definition
| collagen build up and increased cell replication |
|
|
Term
| immune-mediated hepatotoxicity is like type __ HS |
|
Definition
|
|
Term
| most sensitive cells in male reproductive system to toxins? |
|
Definition
|
|
