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Toxicology Exam
| Question | Answer |
|---|---|
| What is the definition of toxicology? | The study of adverse effects of chemicals in living organisms |
| What is the definition of a poison? | An agent that can cause a deleterious response in a biological system. |
| What is the definition of a toxin? | Toxic substances produced by biological systems |
| What is the definition of a toxicant? | Toxic substances produced by, or are by-products, of anthropogenic activities. |
| What is a xenobiotic? | A compound in an organism that is not produced or meant to be present in the organism |
| What are the five principles of toxicology? | Source,Exposure, ADMET, Dose,Target/MOA |
| How can the “target” of toxicology be described? | Where and how the toxin is causing damage. |
| What are four possible sources of toxins? | Environmental exposure, Occupational exposure,Bug bites and stings, Medications |
| List all factors of exposure that can affect potential toxic response | Route, Duration, Single vs. repeated, Frequency |
| What are the major routes of toxic exposure? | Oral, Inhalation, Topical, Parenteral |
| In descending order of effectiveness, list the major and minor routes of exposure for toxic agents. | IV->Inhalation->IP->SQ->SubQ->IM->ID->PO->Dermal |
| Describe possible short-term exposure durations. | Single exposure, Acute exposure: Less than 24 hours |
| Describe possible long-term exposure durations. | ▪ Subacute: 1 month or less ▪ Sub chronic: 1-3 months ▪ Chronic: More than 3 months |
| Can effects from single vs. repeated doses be different? | Yes. |
| Describe the possible effects of a fast absorbing compound. | Likely to produce immediate effect but can also produce a delayed effect. |
| Describe the possible effects of chronic exposure. | An immediate effect may be produced after each exposure. |
| Describe toxication/metabolic activation | Potential poisons are bioactivated in the body to a harmful form. |
| Describe detoxification | Biotransformations that eliminate the ultimate toxicant or prevent its formation. |
| What is the therapeutic index? | A comparison of therapeutically effective dose to toxic dose |
| What equation describes the therapeutic index? | TI = toxic dose / therapeutic dose |
| Describe the margin of safety. | Provides information about the slope for different compounds |
| What equation describes the margin of safety? | MOS = TD1 / ED99 |
| Describe the margin of exposure. | This describes how much someone can be exposed to. |
| What equation describes margin of exposure? | MOE = NOAEL / Exposure |
| What do the varying slopes in toxicologic dose-response curves describe? | The mechanism of action is different for efficacy, toxicity, and lethality |
| Will the target organ always be the site of highest concentration? | No, the target organ is not always the place of highest concentration. |
| What determines toxicity? | The dose at the target. |
| Can the mechanism of action be different at different targets? | Yes |
| What are the three approaches to toxicology? | Descriptive, Mechanistic, Regulatory |
| What does descriptive toxicology describe? | Gross toxic responses using in vitro and in vivo systems |
| What is data from descriptive studies used for? | Safety evaluations for human health and environmental risk assessments, Providing a starting point for elucidating mechanisms |
| What is the purpose of mechanistic toxicology? | To identify and understand cellular, biochemical, and molecular mechanisms causing toxic effects. |
| What is data from mechanistic toxicology used for? | Risk assessment, Design/production of safer alternative chemicals, therapy for poisonings, and treatment of disease, Contributes to knowledge of basic physiology, pharmacology, cell biology, and biochemistry. |
| What is regulatory toxicology? | The science of determining if drugs and chemicals are safe for use. |
| How is regulatory toxicology studied? | Using data from descriptive and mechanistic toxicity, and possibly epidemiology. |
| List the regulatory agencies that use toxicologists. | FDA, EPA, OSHA, NIOSH, CPSC, DOT |
| What fields of study are present when including all three approaches to toxicology? | Risk assessment and toxicogenomics. |
| What is risk assessment? | The process to evaluate the potential for adverse health or environmental effects from exposure to naturally occurring or synthetic agents. |
| What is the goal of risk assessment? | To provide risk managers with a rotational basis for making decisions about managing the use of chemicals or physical agents to protect health and the environment. |
| What factors does risk assessment involve? | Social values, Technical feasibility, Economic factors |
| What is an “Immediate effect”? | Those that occur rapidly after a single administration of a substance |
| What is a “delayed effect”? | Those that occur after the lapse of some time after administration of a substance. |
| What are some extreme examples of delayed effects? | DES and vaginal cancer, TOCP and neurotoxicity |
| Are all toxic effects reversible? | No, some are irreversible |
| What determines reversibility/irreversibility? | The ability of a tissue to regenerate. |
| What organ has a very high ability to regenerate? | The liver |
| In which organ are most injuries irreversible? | The CNS, due to inability of differentiated cells to divide and be replaced. |
| Give two examples of irreversible toxic effects | Cancer and birth defects |
| Where do local toxic effects occur? | Site of first contact |
| Give an example of a toxin that cause local effects? | Chlorine gas |
| What do systemic effects require to induce the effect? | Absorption at the site of entry and distribution to site of action. |
| What kinds of effects do most toxins cause? | Systemic effects. |
| Give an example of a poison that has both local and systemic effects? | Tetraethyl lead |
| Give an example of a poison that can cause indirect systemic effects. | Acid burns |
| List the possible mechanisms of chemical interactions? | Changes in absorption, protein binding, biotransformation, and excretion of one or both interacting compounds. ▪ The response may be increased or decreased due to toxic response at site of action. ▪ Additive, synergistic, potentiation, antagonism |
| Describe the concept of tolerance to a toxic compound | The decreased responsiveness to a toxic effect resulting from prior exposure to a chemical or related compound. |
| What are the two major mechanisms for tolerance? | Dispositional tolerance: decreased amount of toxicant reaching site where toxic effect is produced.Reduced responsiveness of a tissue to a compound |
| What is selective toxicity? | When a toxin is lethal to one species but not the other |
| How can toxic endpoints be described? | On/Off target ▪ Non-organ specific ▪ Organ specific ▪ Idiosyncratic ▪ Allergic reactions |
| Give examples of “On-target” toxicity. | The dose at the receptor is too high, Drug pharmacokinetics change, Receptor numbers change, Drug interacts with correct receptor but wrong tissue (Sleepiness with Benadryl) |
| Describe the pathogenesis of Fibrosis (non-organ specific) | Excessive deposition of collagen and EC matrix proteins cause loss of organ function as tissue is destroyed |
| Where does pulmonary fibrosis occur? | In the alveolar Interstitium. |
| What drugs can cause pulmonary fibrosis? | Amiodarone, Bleomycin, Paraquot |
| What can cause liver fibrosis? | Possibly alcohol |
| What is genotoxicity? | Unscheduled DNA synthesis, sister chromatid exchanges, DNA strand breaks. |
| Is genotoxicity transferrable from cell to cell? | No |
| What is mutagenicity? | Transmissible genetic alterations |
| Where can genotoxicity occur? | Somatic and germ cells |
| What can be the outcomes of genotoxicity? | Cancer, teratogenesis, genetic disorders |
| What are the top causes of non-organ specific cancer? | Tobacco and diet/obesity |
| How does a genotoxic carcinogen damage DNA in cancer patients? | It physically interacts with it to damage or change its structure |
| How does a nongenotoxic carcinogen damage DNA in cancer patients? | It can modify gene expression but does not affect DNA structure, can cause cell to be more susceptible to DNA damage from other sources |
| Describe the initiation step in cancer progression. | A mutation occurs in one or more genes that control key regulatory pathways of the cell |
| Describe the promotion step in cancer progression | Signal transduction pathways are enhanced that are in the initiated cell and its progeny by continuous exposure to the promoting agent (carcinogen) |
| Describe the progression step in cancer progression | A second mutation in the cellular DNA, the cell becomes unstable and malignant |
| What is a complete carcinogen? | Substance capable of initiation, promotion, and progression |
| What is fetal exposure to teratogens determined by? | Maternal ADME of the teratogen, and whether the compound can cross the placenta |
| Do malformations and growth retardation in fetuses always occur together? | No, they can occur separately. |
| Why are lungs susceptible to pulmonary toxicity? | Oxidative burden (imbalance of antioxidants and free radicals, allowing more harmful reactions to occur), Site of deposition of gas exposure, Water solubility of gases |
| What determines deposition location of particles in pulmonary toxicity? | Particle size |
| What determines particle deposition in pulmonary toxicity? | Breathing patterns |
| List acute pulmonary toxicity examples | Airway reactivity (bronchoconstriction/dilation), Pulmonary edema |
| List chronic pulmonary toxicity examples | Fibrosis, Emphysema, Asthma |
| How do airborne pulmonary toxins cause toxicity? | They overload the lungs reducing available oxygen |
| List systemic pulmonary toxins | Bleomycin, Cyclophosphamide, Monocrotaline, Paraquat |
| Why is the nervous system susceptible to neurotoxicity? | Axonal transport , High energy requirements,Presence of myelin Neurotransmission function |
| How does high energy requirements cause nervous system susceptibility? | Neurons are highly dependent on aerobic metabolism. Without it, they cannot function. |
| How does axonal transport cause nervous system susceptibility? | Cells in the NS are very long, and neurons must transport intracellular products down and up the axon. |
| How does the presence of myelin cause susceptibility to neurotoxicity? | Myelin is susceptible to damage by toxic compounds, which can overall interfere with the cells ability to send signals to the rest of the body. |
| How does neurotransmission cause susceptibility to neurotoxicity? | Many drugs and compounds affect the neurons ability to transmit signals. |
| Why is the liver susceptible to hepatotoxicity? | Uptake and concentration roles ,Bioactivation and detoxification capabilities ,Inflammatory and immune response ,Propensity for idiosyncratic responses |
| Why is the kidney susceptible to nephrotoxicity? | Potential toxins in systemic circulation , Process for concentrating urine also concentrates toxins ,Renal transport, accumulation, and metabolism contributes to probability of “In Situ” toxicity, Kidney is sensitive to endogenous vasoconstrictors |
| For what reasons can nephrotoxicity be site-specific? | Blood flow ,Transport and accumulation of chemicals Physiochemical properties of epithelium ,Reactivity of cellular targets ,Balance of bioactivation reactions ,Cellular energetics,Repair mechanisms |
| What can molecules smaller than 600 daltons act as? | Haptens |
| What can large drugs do to the immune system? | Direct activation |
| What are the two main mechanisms in which drugs can activate the immune system? | Hypersensitivity, Autoimmune reactions |
| List the six specialties in toxicology. | Food,Forensic,Occupational,Regulatory,Environmental,Clinical |
| Food is presumed safe unless…? | It contains a poisonous/deleterious substance in an amount injurious to health. |
| What if forensic toxicology the hybrid of? | Analytical chemistry and toxicological principles |
| What is a major challenge of forensic toxicology? | The toxic agent must be isolated from a biological matrix |
| How does forensic toxicology aid in crime solving? | Helps establish cause of death, circumstance of death, and identifies agents used in crimes toward the living. |
| What principles does occupational toxicology use? | Methodology of toxicology towards chemical and biological hazards in the workplace |
| What is the objective of occupational toxicology? | Prevent adverse health effects in workers that arise from work environments. |
| What is the purpose of a regulatory toxicologist? | They set the levels for safe exposure to ▪ environmental contaminants ▪ food additives ▪ medicinals |
| What are environmental toxicologist concerned with? | Impacts of environmental pollutants on non-human organisms and human health. ▪ Ecotoxicology focuses on the impact of toxic substances on population dynamics ▪ Transport, fate, interaction are most important components of these specialties |
| What is clinical toxicology mainly concerned with? | Disease caused by or associated with toxic substances |
| Can pharmacists be clinical toxicologists? | Yes |
| What is the universal telephone number for poison control center access? | 800-222-1222 |
| What is a CSPI? | Certified specialist in poison information |
| What is a DABAT? | Diplomat of the American board of applied toxicology |
| What are the further treatment approaches to treating a poisoned patient after emergency care? | Toxicokinetic based, Pharmacologically based, Inactivation of poison |
| Describe initial emergency care? | Eliminating further exposure, supportive care, and determining poisoning agent. |
| What is the goal of toxicokinetic based treatment? | To decrease the amount of poison in the body to reduce potential end-organ damage. |
| What are the four approaches to toxicokinetic based treatment? | Prevention of absorption, Inhibition of toxication, Enhancement of metabolism, Enhancement of elimination |
| Prevention of absorption | Gastric lavage, emesis, activated charcoal, MD activated charcoal |
| Inhibition of toxication | Inhibiting involved enzymes, such as alcohol dehydrogenase with methanol and EG poisoning by giving ethanol of fomepizole |
| Enhancement of metabolism | Administering cofactors to accelerate metabolic actions of enzymes, but not inducing enzymes themselves. Treating cyanide and acetaminophen poisoning. |
| Why is inactivation of poison used? | To reduce activity of toxins that have entered circulation and are not readily eliminated |
| What is the mechanism of toxin inactivation? | Inactivator binds to the toxin and prevents tissue interaction, Toxin-inactivator complex is cleared, Inactivators must have high affinity for the toxin, Complex must have low toxicity |
| Describe the general structure of heavy metal chelators. | Small molecules with a nucleophilic electron donor to form a metal ligand complex, have higher affinity for binding metal than tissue |
| What are three requirements for heavy metal chelators to work? | Soluble, non-toxic, readily cleared. |
| What does the ideal chelator have low affinity for? | Endogenous ions such as calcium |
| What is an antivenom? | Antibodies against a venom |
| How are antivenoms produced? | Inoculating animals with small amounts of venom to get a humoral response |
| What do antivenoms want to have an affinity for? | High affinity/specificity for its substrate |
| What is the danger with using antivenoms? | Type 3 hypersensitivity reactions |
| Antivenom example | Digoxin immune fab |
| What is the purpose of pharmacological treatment of poison? | To counteract a toxins pharmacological response by administering a drug with opposite pharmacological action, or that bypasses the metabolic pathway that’s been inhibited. |
| What are the four categories of pharm. Mediated treatments? | Receptor antagonist, Receptor agonist, treatment removes poison from active site, treatment passes an inhibited pathway by stimulating down stream targets. |
| Receptor antagonist | Blocks effects of toxin that acts as an agonist. ▪ Examples: Naloxone, atropine, flumazenil (GABAA antagonist to treat benzo overdose) |
| Receptor agonist | Treats agonist effects of the toxin ▪ Examples: physostigmine (increase cholinergic tone, reverse atropine) |
| Treatment removes poison from active site | Treating CN poisoning ▪ Treating CO poisoning with O2 ▪ Treating organophosphate poisoning with pralidoxime |
Created by:
Bmcgraw
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