Term
|
Definition
| LD50/ED50 The ratio of the average lethal dose of a drug to the average effective dose of a drug. |
|
|
Term
| What is the characteristic of a chemical that makes it a “drug”? |
|
Definition
| any chemical that can affect living processes |
|
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Term
| What is “pharmacotherapeutics”? |
|
Definition
| the use of drugs to diagnose, prevent or treat disease or to prevent pregnancy, can alternatively defined simply as the medical use of drugs. |
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Term
| 2. What are the properties of an ideal drug? |
|
Definition
· Effectiveness
· Safety
· Selectivity
· Other desired characteristics include:
o Reversible Action
o Predictability
o Ease of Administration
o Freedom from Drug Interactions
o Low Cost
o Chemical Stability
o Possession of a Simple Generic Name. |
|
|
Term
| What are the properties of an ideal drug? |
|
Definition
· Effectiveness
· Safety
· Selectivity
· Other desired characteristics include:
o Reversible Action
o Predictability
o Ease of Administration
o Freedom from Drug Interactions
o Low Cost
o Chemical Stability
o Possession of a Simple Generic Name. |
|
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Term
| What factors determine the intensity of an individual’s response to a given drug? |
|
Definition
| concentration at the sites of action |
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Term
| How does a nurse’s knowledge of pharmacotherapeutics affect patient care and education? |
|
Definition
| Nurses are the likely the first to observe and evaluate drug responses, and to intervene if required. In order to intervene rapidly and appropriately, nurses must know in advance the responses that a medication is likely to elicit. The nurse is the patient’s last line of defense against medication errors made by others on the healthcare team. |
|
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Term
|
Definition
| description of the drug using the nomenclature of chemistry |
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Term
|
Definition
| assigned by the US Adopted Names Council, there is only one generic name AKA as the nonproprietary name. Less complex than chemical name, but more complex than trade name. Preferred to trade name for general use. |
|
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Term
|
Definition
| AKA proprietary name, is the name under which the drug is marketed. Created by drug companies with the intention of being easy to pronounce, and remember. |
|
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Term
| Why are people usually urged to have their prescriptions filled with “generic drugs”? |
|
Definition
| People are urged to use generic Rx drugs because the cost is less than that of trade/brand name drugs. |
|
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Term
| Why do the generic and trade/brand drugs sometimes differ in bioequivalence? What are the implications when this occurs? |
|
Definition
| Some generic and trade drugs differ in bioequivalence because of fillers that are often added by manufacturers. This can affect the rate and extent of their absorption. A slight increase in absorption can result in toxicity, and a slight decrease can result in therapeutic failure. Sometimes people can take an Rx and have no adverse reaction and then the generic drug and have a reaction to the fillers in it |
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Term
| What did The Federal Pure Food and Drug Act of 1906 do? |
|
Definition
| law made sure that medications had no “adulterants.” |
|
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Term
| The Federal Food, Drug, and Cosmetic Act of 1938 did what? |
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Definition
| Law was to test for toxicity of drugs |
|
|
Term
| The Durham-Humphrey Act of 1952 did what? |
|
Definition
| Drug Prescription Act codified and clarified the distinction between prescription and over the counter drugs. Prescription drugs were defined as either: habit forming; not safe for use except under the supervision of a practitioner; or, for use under the professional supervision of a practitioner. |
|
|
Term
| The Harris-Kefauver Amendment of 1962 did what? |
|
Definition
| was to test the effectiveness of drugs and to instate the first serious set of regulations on drugs because of the thalidomide incident. |
|
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Term
| The Controlled Substance Act of 1973 did what? |
|
Definition
| was passed to put regulations drugs that had the potential to be abused. |
|
|
Term
| The Food and Drug Administration Modernization Act of 1997 did what? |
|
Definition
was to put in new regulations on different aspects of drugs such as: A faster system of getting new drugs for AIDS, cancer and similar diseases.
·Notifications of drug discontinuations prior to it happening, so that patients can get different medications.
·Drug testing on children. Databases for clinical trials.
·Doctors can be informed of off-label uses for drugs. |
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|
Term
| How does legislation related to drugs impact the nurse’s role? |
|
Definition
| Nurses are impacted by these legislations because testing procedures cannot detect all adverse effects before a new drug is released. Because adverse effects may go undetected, when working with a new drug, you should be especially watchful for previously unreported drug reactions. If a patient taking a new drug begins to show unusual symptoms, it is prudent ot suspect that the new drug may be the cause – even though the symptoms are not yet mention in the literature |
|
|
Term
| What is the difference between prescription and over-the-counter drugs? |
|
Definition
Prescription drugs are drugs that have to have doctor’s orders to get.
Over-the-counter drugs are defined as drugs that can be purchased without a prescriptio |
|
|
Term
| What does it mean when a drug is used for an “off label” purpose? |
|
Definition
| An “off-label” use is a use that has not been evaluated by the FDA |
|
|
Term
| How is it determined that a drug will be available OTC? |
|
Definition
| The FDA determines whether or not a drug will be available OTC |
|
|
Term
| How do drugs differ from herbal supplements? |
|
Definition
| Herbal medicines can be defined as the use of plant-derived products to promote health and relieve symptoms of disease while drugs are chemicals formulated for the same purpose. The FDA does not regulate herbs because they are considered a “dietary supplement.” While drugs are presumed dangerous until rigorous testing reveals an absence of serious toxicity, dietary supplements are considered safe until proved hazardous. |
|
|
Term
| Why should nurses be concerned about the herbal supplements their patients may be taking? |
|
Definition
| Nurses should be concerned because there can be interactions between herbal supplements and many drugs |
|
|
Term
| What is the meaning of “controlled substances” and the various “schedules”? |
|
Definition
| Controlled Substance: Drugs with potential for abuse causing physical and/or psychological dependency. Only medically licensed personal possessing a DEA number may distribute these drugs. Written record of all transactions (purchased or dispensed) must be recorded and submitted to the DEA every 2 years. Potential for abuse increases, as Schedule numbers, IV, III, II, get smaller. When state or federal law conflict regarding drug distribution the more restrictive (stringent) of the two takes precedence. |
|
|
Term
| What is a Schedule I (C-V) drug? |
|
Definition
| very high potential for abuse with no approved medical use in the U.S. (Example: Heroin) |
|
|
Term
| What is a Schedule II (C-II) drug? |
|
Definition
| highest potential for abuse for prescribed drugs. Orders must be typed or filled out in ink and signed by the prescribing physician. Verbal requests may be accepted for emergencies with a written prescription submitted within 72 hrs. No refills. If a refill is needed a new prescription must be written to continue therapy. Example: Morphine, Oxycodone, Fentanyl |
|
|
Term
| What is a Schedule III (C-III) drug? |
|
Definition
| – potential for abuse. Up to 5 refills per prescription in a 6-month period. After 6 months a new prescription must be submitted. Example: Hydrocodone Syrup, Vicodin (Hydrocodone & Tylenol), Testosterone (Steroid), Tylenol #3. |
|
|
Term
| What is a Schedule IV (C-IV) drug? |
|
Definition
| potential for abuse. Up to 5 refills per prescription in a 6-month period. After 6 months a new prescription must be submitted. Example: Alprazolam, Diazepam (Valium), Lorazepam, Triazolam. |
|
|
Term
| What is a Schedule V (CV)drug? |
|
Definition
| Same regulations as C-III and C-IV but may be dispensed w/o a prescription with certain conditions: (1) dispensed by pharmacist (2) limited amount dispensed (doesn’t say how much) (3) must be 18 yrs. or older to receive (4) pharmacist records transaction (5) if state and local laws do not prohibit dispensing C-V without a prescription. Example: diphenoxylate plus atropine. |
|
|
Term
| What are the practice implications for the nurse when considering "controlled substances" and their various schedules? |
|
Definition
| many hospital require that floor stocks of controlled substances be counted at the beginning and end of each shift. |
|
|
Term
| what is Preclinical Testing? |
|
Definition
| Testing here determines toxicity, pharmacokinetic properties, and potential useful biologic effects. Preclinical lasts 1-5 yrs. If preclinical is successful the drug developer applies to the FDA for Investigational New Drug status to begin testing on humans in clinical trials. |
|
|
Term
| How long do clinical trials last? |
|
Definition
|
|
Term
| What is Phase I of clinical trials? |
|
Definition
| Usually conducted on normal volunteers. However if a drug is likely to have severe side effects, as many anticancer drugs do, the trial is done in volunteer patients who have the disease under consideration. Goals of Phase I – Evaluation of drug metabolism, and Determination of effects in humans. |
|
|
Term
| What are Phase II & III of the clinical trials? |
|
Definition
| In these trials, drugs are tested in patients. Objective: to determine (1) therapeutic affects (2) dosage range and (3) safety. 500-5000 patients receive the drug but only a few hundred take it for more than 3-6 months. Upon completion of Phase III the drug manufacturer applies to the FDA for conditional approval of a New Drug Application. If approved, Phase IV may begin |
|
|
Term
| What is Phase IV: of FDA drug testing? |
|
Definition
| Post marketing Surveillance: Drug is released for general use, permitting observation of its effects in a large population. This is where adverse effects can show up, like with the drug Vioxx and Celebrex (recent recalls). Physicians report new drug data voluntarily to determine the drugs success |
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|
Term
| What guidelines does Lehne give when it comes to new drugs? |
|
Definition
| Be neither the first to adopt the new nor the last to abandon the old”. What are the potential benefits of the drug as opposed to its potential for harm (Risk to Benefit factor)? New drugs generally present greater risks than old ones. The author feels that new drugs present a risk of adverse effects until proven safe over time and that in many cases new drugs don’t offer any greater benefit over old drugs. That means we are put in the middle of the prescribing Physician who wants to use a new drug and the patient’s risk-to-benefit factor and identifying high risk patient using a new drug (my conclusion). |
|
|
Term
| What guidelines does Lehne give when it comes to new drugs? |
|
Definition
| Be neither the first to adopt the new nor the last to abandon the old”. What are the potential benefits of the drug as opposed to its potential for harm (Risk to Benefit factor)? New drugs generally present greater risks than old ones. The author feels that new drugs present a risk of adverse effects until proven safe over time and that in many cases new drugs don’t offer any greater benefit over old drugs. That means we are put in the middle of the prescribing Physician who wants to use a new drug and the patient’s risk-to-benefit factor and identifying high risk patient using a new drug (my conclusion). |
|
|
Term
| What is meant by “patient compliance” and how can the nurse increase it? |
|
Definition
| Patient compliance is getting the patients to take his/her medications according to instructions; such as, at the right time, in the right dose, and by the right route. Increase compliance thru patient education about the drugs they are taking, what the drugs will do, and why it is important to take them as directed |
|
|
Term
| Describe the nurse’s responsibilities related to medication administration. |
|
Definition
At one time, a nurse’s responsibility regarding medications focused mainly on the Five Rights of Drug Administration à give the right drug to the right patient in the right dose by the right route at the right time. Today, nurses’ responsibility goes beyond the Five Rights. Nurses are especially important within the system because it is the nurse—not the physician—who follows the patient’s status more closely. Nurses are the first ones to observe and evaluate drug responses. The stronger your knowledge of pharmacology the more you will be able to anticipate drug responses and not simply react to them after the fact.
Since it is the nurse who actually administers drugs, the nurse is the last person to check medications prior to administration. Consequently, you are the patient’s last line of defense against medications errors. |
|
|
Term
| What are the six Rights of Drug Administration used by nurses? |
|
Definition
Right drug
Right dose
Right patient
Right time
Right route
Right documentation |
|
|
Term
| What is homeostasis and how is it regulated? |
|
Definition
| Homeostasis may be defined as a dynamic steady state, representing the net effect of all turnover reactions. The idea homeostatic balance represents an idea;. Actually, in every self-regulating system some degree of deviation occurs from what is optimal or normal for that system – a range over which a given value is maintained. Parameters such as temperature, cardiac output, blood pressure, oxygen and carbon dioxide levels, acid-base balance, fluid volume, and electrolyte composition are closely regulated to maintain homeostasis. Most homeostatic control mechanisms in the body, function on the principle of negative feed back, which tends to favor stability. In order to be regulated, the variable to be controlled must be sensed. Sensory neurons and endocrine glands are primary homeostatic sensors. Sensors then provide feedback to a regulatory center (usually the brain), which integrates all relevant input and initiates a response. Effectors (muscles and glands) carry out the responses. |
|
|
Term
|
Definition
| Disease can be view as a disruption of homeostasis. Disease represents the sum of the deviations from normal. |
|
|
Term
| What factors affect the determination of “normal” in a given person? |
|
Definition
Genetic variations
Cultural considerations
Age differences
Gender differences
Situational differences
Time variation
When assessing a person’s health status, a change in some value or factor is more significant than the actual value of the particular factor. A blood pressure of 90/70 mm Hg may not be significant if that is the usual value. However, if a person usually has a blood pressure of 120/80 mm Hg a reading of 90/70 mm Hg it would be very significant. |
|
|
Term
|
Definition
| the study of the cause or reason for a disorder. |
|
|
Term
| What is the impact of genetics upon disease? |
|
Definition
| Genetics is directly related to human disease as well as environmental interactions. Abnormal proteins can be made when there are mutated genes, which can cause the protein to not meet its intended function. Some mutations are lethal while some are only lethal when the person is placed in a certain environment. Other proteins can cause problems without certain environmental conditions. This information can be used to see how inheritance and genes can be directly related or cause certain diseases. |
|
|
Term
| What is an “idiopathic” etiology of disease? |
|
Definition
| An idiopathic disease has an undetermined cause. |
|
|
Term
| What is an "iatrogenic” etiology of disease? |
|
Definition
| An iatrogenic condition one that is unintended due to a medical treatment. |
|
|
Term
| What is a “psychogenic” disease? |
|
Definition
| A psychogenic disease is an illness that stems from an emotional or mental cause. |
|
|
Term
| 17. What is the difference between signs and symptoms? |
|
Definition
| Signs are manifestations of the disease that are objectively identifiable by an observer (nurse). Symptoms are subjective feelings and can only be reported by the affected individual. Examples of symptoms are nausea and pain. Examples of signs are fever and reddening of the skin. |
|
|
Term
|
Definition
| the time between the exposure of a tissue to a harmful agent and the first signs and symptoms that appear. (In infectious diseases this is called the incubation period.) |
|
|
Term
|
Definition
| refers to the appearance of the first signs and symptoms indicate the onset of the disease such as fever or headache. |
|
|
Term
| What is the Subclinical stage: |
|
Definition
| during which is the patient appears to be able to function normally although the disease processes are established. |
|
|
Term
| What is the Convalescence stage? |
|
Definition
| the stage of recovery after a disease, injury or surgery |
|
|
Term
|
Definition
| is a relatively sudden increase of severity of a disease or any of its signs or symptoms. |
|
|
Term
|
Definition
| a condition that has severe signs or symptoms, but runs a short amount of time. |
|
|
Term
| What is meant by Chronic? |
|
Definition
| a condition lasts for a long time. |
|
|
Term
| What is Primary prevention? |
|
Definition
| Preventing disease by reducing susceptibility or exposure. Examples are improving nutrition, housing or sanitation, immunizations, health education programs, and public health measures (like for clean air and water). |
|
|
Term
| What is Secondary prevention? |
|
Definition
| The early detection, screening and management of disease. Examples are yearly physicals, Pap smears, mammograms, prenatal diagnosis of certain genetic diseases, and blood tests. |
|
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Term
| What is Tertiary prevention? |
|
Definition
| Used for advanced disease or disability, it includes rehab and supportive care to alleviate the disability and attempts to restore effective functioning. Most 3° preventions are medical or surgical. Physical therapy, radiation therapy and drugs are examples of medical prevention. |
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Term
| How does the amphipathic structure of the lipid bilayer cell membrane lead to selective permeability to lipid- and water-soluble molecules? |
|
Definition
| Lipids have a molecular structure that is amphipathic, meaning they have both a hydrophilic and a hydrophobic end. This characteristic causes lipids to spontaneously form bilayers that leave both ends “satisfied” and the bilayer is essentially sealed. Lipid-soluble molecules (those that are non-polar or have very low polarity) are able to pass though via simple diffusion, but water-soluble molecules have charges so they are repelled by the large hydrophobic region/layer and must cross the membrane via protein channels or carriers. |
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Term
| How does water pass through the cell membrane? |
|
Definition
| Water moves across the membrane via channels called aquaporins. It also crosses during osmosis when Na+, K+ and other ions move down their electrochemical gradients via facilitated diffusion (which is passive transport through membrane proteins), only water moves in the opposite direction going from an area of low solute concentration to high. |
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|
Term
| By what mechanisms are large and small molecules transported across cell membranes? |
|
Definition
| Large molecules are transported across the cell membrane through endocytosis. Endocytosis is where the large molecule is engulfed by membrane-bound vesicles and carried across the cell membrane. The large molecule is then secreted into the other side of the cell membrane. Carriers or channels transport small molecules across the cell. Carrier proteins can either be active or passive, while channel proteins are only passive. |
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|
Term
| How do carrier-mediated and channel-mediated transport systems differ? |
|
Definition
| Carrier mediated transport systems can use active or passive transport. They are very specific for certain molecules, and can also move two different ions at a time (Example: Na+ and K+ at the same time). Channel-mediated transport systems can only use passive transport. They also contain gates, which open and close to let molecules through. Channel transportation is very fast and also very selective for certain molecules. |
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|
Term
| Why must cells continuously synthesize ATP? |
|
Definition
| Cells must continually synthesize ATP, because cells require energy to function. Since ATP cannot cross the plasma membrane, be shared between cells or stored, the only way for a cell to get ATP is to synthesize it. Without synthesizing ATP, the cell will die. |
|
|
Term
| How is cellular ATP produced and used in a cell? |
|
Definition
| Cellular ATP is produced throughout three processes: Glycolysis, Krebs cycle, and Oxidative Phosphorylation. It is used in the cell for pumps (Na+ - K+ pumps), biosynthesis, movement, and to change the electrochemical gradient. ATP can either be used directly or indirectly |
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|
Term
| What are the consequences of hypoxia to cellular function? |
|
Definition
| Hypoxia is lack of oxygen in the cell. Since oxygen is needed for the synthesis of ATP, a decrease in oxygen will mean a little or no synthesis of ATP. Thus, the cell will become damage and likely die, unless it can find a source of oxygen. |
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|
Term
| By what means do cells communicate with one another? |
|
Definition
·Gap junctions
·Direct cell-to-cell contact unctions
·signaling through secreted ligands:
· Synaptic signaling
· Paracrine signals
· Endocrine signals |
|
|
Term
|
Definition
| connecting channels between adjacent cells that directly connect the cytoplasms allowing the passage of small molecules from one cell to the next. |
|
|
Term
| What is Direct cell-to-cell contact? |
|
Definition
| plasma membranes or the extracellular molecules, receptors with signaling molecules present on the membrane surfaces. |
|
|
Term
| What is the best understood form of cell communication? |
|
Definition
| signaling through secreted ligands: |
|
|
Term
| What are the secreted ligands used for cellular communication? |
|
Definition
·Synaptic signals
·Paracrine
·Endocrine |
|
|
Term
| where does synaptic signaling take place? |
|
Definition
| cells of the nervous system |
|
|
Term
| What are paracrine signals? |
|
Definition
| chemicals secreted in to a localized area, and rapidly destroyed, so that only cells in the immediate area are affected. |
|
|
Term
| What are Endocrine signals? |
|
Definition
| are hormones, secreted by specialized cells. The hormones travel through the bloodstream to target cells widely distributed throughout the body. |
|
|
Term
| What is the ligand a cell releases to activate itself? |
|
Definition
|
|
Term
| Explain how insoluble molecules in the extracellular space communicate/affect cells via cell surface receptor mechanisms. |
|
Definition
| Most hormones, local chemical mediators, and neurotransmitters are water soluble molecules that are unable to pass through the lipid bilayer of the cell. These ligands exert their effects through binding with a receptor on the surface of the target cell, which then changes or transduces the external signal into an intracellular message. |
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|
Term
| Name the 3 major classes of cell surface receptor proteins. |
|
Definition
Ion channel linked
Enzyme linked
G protein linked |
|
|
Term
| How do ion channel-linked receptors work? |
|
Definition
| They bind neurotransmitters, causing specific ion channels in the membrane to open or close. |
|
|
Term
| How do Enzyme-linked receptors work? |
|
Definition
| They catalyze enzyme reactions when they are activated by appropriate ligands. |
|
|
Term
| Describe the mechanism of G-protein linked receptors. |
|
Definition
| G-protein linked receptors are activated by appropriate ligands causing the G-protein to be activated inside the cell. The G-protein in turn activates a 2nd messenger (in our case cAMP, IP3, DAG Ca2+, and cGMP) and the 2nd messenger causes a cascade of enzymatic reactions that result in genes in the nucleus being turned on and/or off. |
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|
Term
| How is an action potential generated? |
|
Definition
| An action potential is triggered by membrane depolarization. In nerve and muscle cells, the usual trigger for depolarization is binding of a neurotransmitter to cell surface receptors. Transmitter binding causes channels or pores in the membrane to open , allowing ions (primarily Na+) to enter the cell. This influx of positive ions results in a shift I the membrane potential to a less negative value, resulting in depolarization. Threshold is reached when a patch of the membrane becomes sufficiently depolarized to activate voltage-gated sodium channels in the membrane. At threshold, these channels open rapidly and transiently to allow the influx of Na+ ions. This phase of rapid depolarization is terminated when the fast Na+ channels suddenly close and the repolarization phase begins. Two major factors contribute to cellular repolarization: closing Na+ channels stops sodium inflow, and opening of voltage-gated K+ channels allowing K+ to flow out of the cell. These K+ channels respond to depolarization of the membrane in the same manner as fast Na+ channels, but they take much longer to open and close. The loss of positive intracellular potassium ions helps to quickly return the membrane potential to its negative RMP value. |
|
|
Term
| What are action potentials? |
|
Definition
| Action potentials are rapid, self-propagating electrical excitations of the membrane that are mediated by ion channels that open and close in response to changes in voltage across the membrane (voltage-gated ion channels). |
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|
Term
| How does high extracellular potassium affect the resting membrane potential? How does this present clinically? |
|
Definition
| If the extracellular K+ level is increased fewer K+ ions will leave the cell, owing to the reduced concentration gradient. These extra positive intracellular ions will neutralize more of the negative cellular anions, and the cell will hypopolarize, or becomes less negative. Clinically the patient with hyperkalemia will lead to spastic paralysis…twitchy. |
|
|
Term
| How does low extracellular potassium affect the resting membrane potential? How does this present clinically? |
|
Definition
| If extracellular K+ levels fall, more K+ will exit the cell, owing to the greater concentration gradient. Fewer intracellular anions will be neutralized, and the cell interior will become more negative, or hyperpolarized. Clinically hypokalemia leads to flaccid paralysis…floppy. |
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|
Term
| What is the relationship between stress and disease? |
|
Definition
| Cortisol is the most potent glucocorticoid. Cortisol acts as an immunosuppressant, as it affects the immune system by affecting natural killer (NK) cells, macrophage production of cytokines, T cells, and B cells. Cortisol literally reduces the numbers of nearly all immune response cells, including lymphocytes, monocytes, eosinophils, and basophils. Cortisol is essential to meet the demands of the alarm stage of stress. However, high levels of cortisol activity in response to stress are intended to be self-limiting. Ideally the offending stressor is coped with or adapted to allowing the high cortisol activity to signal the shutdown of the hypothalamic-pituitary-adrenal (HPA) axis and immune system stress responses. If the stress response, or alarm, continues, the system adapts by no longer responding to cortisol without reducing cortisol activity. Severe, prolonged, or persistent increase in cortisol activity is thought to play a major role in the stress-disease process. |
|
|
Term
| How do acute and chronic stresses differ? |
|
Definition
| Stress is defined as a state of tension that can lead to the disruption of or threaten homeostasis. Acute stress is short term, such as the alarm stage, or the fight or flight response. Chronic stress is long term, and can cause diseases such as asthma, palpitations, headaches, menstrual irregularity, rashes, and digestive disturbances, among others. |
|
|
Term
| What is desensitization and how does it affect the stress response? |
|
Definition
Desensitization - training of the hypothalamus to react less forcefully to a stressor/threat. Repeated practice of ignoring specific stressor prevents the inappropriate triggering of the GAS. The result is a more acceptable level of stress response.
How it affects stress response - changes brain waves from Beta to Alpha (alpha are slower and more normal). Accomplished by meditation and visualization exercises |
|
|
Term
| How do genetics, age, gender, culture, and ethnicity influence an individual’s stress response? |
|
Definition
Cultural – perception of health/illness is different in every culture and can be based on religious ideology.
Age – Aging itself is stressful. Furthermore, stress and stress-related mechanism augment age-related changes in the body.
Genetics – physiology is different between each individual, hypothalamus might function differently.
Gender – women may get menstrual irregularity, while men may respond to stress by becoming impotent. |
|
|
Term
| What is the physiological response to stress? |
|
Definition
| endocrine system linked to nervous system and every other physiologic system even the immune system. Hair loss, tension, asthma, heart palpitations, digestive disorders, irritable bowel, tics etc are responses to stress. |
|
|
Term
| How do the neuroendocrine and immune systems relate to the stress response? |
|
Definition
| Neurocrine system is activated by stress. Hormones released during stress effect immune system. Neurocrine systems (SNS) enable the body to react quickly to the stressor. SNS activates the hypothalamus and pituitary gland, which release hormones. Once pituitary gland is activated it cannot turn off until desensitization occurs. |
|
|
Term
| Define “pharmacokinetics” |
|
Definition
| Pharmacokinetics is the study of drug movement through the body. There are four component processes that are associated with pharmacokinetics: absorption, distribution, metabolism, and excretion. |
|
|
Term
|
Definition
| is the movement of a drug from its site of administration into the blood. |
|
|
Term
|
Definition
| Drug movement from the blood to the interstitial space of tissues and from there into cells. |
|
|
Term
| What is Metabolism (biotransformation)? |
|
Definition
| Metabolism is the enzymatically-medicated alteration of drug structure. |
|
|
Term
|
Definition
| The movement of drugs and their metabolites out of the body. (L p 24) |
|
|
Term
| What is the impact of drug ionization? |
|
Definition
·The ionization of drugs is pH dependent. When the pH of the fluid on one side of a membrane differs from the pH of the fluid on the other side, drug molecules will tend to accumulate on the side where the pH most favors their ionization. Accordingly, since acidic drugs tend to ionize in a basic media, and since basic drugs tend to ionize in acidic media, when there is a pH gradient between 2 sides of a membrane,
oAcidic drugs will accumulate on the alkaline side.
oBasic drugs will accumulate on the acidic side.
·The process whereby a drug accumulates on the side of a membrane where the pH most favors its ionization is referred to as ion trapping or pH partitioning |
|
|
Term
| How do drugs cross the cell membranes of the organs and tissues involved in pharmacokinetics? |
|
Definition
There are three ways that drugs cross cell membranes:
·Channels (Ion Channels)
·Carrier Proteins
·Direct penetration of the membrane |
|
|
Term
|
Definition
| AKA ion channels are Passive only, Very fast, Channels are “gated” (ligand, voltage, or mechanically gated) |
|
|
Term
| Describe carrier proteins. |
|
Definition
| Active or Passive, Slow, May be coupled so 2 ions must move, Very selective, |
|
|
Term
| What kind of drugs can directly penetration the membrane? |
|
Definition
| Many drugs are too large to pass through channels, and most do not have transport system, so most drugs must be lipid soluble to cross the cell membrane. |
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Term
| What do the rate and amount of drug absorption affect? |
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Definition
| Absorption is the movement of a drug from it site of administration into the blood. The rate of absorption determines how soon effects will begin, and the amount of absorption helps determine how intense effects will be. (L p 28) Faster absorption equals short effect and slower absorption equals a longer effect. |
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Term
| What are the common routes of drug administration that fall under “enteral” ? |
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Definition
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Term
| What are the common routes of drug administration that fall under “parenteral”? |
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Definition
| commonly used parenteral means by injection. Principal parenteral routes are Intravenous, Intramuscular, and Intradermal |
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Term
| What are the advantages of Oral administration of a drug? |
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Definition
| Easy, convenient and inexpensive (as in, no cost for the process of administration.) Safer than injection: no risk of fluid overload, infection or embolism. Reversible: emesis (vomiting) can be induced to prevent absorption if needed. Activated charcoals, a compound that absorbs drugs while they are still in the GI tract can be administered to prevent harm from orally administered drugs. |
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Term
| What are the disadvantages of Oral administration of a drug? |
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Definition
| Disadvantages: (1) Absorption is highly variable from patient to patient. (2) Some drugs become inactivated by oral administration; such as from digestive enzymes in the stomach (penicillin G is destroyed this way). (3) Some drugs are inactivated by the liver in the “first pass effect” (see 5 d.) after being absorbed in the intestine (insulin is not an oral drug because of this) (4) Patient compliance is also a problem, as oral drug administration requires a conscious, cooperative patient. (5) Some drugs can cause local irritation of the GI tract, which can result in discomfort, nausea, and vomiting. |
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Term
| What factor affect the rate of absorption with the oral administration of a drug? |
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Definition
| Factors affecting rate of absorption: Because of multiple factors, the rate and extent of drug absorption following oral administration can be highly variable. Factors that can influence absorption include (1) solubility and stability of the drug, (2) gastric and intestinal pH, (3) gastric emptying time, (4) food in the gut, (5) co-administration of other drugs, and (6) special coatings on drug preparation. |
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Term
| What are the factors affecting rate of absorption with the intravenous administration of a drug? |
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Definition
| When a drug is administered IV, there are no barriers to absorption. Recall that absorption is defined as the movement of the drug from its site of administration into the blood. Since IV administration puts a drug directly into the blood, all barriers are by passed. |
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Term
| What are the factors affecting rate of absorption with the Intramuscular and Subcutaneous administration of a drug? |
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Definition
| When a drug is injected IM, the only barrier is the capillary wall. Like IV administration, IM administration presents no significant barriers to absorption. |
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Term
| What are the advantages of intravenous administration of drugs? |
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Definition
| Rapid onset: While this is not always important, it is clearly beneficial in emergencies. Control: Since the entire dose is administered directly into the blood, we have precise control over levels of drug in the blood. Use of large fluid volumes: Some drugs that require parenteral administration are poorly soluble in water and therefore must be dissolved in a large volume. Use of irritant drugs: Certain drugs, in high concentrations can cause severe local injury. However, when administered through a freely flowing IV line, these drugs are rapidly diluted in the blood, thereby minimizing the risk of injury. |
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Term
| What are the disadvantages of intravenous administration of drugs? |
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Definition
| High cost, Difficulty, and Inconvenience: IVs are expensive and take special training to set up. Because the patient is tethered to lines and bottles, their mobility is limited. Irreversibility: Once a drug has been injected, there is no turning back; the drug is in the body and cannot be retrieved. Fluid overload: this can be a significant problem for patients with hypertension, kidney disease, or heart failure. Infection: This can occur from injecting a contaminated drug. Embolism: IV administration carries the risk of embolism (blood vessel blockage). |
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Term
| What are the disadvantages of Intramuscular and Subcutaneous administration of drugs? |
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Definition
| The major drawbacks of IM administration are discomfort (painful) and inconvenience. Also, IM injection can cause local tissue injury and possible nerve damage if injection is done improperly. |
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Term
| What are the advantages of Intramuscular and Subcutaneous administration of drugs? |
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Definition
| The IM route is used for administration of poorly soluble drugs. Another advantage of the IM route is that we can use it to administer depot preparations (preparations from which the drug is absorbed slowly over an extended time.) |
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Term
| What is “bioavailability” and what is its significance? |
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Definition
| Bioavailability is the ability of a drug to get to general circulation from site of administration. Differences in bioavailability are of greatest concern for drugs with a narrow therapeutic range. When the therapeutic range is narrow, a relatively small change in drug level can produce a significant change in response: A small decline in drug level may cause therapeutic failure, whereas a small increase in drug level may cause toxicity. Under these conditions, differences in bioavailability could have a significant impact. |
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Term
| What is the primary rate-limiting factor of drug distribution? |
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Definition
The primary rate-limiting factor is the rate of absorption into the blood. This bioavailability is affected by:
·Route of administration (Enteral vs. parenteral, also the form of the drug, liquid, tablet, etc.
·Surface area/ cells available.
·Perfusion/Blood flow at site of absorption.
·Lipid solubility, more limpidity – faster movement across membranes.
(Class notes) |
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Term
| What is the blood-brain barrier and what is its significance? |
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Definition
| The BBB refers to the unique capillaries found in the CNS, in which there are a series of tight junctions between the cells that compose the walls of most capillaries. These junctions are so tight that they prevent drug passage. Consequently, in order to leave the blood and reach sites of action within the brain, a drug must be able to pass though cells of the capillary wall. Only drugs that are lipid soluble or have a transport system can cross the BBB to a significant degree. As a consequence, potentially toxic substances are prevented from crossing this barrier and injuring the brain. On the other hand, substances for CNS therapy are also prevented from entering the CNS. The BBB can impede access of antibiotics to CNS infections. The BBB is not fully developed at birth and neonates and newborns are extremely susceptible to CNS poisons. |
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Term
| What is the placental barrier and what is its significance? |
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Definition
| The placental barrier is a series of membranes that separate the maternal and fetal circulation. It is NOT, however, a barrier to the passage of drugs and is subject to the same factors of other membranes in regard to the passage of drugs. Lipid soluble, non-ionized compounds are easily passed between the fetal and maternal, etc. It is significant because certain drugs that are able to pass through this membrane can cause serious birth defects and/or drug dependencies. |
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Term
| Explain plasma protein binding and its effect upon serum drug levels. |
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Definition
| Plasma albumin is the most important protein to which drugs can bind due to the fact that it is the most abundant protein in the plasma. The binding between Albumin and drugs, as a result, a drug may exist either bound or unbound (free). Because of its size albumin always remains in the bloodstream and consequently, any drug bound to it will also say in the bloodstream. This is significant because it does not allow the drugs to reach their sites of action, metabolism, or excretion. The percentage of drug molecules that are bound is determined by the strength of the attraction between albumin and the drug. An important consequence of protein binding is restriction of drug distribution. In addition to restricting the distribution of drugs, protein binding can be a source of drug interactions. Because the number of binding sites on albumin is limited, drugs with the ability to bind albumin will compete with one another for binding sites. As a result, one drug can displace another from albumin, causing the free concentration of the displaced drug to rise. By increasing levels of free drug, competition for binding can increase the intensity of drug responses. If the intensity increases excessively, toxicity can result. |
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Term
| Where does most drug metabolism occur? What are the lesser sites of drug metabolism? |
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Definition
| Most drug metabolism occurs in the liver and is performed by the hepatic microsomal enzyme system, also known as the P450 system. (L p.35) "Lesser sites of drug metabolism" are the kidney and the intestine, and of the two, the kidney metabolizes more. But, if metabolism is necessary to allow excretion, it is mostly done by the liver. (Dr. E’s answer on the discussion page 1/22/06). |
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Term
| What is the role of the P450 system? What is meant when a drug is said to induce metabolism? |
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Definition
| The P450 system metabolizes certain drugs and other endogenous compounds. A drug is said to induce metabolism when it acts on the liver to increase the rates of drug metabolism, by causing the liver to synthesize drug-metabolizing enzymes |
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Term
| What are the five potential consequences of drug metabolism. |
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Definition
·Accelerated Renal Drug Excretion
·Drugs inactivation
·Increased Therapeutic Action
·Activation of Prodrugs
·Increased or Decreased Toxicity |
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Term
| What is "accelerated Renal Drug Excretion"? (One of the consequences of drug metabolism.) |
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Definition
| The kidney is unable to excrete drugs that are highly lipid-soluble. The liver converts lipid-soluble drugs into more polar (less lipid-soluble) compounds, making it possible for the kidney to excrete many drugs |
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Term
| What is "drug inactivation?" (One of the consequences of drug metabolism.) |
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Definition
| Drug metabolism can convert pharmacologically active compounds to inactive forms. |
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Term
| What is increased "Therapeutic Action?" (One of the consequences of drug metabolism.) |
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Definition
| Metabolism can increase the effectiveness of some drugs. |
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Term
| What is the "activation of Prodrugs"? (One of the consequences of drug metabolism.) |
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Definition
| A prodrug is a compound that is pharmacologically inactive as administered and then undergoes conversion to its active form within the body. |
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Term
| What is "Increased or Decreased Toxicity?" (One of the consequences of drug metabolism.) |
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Definition
| By converting drugs into inactive forms, metabolism can decrease toxicity. Conversely, metabolism can increase the potential for harm by converting relatively safe compounds into forms that are toxic. |
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Term
| Define the first-pass effect. What routes are affected? How is it compensated for in drug administration? |
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Definition
| The term first-pass effect refers to the rapid hepatic inactivation of certain oral drugs. When drugs are administered orally, they are absorbed from the GI tract and carried directly to the liver via the hepatic portal circulation. If the capacity of the liver to metabolize a drug is extremely high, that drug can be completely inactivated on its first pass through the live. As a result, no therapeutic effects will occur. To circumvent the first-pass effect, a drug that undergoes rapid hepatic metabolism is often administered parenterally. This permits the drug to temporarily bypass the liver, thereby allowing it to reach therapeutic levels in systemic blood. |
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Term
| How are drugs and drug metabolites excreted? Where does most drug excretion occur? |
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Definition
| Drug excretion is defined as the removal of drugs from the body. Drugs and their metabolites can exit the body in urine, bile, seat, saliva, breast milk, and expired air. The most important organ for drug excretion is the kidney. |
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Term
| What are the steps of renal drug excretion? |
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Definition
·Glomerular filtration
·Passive tubular reabsorption
·Active tubular secretion |
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Term
| What is Glomerular filtration and what factors affect it? |
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Definition
| Glomerular filtration – as blood passes through the glomerulus capillaries, fluids and small molecules–including drugs–are forced through the pores of the capillary wall. Blood cells and other large molecules are too pig to pass through the pores in the capillary walls. Albumin is too large to pass through the pores; therefore any drug bound to it will also remain in the blood stream. |
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Term
| What is Passive tubular reabsorption? and What factors can affect it? |
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Definition
| Passive tubular reabsorption – at the distal tubule, the drug concentrations in the blood are lower than drug concentration in the tubule. This concentration gradient acts as a driving force to move drugs from the lumen of the tubule back into the blood. Since lipid-soluble drugs can readily cross the membranes that compose the tubular and vascular wall, drugs that are lipid soluble undergo passive reabsorption from the tubule back into the blood. In contrast, drugs that are not lipid soluble (ions and polar compounds) remain in the urine to be excreted. |
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Term
| What is Active tubular secretion? and what factors can affect it? |
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Definition
| Active tubular secretion - There are active transport systems in the kidney tubules that pump drugs from the blood to the tubular ruin. The tubules have two classes of pumps, one for organic acids and the other for organic bases. These pumps have a relatively high capacity and play a significant role in excreting certain compounds. |
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Term
| Define Plasma drug level; peak, trough, and toxic plasma levels, and explain its relationship to the time course of drug responses (i.e., onset, peak, and duration): |
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Definition
| Pharmacokinetic processes determine the plasma concentration of a drug, called the plasma drug level. Peak is the time of maximum plasma concentration of a drug. Toxicity occurs when plasma levels climb too high. The plasma level at which toxic effects begin is termed the toxic concentration (L p. 39, class notes). When a drug is administered repeatedly, its level will fluctuate between doses. The highest level is the peak, and the lowest level is referred to as the trough concentration. How high the peaks and how low the troughs are depends upon the drug’s therapeutic range. |
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Term
| Define Minimum effective concentration (MEC) and explain its relationship to the time course of drug responses (i.e., onset, peak, and duration): |
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Definition
| MEC is defined as the plasma drug level below which therapeutic effects will not occur. Hence to be of benefit, a drug must be present in concentration at or above the MEC. Onset occurs when the plasma drug level reaches MEC. |
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Term
| Define Therapeutic range and explain its relationship to the time course of drug responses (i.e., onset, peak, and duration): |
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Definition
| Therapeutic range is the plasma drug level that falls between the MEC and the toxic concentration. When plasma levels are with in the therapeutic range, there is enough drug present to produce therapeutic responses, but no so much that toxicity results. The peak of the drug concentration should occur within this range. Drugs that have a narrow therapeutic range are difficult to administer safely. Conversely, drugs that have a wide therapeutic range can be administered safely with relative ease. ( |
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Term
| Define Loading and maintenance doses.and explain their relationship to the time course of drug responses (i.e., onset, peak, and duration): |
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Definition
| For drugs whose half-lives are long, achieving plateau (see question 8) could take days or even weeks. When plateau must be achieved more quickly, a large initial dose can be administered. This large initial dose is called a loading dose. After high drug levels have been established with a loading does, plateau can be maintained by giving smaller does. These smaller doses are referred to as maintenance doses. |
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Term
| Define Half-life and explain its relationship to the time course of drug responses (i.e., onset, peak, and duration): (Explain how a drug’s half-life can be used to determine its anticipated serum level). |
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Definition
| Drug half-life is defined as the time required for the amount of drug in the body to decrease by 50%. A few drugs have half-lives that are extremely short – on the order of minutes. In contrast, the half-lives of some drugs exceed 1 week. Drugs with short half-lives leave the body quickly. Drugs with long half-lives leave slowly. |
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Term
| What is the plateau principle? |
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Definition
| Administering repeated doses of a drug will cause that drug to build up in the body until a plateau (steady level) has been achieved. If a second dose of a drug is administered before all of the prior does has been eliminated, total body stores of that drug will be higher after the second dose than after the initial dose. As succeeding doses are administered, drug levels will climb even higher. The drug will continue to accumulate until a state has been achieved in with the amount of drug eliminated between does equal the amount administered. When the amount of drug eliminated equals the amount administered, average drug levels will remain constant and plateau will have been reached. |
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Term
| What does the plateau principle mean to the nurse? |
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Definition
| A nurse should understand the plateau principle determine the dosage of continual efficacy of a drug. It is important to know the therapeutic range of the drug so as to keep the peak of the plateau below the toxic concentration range and to keep the trough above the MEC. |
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Term
| Define the term “pharmacodynamics.” |
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Definition
| Pharmocodynamics is the study of the biochemical and physiologic effects of drugs and the molecular mechanisms by which those effects are produced, OR, what drugs do at the cells (when they arrive) and how they do it; drugs modify existing functions, they don’t create new ones |
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Term
| What is the “dose-response relationship” and what is its significance? |
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Definition
| The Dose-response relationship is the relationship between the size of an administered dose and the intensity of the response produced. The dose-response relationship determines the minimum amount of drug we can use, the maximum response a drug can elicit and how much we need to increase the dosage to produce the desired increase in response. Dose-response curve relates to Efficacy & Potency. |
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Term
| Using a dose-response curve, illustrate and differentiate the concepts of potency and efficacy. |
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Definition
Maximum efficacy is defined as the largest effect that a drug can produce. Maximum efficacy is indicated by the height of the dose-response curve.
The term Potency refers to the amount of drug we must give to elicit an effect. Potency is indicated by the relative position of he dose-response curve along the x (dosage) axis.
See charts on pages 44-45 Lehne |
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Term
| 12. Explain how receptors determine selective drug action. |
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Definition
| As a rule, each type of receptor participates in the regulation of just a few processes. If a drug interacts with only one type of receptor and if that receptor type regulates just a few processes, then the effects of the drug will be limited. Conversely, if a drug interacts with several different receptor types, then that drug is likely to elicit a wide variety of responses. The shape of the drug is complementary to the shape of the receptor, which determines the selectively of the drug action. |
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Term
| What is the simple occupancy theory of drug receptor interaction? |
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Definition
| The simple occupancy theory of drug receptor interaction says that 1) the intensity of the response to a drug is proportional to the number of receptors occupied by that drug. 2) a maximal response will occur when all available receptors have been occupied. This theory says that two drugs acting on the same receptors should produce the same maximal effect, but it does not explain why one drug should be more potent than another, nor can this theory explain how one drug can have higher maximal efficacy than another. That is, according to this theory, two drugs at the same receptor should produce the same maximal effect, providing that their dosages were high enough to produce 100% receptor occupancy. However, we have seen this is not true. The simple occupancy theory assumes that all drugs acting at a particular receptor are identical with respect to 1) the ability to bind to the receptor and 2) the ability to influence receptor function once binding has taken place. |
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Term
| What is the modified occupancy theory? |
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Definition
| · The modified occupancy theory explains things that the simple occupancy cannot and is based on different assumptions. The modified drug theory says that two drugs can occupy the same number of receptors but produce effects of different intensity. The modified theory gives two qualities to drugs, affinity and intrinsic activity. |
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Term
|
Definition
o Affinity is the strength of the attraction between the drug and its receptor. High affinity = strong attraction, Low affinity = weakly attracted. Affinity is related to potency because drugs with a high affinity are effective in low doses, which means that drugs with high affinity are very potent; conversely, drugs with low affinity must be present in high concentrations to bind to their receptors. Accordingly, drugs with low affinity are not very potent.
o Intrinsic activity is the ability of a drug to activate a receptor on binding. High intrinsic activity = intense receptor activation. Low intrinsic activity = slight activation. The intrinsic activity is related to efficacy |
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Term
| What is Intrinsic activity? |
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Definition
| o Intrinsic activity is the ability of a drug to activate a receptor on binding. High intrinsic activity = intense receptor activation. Low intrinsic activity = slight activation. The intrinsic activity is related to efficacy because drugs with high intrinsic activity have high maximal efficacy and vice versa. |
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Term
|
Definition
| Agonists are molecules that activate receptors. Examples are neurotransmitters, hormones. Drugs that mimic the body’s own regulatory molecules are call agonists. |
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Term
| What is a Partial agonist? |
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Definition
| Partial agonist: is an agonist that only has moderate intrinsic activity which means that the maximal effect that it can produce is lower than that of a agonist. They can act as agonists as well as antagonists. For example if a patient is already taking a full agonist drug for pain relief and is then give a large does of a partial agonist for the same receptors, the partial agonist will occupy the receptor and prevent their activation by the full agonist. As a result, rather than experiencing the high degree of pain relief that the full agonist can produce, the patient will experience only the limited relief that the partial agonist can produce. In this situation the partial agonist is acting as an antagonist. |
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Term
|
Definition
| Antagonists produce their effects by preventing receptor activation by endogenous regulatory molecules and drugs. They virtually have no effects of their own on the receptor. According to the modified occupancy theory, an antagonist is a drug with affinity for a receptor but with no intrinsic activity. Antagonists produce their effects by preventing the activation of receptors by agonists (antagonist drugs used in treatment of overdose). |
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Term
| What is a noncompetitive antagonist? |
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Definition
| Noncompetitive is where antagonists bind irreversibly to receptors. Noncompetitive reduce the number of receptors available to the agonist. If sufficient antagonist is present, agonist effects will be blocked completely. Because the binding of Noncompetitive antagonist is irreversible, inhibition by these agents cannot be overcome – no matter how much agonist may be available. The effects of noncompetitive antagonists wear off as the cell replaces the receptors to which they are bound. |
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Term
| What is a competitive antagonist? |
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Definition
| Competitive antagonists bind reversibly to receptors. If an agonist and an antagonist have an equal affinity for a receptor then the one which is present in the highest concentration will occupy the receptor. |
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Term
| Explain Up and down regulation. |
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Definition
| Receptors are dynamic components of the cell. In response to continuous activation or continuous inhibition, the number of receptors on the cell surface can change, as can their sensitivity to agonist molecules. For example, when the receptors of a cell are continually exposed to an agonist, the cell usually becomes less responsive. When this occurs, the cell is said to be desensitized or refractory, or to have undergone down –regulation. Several mechanisms may be responsible, including destruction of receptors by the cell and modification of receptors such that they respond less fully. Continuous exposure to antagonist has the opposite effect, causing the cell to become hypersensitive. One mechanism that can cause hypersensitivity is synthesis of more receptors. |
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Term
| 15. Explain the concept of interpatient variability in terms of ED50. What factors contribute to individual variation in drug response (consider especially the effect of age and disease upon pharmacokinetics)? What are the clinical implications for nurs |
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Definition
| “ED50 is an abbreviation for the average effective dose. The ED50 is defined as the dose that is required to produce a defined therapeutic response in 50% of the population.” The ED50 is considered the standard dose of a drug. After evaluating a patient’s response to this “standard” dose, we can then adjust subsequent doses up or down in accordance with the patients needs. Because initial doses are approximations, it would be wise not to challenge the doctor if the prescribed initial dose differs by a small amount (10-20%) from the recommended doses in a published drug reference. Administer the dose and subsequent doses can be adjusted as needed. Of course, if the physician’s order calls for a dose that differs from the recommended dose by a large amount, that order should be challenged. Because of variability in responses, nurses, patients, and other concerned individual must evaluate actual responses and be prepared to inform the prescribing physician about these responses so that proper adjustments in dosage can be made. |
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Term
| What is “therapeutic index” and how is it interpreted? |
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Definition
The therapeutic index is the measure of a drug’s safety. The therapeutic index is defined as the ratio of a drug’s LD50 to its ED50:
THERAPEUTIC INDEX (TI) = LD50/ED50
A therapeutic index indicates that a drug is relatively safe. Conversely, a small therapeutic index indicates that a drug is relatively unsafe. The highest dose required to produce therapeutic effects must be substantially lower than the lowest dose capable of causing death. |
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Term
| What are common side effects/adverse responses to drug therapy? |
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Definition
| Drugs can adversely affect all body systems in varying degrees of intensity. Mild reactions: Drowsiness, nauseas, itching, and rash. Severe reactions (can cause death): respiratory depression, neutropenia, hepatocellular injury, anaphylaxis, and hemorrhage. |
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Term
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Definition
| Some patients are more vulnerable than others. Adverse reactions are most common in the elderly and in the very young. Patients over 60 account for nearly 50% of all the cases. |
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Term
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Definition
| as decreased responsiveness to a drug as a result of repeated drug administration. Patients who are tolerant to a drug require higher doses to produce the same effects that were achievable with lower doses before tolerance had developed. |
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Term
|
Definition
| a state in which the body has adapted to prolonged drug exposure in such way that an abstinence syndrome will result if drug use is discontinue. Dependence develops when using certain drugs as opioids, alcohol, barbiturates and amphetamines. |
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Term
|
Definition
| a disease process characterized by the continue use of specific psychoactive substance despite, physical, psychological, or social harm. |
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Term
| Differentiate the etiology of drug allergies and idiosyncratic responses. |
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Definition
An allergic reaction is an immune response. For an allergic reaction to occur there must be prior sensitization of the immune system. Once the immune system has been sensitized to a drug, re-exposure to that drug can trigger an allergic response.
Idiosyncratic effect is defined as an uncommon drug response resulting from a genetic predisposition. |
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Term
| What does it mean if a drug is found to be carcinogenic |
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Definition
| Carcinogenic is the ability of certain medications and environmental chemicals that cause cancer. Several of the drugs used to treat cancer are among the drugs with the greatest carcinogenic potential |
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Term
| How can ADRs be minimized? |
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Definition
| The responsibility to reducing ADRs lies with everyone associated with drug manufacture and use. The pharmaceutical industry must strive to produce the safest possible medicines; the prescriber must select the least harmful medicine for a particular patient; the nurse must evaluate patients for ADRs and must educate patients in a way to avoid or minimize harm; and patient and their families must watch for signs that an ADR may be developing and should seek medical attention if they appear. |
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Term
| What are the consequences of drug-drug interactions? |
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Definition
·One drug may intensify the effect of the other. This type of interaction is called potentiative and may be beneficial or detrimental. A potentiative interaction that enhances therapeutic effects is clearly beneficial. Conversely, a potentiative interaction that intensifies adverse effects is clearly detrimental.
·Interactions that result in reduced drug effects are often termed inhibitory, and can be beneficial or detrimental. Inhibitory interactions that reduce toxicity are beneficial. Conversely, inhibitory interactions that reduce therapeutic effects are detrimental.
·The combination of two drugs produces a new response not seen with either agent alone (Unique response.) |
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Term
| What are the mechanisms of drug-drug interactions? |
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Definition
1.Direct or chemical or physical interaction. Some drugs because of their physical or chemical properties can undergo direct interaction with other drugs. Direct interactions occur most commonly when drugs are combined in IV solutions. Frequently, the interaction produces a precipate. If this happens that solution should be discarded. Because drugs can interact in solution, never combine two or more drugs in the same container unless it has been established that indirect interaction will not occur. It is difficult that interactions happen within the patient because drugs are diluted in the body water following administration.
2.Pharmacokinetic Interactions. When two drugs are taken together. One may alter the absorption, distribution, metabolism or excretion of the other.
3. Pharmacodynamic Interactions.
·Interactions in which the interacting drugs act at the same site. They are almost always inhibitory and occur when an antagonist drug blocks access of agonist drug to its receptors. These interactions may reduce therapeutic effects (undesirable), other reduce toxicity and are of obvious benefit.
·Interactions in which the interacting drugs act at separate sites. When two drugs influence the same physiologic process, then one drug can alter responses produce by the other. Interactions resulting from effects produced at different sites may be potentiative or inhibitory |
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Term
| How might a drug-drug interaction alter absorption? |
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Definition
·By elevating gastric pH, antacids can decrease the ionization of basic drugs in the stomach, thereby increasing the ability of basic drugs to cross membranes and be absorbed. Antacids have the opposite effect on acid drugs.
·Laxatives can reduce absorption of other drugs by accelerating their passage through the intestine.
·Drugs that depress peristalsis (e.g., morphine, atropine) prolong drug transit in the intestine, thereby increasing the time of absorption.
·Drugs that induce vomiting can decrease absorption of oral drugs.
·Cholestyramine and certain other adsorbent drugs, which are administered orally but do not undergo absorption can adsorb other drugs onto themselves, thereby preventing absorption of the other drug into the blood.
·Drugs that reduce regional blood flow can reduce absorption of other drugs from the region. |
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Term
| How might a drug-drug interaction alter distribution? |
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Definition
·By elevating gastric pH, antacids can decrease the ionization of basic drugs in the stomach, thereby increasing the ability of basic drugs to cross membranes and be absorbed. Antacids have the opposite effect on acid drugs.
·Laxatives can reduce absorption of other drugs by accelerating their passage through the intestine.
·Drugs that depress peristalsis (e.g., morphine, atropine) prolong drug transit in the intestine, thereby increasing the time of absorption.
·Drugs that induce vomiting can decrease absorption of oral drugs.
·Cholestyramine and certain other adsorbent drugs, which are administered orally but do not undergo absorption can adsorb other drugs onto themselves, thereby preventing absorption of the other drug into the blood.
·Drugs that reduce regional blood flow can reduce absorption of other drugs from the region. |
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Term
| How might a drug-drug interaction alter metabolism? |
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Definition
| Some drugs increase the metabolism of other drugs; some drugs decrease the metabolism of other drugs. Drugs that increase the metabolism of other drugs do so by inducing synthesis of hepatic drug-metabolizing enzymes. Drug that decrease the metabolism of other drugs do so by inhibiting those enzymes |
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Term
| How might a drug-drug interaction alter Renal Excretion? |
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Definition
| Drugs can alter all three phases of renal excretion (filtration, reabsorption, and active secretion). |
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Term
| What is combined toxicity? |
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Definition
| drugs with overlapping toxicity |
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Term
| What are the nursing implications for drug-drug interactions? |
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Definition
·Interactions that increase therapeutic effects or reduce toxicity are desirable. Conversely, interactions that reduce therapeutic effects or increase toxicity are detrimental.
·The risk of serious drug interaction is proportional to the number of drugs that a patient is taking.
·Interactions are special important for drugs that have a low therapeutic index.
·Minimized the number of drugs a patient receive.
·Take a thorough drug history, and make a special effort to ensure that the patient’s drug profile is completed.
·Additional measures for reducing adverse interactions include adjusting the dosage when an inducer of metabolism is added or deleted from the regimen; adjusting the timing of administration to minimize interference with absorption, and monitoring for early signs of toxicity when combinations of toxic agents cannot avoided. |
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Term
| What is the role of the placebo effect in health care? |
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Definition
| A Placebo is a preparation that is devoid of intrinsic pharmacologic activity. The placebo effect is defined as that component of a drug response that is caused by psychological factors and NOT by the biochemical or physiologic properties of the drug. It is impossible to assess with precision the contribution that psychologic factors make to the overall response to any particular drug; it is widely believed that with practically all medications, some fraction of the total response results from a placebo effect. Not all placebo responses are beneficial; placebo responses can also be negative. The patients attitude (positive) may help promote beneficial effects so it is desirable that all members of the healthcare team present the patient with an optimistic (but realistic) assessment of the effects that therapy is likely to produce. The positive placebo effect can decrease when the nurse on the day shift expresses optimism and the night shift nurse expresses pessimism about the drug therapy |
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Term
| What are the concerns related to drug therapy in pregnancy |
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Definition
Half to two thirds of pregnant women take at least one medication and the majority takes more. Some drugs are used to treat pregnancy-related conditions like nausea, constipation, pre-clampsia or chronic diseases like hypertension, diabetes, and epilepsy.
Concerns are the balance between “risk to benefit” considerations of drug therapy without knowing what the risks really are (78). Remember that clinical testing on women and children was only approved in the 1990’s so there is a lack of clinical drug information for women in general (study guide #1 (17)). The author says the health of the fetus depends on the health of the mother and drug therapy should not be avoided (78)
Pregnancy brings on physiologic change that can alter drug disposition like changes in the liver, kidney, and GI tract. These changes may affect drug dosage. Example: renal blood flow doubles in the third trimester with a large increase in glomerular filtration rate. This accelerates the clearance of drugs that are eliminated by glomerular filtration. To compensate the drug dosage would be increased. For some drugs, hepatic metabolism increases during pregnancy. Tone and motility of the bowel decrease in pregnancy, which allows more time for oral and gastric tube fed drugs to be absorbed. In theory this could increase levels of drug absorption whose absorption would normally be poor hence producing a prolonged effect. Dosage reduction may be needed in this case. Lipid soluble drugs cross the placenta easily while ionized, highly polar, or protein bound drugs cross with difficulty. Nonetheless, the clinician should assume that any drug taken during pregnancy will reach the fetus |
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Term
| What are the concerns related to drug therapy during breast-feeding? |
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Definition
Breast Feeding: Very little research done (82). Nearly all drugs can enter breast milk but extent varies greatly. Same physiology applies to breast milk as the placenta. To reiterate, lipid soluble drugs cross the breast tissue membrane easily while ionized, highly polar, or protein bound drugs cross with difficulty (83).
Options to minimize risk to fetus:
·Dosage taken after breast feeding
·Avoid drugs with long half life
·Drugs that tend to be excluded from milk
·Drugs that produce the least effect to infant (Table 9-4)
·Avoid known hazardous drugs (Table 9-3) |
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Term
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Definition
| production of birth defects |
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Term
| What are the FDA Pregnancy Risk Categories and how are they interpreted? |
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Definition
Category A – least dangerous. Controlled studies on pregnant women demonstrate no fetal harm.
Category B – Slightly more risk than category A. Animal studies show no fetal risk, but controlled studies have not been done on women.
Category C – Greater risk than Category B. Animal studies show risk of fetal harm but no studies on women yet OR no study on women or animals.
Category D – Proven Risk of Fetal Harm. Potential benefits of use during pregnancy may be acceptable despite the risks (life threatening). Label WARNING statements.
Category X – most dangerous. Proven risk of fetal harm (abnormalities). Risk to fetus outweighs therapeutic benefit. See “Contraindications” section of drug labeling. |
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Term
| Using your knowledge of the functions of the SNS and the PSNS by receptor and sub-receptor type, explain the concept of receptor selectivity as it applies to ANS drugs. |
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Definition
| “Selectivity is one of the most desirable qualities a drug can have, since a selective drug is able to alter a disease process while leaving other physiologic processes largely unaffected.” For example, a B1 agonist drug will affect only B1 receptors and can increase HR and cause urinary retention, but otherwise shouldn’t affect other organs. (L p. 95) There are different kinds receptors on organs in the PSNS and SNS. Drugs given to control the heart, lungs and other organs can be specific to the desired response because the PSNS and SNS are opposing systems, that is, they pretty much do the opposite of one another. |
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Term
| Explain the mechanisms of action, anticipated side/adverse effects, and potential uses for Adrenergic agonists (Sympathomimetic) |
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Definition
·Mechanism of Action- Activate adrenergic receptors, which cause reactions similar to turning on fight vs. flight response. Do this by:
·Direct receptor binding- most common mechanism, mimick natural NT (NE and epi)
·Enhancing NT release- by acting on sympathetic nerve terminals it causes NT release.
·Inhibiting NT reuptake- Reuptake is the major way to end adrenergic stimulation, blocking reuptake will prolong receptor activation.
·Inhibiting NT Inactivation- By inhibiting monamine oxidase (MAO), which can inactivate NE, adrenergic agonists can enhance receptor activation.
·Side Effects- Hypertension, which can lead to reflex bradycardia, altered HR, anginal pain, hyperglycemia in patients with diabetes.
·Potential uses- Treatment of heart failure, relieve asthma, delay pre-term labor. |
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Term
| Explain the mechanisms of action, anticipated side/adverse effects, and potential uses for Alpha1/beta blockers (Adrenergic Antagonists; Sympatholytic) |
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Definition
·Mechanism of Action- Directly block alpha1, B1 and B2 receptors; acts like PSNS – “rest and digest”.
·Side Effects- Dizziness, fainting, bradycardia, reflex tachycardia, nasal congestion, inhibition of ejaculation, sodium retention, increased blood volume, and can cause heart failure.
·Potential Uses- Treat hypertension by vasodilation, decrease toxicity from adrenergic agonist drugs, treat heart failure, treat myocardial infarction and cardiac dysrhythmias. |
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Term
| Explain the mechanisms of action, anticipated side/adverse effects, and potential uses for Cholinergic (Muscarinic agonists; Direct-acting parasympathomimetic) |
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Definition
·Mechanism of Action- Direct interaction with muscarinic receptors; responses resemble stimulation of PSNS – “rest and digest”.
·Side Effects- Hypotension, bradycardia, abdominal cramps, increased salivation, diarrhea, exacerbation of asthma.
·Potential Uses- Treatment of urinary retention is primary use, but can also treat GI disorders. |
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Term
| Explain the mechanisms of action, anticipated side/adverse effects, and potential uses for anticholinergic (Muscarinic antagonist/blocker; Direct-acting parasympatholytic; Antimuscarinic) |
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Definition
·Mechanism of Action- Competitively block the actions of Ach at muscarinic receptors, but have no direct effects of its own.
·Side Effects- Dry mouth, blurred vision, urinary retention, constipation, tachycardia.
·Potential Uses- To increase HR, decrease salivary/bronchial/sweat glands, decrease acid secretions in stomach, bronchial relaxation, decrease GI motility, decrease pee, mild CNS excitation. |
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Term
| Explain the mechanisms of action, anticipated side/adverse effects, and potential uses for Acetylcholinesterase Inhibitors (Indirect-acting parasympatholytic) Cholinesterase inhibitors |
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Definition
·Mechanism of Action- Prevent degredation of Ach by acetylcholinesterase and lack selectivity. There are ‘reversible’ short term and ‘irreversible’ long term inhibitors.
·Side Effects- Excessive salivation, increased gastric secretions, increased GI motility and urination, and depolarizing neuromuscular blockade = paralysis of respiratory muscles = dead.
·Potential Uses- Reversible inhibitor: Oral therapy of myasthenia gravis (muscle weakness, rapid fatigue).
Irreversible inhibitor: Treatment of glaucoma. |
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