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2011-10-23 01:50:54
Ch1 Pharmocology

Module 7 Test 3
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  1. What is Drug?
    any chemical that can affect living processes
  2. What is Pharmacology?
    the study of drugs and their interactions with living systems
  3. Clinical Pharmacology
    the study of drugs in humans. This discipline includes the study of drugs in patients as well as in healthy volunteers (during new drug development
  4. Therapeutics
    also known as pharmacotherapeutics, is defined as the use of drugs to diagnose, prevent, or treat disease or to prevent pregnancy. Alternatively, therapeutics can be defined simply as the medical use of drugs.
  5. Describe the properties of an ideal drug?
    • 3 most important:
    • Effectivness: An effective drug is one that elicits(vizivaet) the responses for which it is given. Effectiveness is the most important property a drug can have.
    • Safety: A safe drug is defined as one that cannot produce harmful effects—even if administered in very high doses and for a very long time. There is no such thing as a safe drug. All drugs have the ability to cause injury, especially with high doses and prolonged use.
    • Selectivity: A selective drug is defined as one that elicits only the response for which it is given. A selective drug would not produce side effects. There is no such thing as a selective drug: All medications cause side effects.
    • Other Ideal Drug Properties:
    • Reversible action: drug actions need to subside withing an appropriate time.
    • PRedictability
    • Ease of administration
    • Freedom fromdrug interactions
    • Lowcast
    • chemical stability - some drugs lose effectiveness during storage
    • simple generic name
    • From the preceding, we can see that available medications are not ideal. No drug is safe. All drugs produce side effects. Drug responses may be difficult to predict and may be altered by drug interactions. Drugs may be expensive, unstable, and hard to administer. Because medications are not ideal, all members of the healthcare team must exercise care to promote therapeutic effects and minimize drug-induced harm.
  6. Therapeutic Objective
    • Maximum benefit
    • MInimum Harm
  7. Pharmocokinetics
    Pharmacokinetic processes determine how much of an administered dose gets to its sites of action. There are four major pharmacokinetic processes: (1) drug absorption, (2) drug distribution, (3) drug metabolism, and (4) drug excretion. Collectively, these processes can be thought of as the impact of the body on drugs
  8. Pharmocodynamics
    Once a drug has reached its sites of action, pharmacodynamic processes determine the nature and intensity of the response. Pharmacodynamics can be thought of as the impact of drugs on the body. In most cases, the initial step leading to a response is the binding of a drug to its receptor. This drug-receptor interaction is followed by a sequence of events that ultimately results in a response. As indicated in Figure 1-1, the patient's “functional state” can influence pharmacodynamic processes.
  9. Factors that determine the intensity of a drug's response in the human body?
    • prescribed dose
    • administred dose
    • concentration at sites of action
    • Intesity of response
    • the intensity of the response is determined by the concentration of a drug at its sites of action. As the figure suggests, the primary determinant of this concentration is the administered dose. When administration is performed correctly, the dose that was given will bear a close relationship to the dose that was prescribed. The steps leading from prescribed dose to intensity of the response are considered below.
    • Administration: 6 rights (right dosage, rount, timeing) and paient adherence (strogoe soblyudenie) right time
    • Individual Variation: Age, Gender, Weight, Genetic Factors, drug interaction
    • Pharmocokinetics: absorption, distribution, metabolism, excretion
    • Pharmocodynamics: drug-receptor interaction, patient's functional state, placebo effects.
  10. Pharmokokinetics - 1 Drug Absorption
    • movement of a drug from its site of administration into the blood. The rate of absorption determines how soon effects will begin. The amount of absorption helps determine how intense effects will be.
    • Rate of Dissolution.
    • Before a drug can be absorbed, it must first dissolve. Hence, the rate of dissolution helps determine the rate of absorption. Drugs in formulations that allow rapid dissolution have a faster onset than drugs formulated for slow dis
    • Surface Area.
    • The surface area available for absorption is a major determinant of the rate of absorption. The larger the surface area, the faster absorption will be.solution
    • Blood Flow.
    • Drugs are absorbed most rapidly from sites where blood flow is high. Why? Because blood containing newly absorbed drug will be replaced rapidly by drug-free blood, thereby maintaining a large gradient between the concentration of drug outside the blood and the concentration of drug in the blood. The greater the concentration gradient, the more rapid absorption will be.
    • Lipid Solubility.
    • As a rule, highly lipid-soluble drugs are absorbed more rapidly than drugs whose lipid solubility is low
    • pH Partitioning.(respredelienie)
    • pH partitioning can influence drug absorption. Absorption will be enhanced when the difference between the pH of plasma and the pH at the site of administration is such that drug molecules will have a greater tendency to be ionized in the plasma.
  11. 2. Distribution
    • Movement of drug through body from Blood into the tissue
    • Leaving the vascular system and entering tisues and cells
    • Blood brain barrier: In central nervous system. There are tight junctions between the cells that compose the walls. Prevent drug passage. Only those can pass that are lipid soluble and have a transport system can pass to only a small degree. Also BBB has P-glycoprotein that pums the drug out of the brain back into the capilary system.
    • Placental drug transfer: some drugs to pass placenta.
  12. 3.Drug Metabolism
    also known as biotransformation, is defined as the enzymatic alteration of drug structure. Most drug metabolism takes place in the liver.
  13. 6 therapeutic Consequences of drug Metabolism
    • Accelerated Renal Drug Excretion.
    • The most important consequence of drug metabolism is promotion of renal drug excretion. enzymes convert highly lipid soluble drugs into less lipid soluble so that the kidneys can exrete them out of the body.
    • Drug Inactivation.
    • Increases therapeutic actions: metabalism can incrase effectivness of some drugs
    • Activation of Produrugs: A prodrug is a compound that is pharmacologically inactive as administered and then undergoes conversion to its active form within the body.
    • Increases or Decrease Toxicity: 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.
  14. Special Considerations in Drug Metabolism
    • Age: in infants metabolism of drugs is limited. Body mass, gender, genetics, environemnt, fluids
    • First-Pass effect: relates to the oral drugs get rapidly inactive by the liver. Oral drugs are absorbed from the GI tract, they are carried directly to the liver via the hepatic portal vein. To bypass this even the drug is administred via parenteral way this way it can temporarily bypass the liver.
    • Nutritional status: in the mulnurished person drug metabolism can ve compromised.
    • Copmetition between drugs: When two drugs are metabolized by the same metabolic pathway, they may compete with each other for metabolism, and thereby decrease the rate at which one or both agents are metabolized. If metabolism is depressed enough, a drug can accumulate to dangerous levels.
  15. 4. Excretion
    • Primarily done by the kidneys
    • Other routes:
    • Breat milk
    • Bile - stool
    • Lungs - anastethics are excreted throug
    • Sweat and saliva.
  16. Time course of drug response
    • Plasma drug level - levels of drug in the blood correlate with rherapeutic and toxic responses
    • Non - therapeutic - plasma drug level below MEC (minimum effective concentration)
    • Toxic Concentration - plasma drug levels climb too high
    • Therapeutic range: the objective of drug dosing is to maintaintplasma drug levels within the therapeutic range.
    • Drugs that have wide therapeutic range can be administred safly with realtive easy. Narrow range difficult to administre safely.
    • Drug Half-life: the time required for the amount of drug in the body to decrease by 50%. somehave short halfe life some have longhave lifes.
  17. 7 Aspect of drug therapy
    • (1) preadministration assessment: collect baseline to be able to asses an adverse effect of the drug you gave. Identify High-risk patients. and Capacity for self-care: Visual acuity, Manual dexterity, intellectula ability, memory, finance, cultural attitudes
    • (2) dosage and administration: more than one indication, more than once route, read order carefully, verify identity of the patient, verify calculations, understand the reason for the drug's use.
    • (3) evaluating therapeutic effects of drug: assess and record patient response to drug. Promote patient's adherence to medication regime. Utilize non-drug measure to enhance drug's effect.
    • (4) minimizing adverse effects: know what could happen and know what to do if it happens. reducing drug interactions. timing - spread medication out, know signes and symptoms of toxicity of medication.
    • (5) minimizing adverse interactions
    • (6) making PRN decisions
    • (7) managing toxicity.
  18. Peak level of drug action
    the highest level that it gets in the blood stream. Don't wanna get above that.
  19. Trough level of drug action
    the lowest level in the blood stream
  20. Therapeutic range
    between the peak and trough level
  21. Therapeutic index
    is a measure of a drug's safety. on animals. High index - safe to take. Low index - durg is ralative unsafe.
  22. Onset of action of drug
    when you start feeling the effect of the drug.
  23. Pharmocodynamics
    how drugs effect the body
  24. Dose-response relationship
    • relationship between the size of an administered dose and the intensity of the response produced) is a fundamental concern in therapeutics. Dose-response relationships determine the minimum amount of drug we can use, the maximum response a drug can elicit, and how much we need to increase the dosage in order to produce the desired increase in response.
    • Maximal efficacy - the largest effect that a drug can produce.
    • Relative potency- amoun of drug we must give to elicit an effect.
    • Just understand that dose and response are related.
  25. Drug-receptor interactions
    • Recepotros any functional macromolecule in a cell to which a drug binds to produce its effects.
    • As suggested by the equation, binding of a drug to its receptor is usually reversible.
    • Under physiologic conditions, receptor activity is regulated by endogenous compounds (neurotransmitters, hormones, other regulatory molecules). When a drug binds to a receptor, all that it can do is mimic or block the actions of endogenous regulatory molecules. By doing so, the drug will either increase or decrease the rate of the physiologic activity normally controlled by that receptor.
  26. Funtion of agonists
    • are molecules that activate receptors
    • When drugs act as agonists, they simply bind to receptors and mimic the actions of the body's own regulatory molecules.
  27. Function of Angatonists
    • produce their effects by preventing receptor activation by endogenous regulatory molecules and drugs.
    • Antagonists have virtually no effects of their own on receptor function
    • an antagonist is a drug with affinity for a receptor but with no intrinsic activity. Affinity allows the antagonist to bind to receptors, but lack of intrinsic activity prevents the bound antagonist from causing receptor activation.
  28. Function of Partial agonist
    • A partial agonist is an agonist that has only moderate intrinsic activity. As a result, the maximal effect that a partial agonist can produce is lower than that of a full agonist
    • Serve as agonist and antagonist. ex. if a full dose of a drug given a parital antagonist can block that effect and the patient will fill only half of the effect of the drug so it is acting as antagonist.
  29. Drug-drug interaction
    • 3 possible outcomes
    • 1. One drug may intesify the effects of the other
    • 2. reduce the effects of the other
    • 3. combination may produce a new response not seen in either drug alone.
    • any 4 of phyrmocokinetic processes can be affected
  30. Food-drug interaction
    • timing of drug administration: at bedtime, in morning, with meals or not.
    • Similar affect as drug-drug
    • ex. grapefruit juice affect - can make drugs toxic
    • Lecorice - increase the level of Digoxin in the blood causing toxicit
    • Alcohol and Acetomenofin - bothe metabalize in the liver, causing liver damage
  31. Herb-drug interaction
    interact with conventional drugs. Bigest concern are intearactions what reduce veneficial responses to convenional drug and intereactions tha increase toxocity. This info is lacking.
  32. Primary effect and Secondary effect
    • Primary: is a therapeutic effect of medications are effects that are predicted, intended and desired.
    • THe reason the drug was prescribed
    • Secondary: all other consequences (unintended, nontherapeutc.)
  33. sife effects
    a nearly unavoidable secondary drug effect produced at therapeutic doses.
  34. Toxicity
    an adverse drug reaction caused by excessive dosing
  35. Allergic reaction
    • 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.
    • the intensity of allergic reactions is largely independent of dosage
  36. Anaphylitic reaction
    is a life-threatening response characterized by bronchospasm, laryngeal edema, and a precipitous drop in blood pressure
  37. Idiosyncratic Effect
    an uncommon drug response resulting from a genetic predisposition
  38. Ways to minimized ADRs
    • produce the safest medicine possible
    • the prescriber must select ht eleast harmful medicine
    • thenurse must evalute patients for ADRs and educate in ways to avoid or minimize harm
    • patients and their families must watch for signs that an ADr
  39. Types of medication Errors
    • 13 major categories on page 70 of Pharmocology table 7-3
    • 3 most common: overdose, wrong drug, suing wrong route
    • Can be direct and indirect harm
    • Direct harm - givin an excessive dose can cause adverse effect and death
    • indirect harm - too little medication lead to harm through failure to adequately treat the patients' illness.
  40. Causes of Medicaiton Errors
    • page 70 table 7-4
    • Human factors (performane or knowledge deficits)
    • Communication mistake (illegible presriber handwriting)
    • Confusion of similarities in drug names
    • Name confusion - 90 of all errors.
  41. Ways to reduce medicaiton errors
    • At the heart of efforts to reduce medication errors is a change in institutional culture—from a punitive system focused on “naming, blaming, and shaming” to a nonpunitive system in which medication errors can be discussed openly, thereby facilitating the identification of errors and the development of new safety procedures.
    • Effective measures for reducing medication errors include (1) using a safety checklist for high-alert drugs; (2) replacing handwritten medication orders with a computerized order entry system; (3) having a clinical pharmacist accompany ICU physicians on rounds; (4) avoiding error-prone abbreviations; (5) helping and encouraging patients and their families to be active, informed participants in the healthcare team; and (6) using a computerized bar-code system that (a) identifies the administering nurse and (b) ensures that the drug is going to the right patient and that adverse interactions are unlikely.
  42. CHemical, generic and trade name clasicifications
    • Chemical name: rarely used, it is the exact description of the drug's chemical compositon and molecular structure
    • Generic: when the developing manufacturer is ready to market a drug then the name is assigned and it is usually similar to the chemical name, but it is simpler. It is also the oficial name
    • When the drug is markted, the manufacturere sells in under a brand (trade or proprietary) name. Has a registration mark and capitalized
  43. Drug classification
    • If you learn the common characteristscs ofr a drug classification, then when you encounter a new drug, you will be able to associate it withits classification and make inferences about its basic characteristcs.
    • by usage
    • by body systems
    • by chemical or pharmocological class
  44. Agencies and legislation that help to ensure drug quality and safety
    • FDA of the U.S. Department of Health and Human Services regulates manufactre and sale of all medications and monitors their safety and effectiveness.
    • Both the United States and Canada have controlled substances legislation that define which medications are controlled substances and define categories for classifying these medications according to dependence and addictive properties.
    • In Canada, this legislation is known as the Canadian Narcotic Control Act of 1961.
    • In the United States, there is the Controlled Substances Act of 1970.
  45. Sources of obtaining drug information
    • Nursing drug Handbook
    • Physician's Desk Reference (PDR)
    • Pharmocology Texts
    • Internet-based Formularies
    • Pharmocist
    • Medication Package inserts
    • Institutional Medication policies and Precedures
  46. How does excretion occures at the Kidneys, liver, GI tract, lungs, and exocrine glands
    • Kidneys: primary site of excretion. Adequate fluid intake neede to excrete via urine
    • Liver and GI tract: broken down by liver and excreted into the GI tract and eliminated into feces. Somefat soluble agents are reabsorbed by the bloodstrea, distributed to the target site, and returned to ht e liver. Then excreted via kidney.
    • Lungs: most drugs removed by the lungs are not metabalized first. Drug administred by inhalation and removed by exhalation. Some alcohols can be excreted in limited amounts by they lungs.
    • Exocrine glands: Drug excretion through (sweat and salivary) is limited. The elimination of metabolites in sweat is frequently responsible for such side effects as dermititis. Drug secreated in the saliva are usually swallowed and absorbed as other oral meds.