Pharm 1

  1. Drug
    any chemcial that can affect living process
  2. Pharmacology
    • study of drugs and their interactions with living systems
    • physical chemical properties/biochemical physiologic effects
  3. Clinical Pharmacology
    study of drugs in humans, in patients, in healthy volunteers
  4. Therapeutics (Pharmacotherapeutics)
    • use of drugs to diagnose, prevent, or treat disease
    • or to prevent pregnancy
    • medical use of drugs
  5. Properties of an Ideal Drug (there is no such thing as an ideal drug)
    • EFFECTIVENESS: elicits for which given, most important
    • SAFETY: no harmful effects
    • SELECTIVITY: only the intended response
    • Reversible Axn: some drugs we want reversed, some we dont
    • Predictability: unique patients- tailor to individual
    • Ease of Admin: simple/convenient, enhance pt adherence, decr. med errors
    • Freedom from Drug Interxns: safety
    • Low Cost: can be a huge financial burden
    • Chemical Stability: can lose effectiveness during storage or when dissovled
    • Possess a Simple Generic Name: trade name much simpler, but generic is preferred
  6. Therapeutic Objective
    provide maximum benefit with minimum harm
  7. 5 Rights (plus 2)
    Right Drug to the right Patient in the right Dose by the right Route at the right Time, with the right Documentation and before the Expiration Date
  8. Must Give Patient During Pharm. Pt. Educ.
    • Drug name + therapeutic category
    • Dosage size + schedule
    • Route + technique of admin
    • Expected therapeutic response + when should develop
    • Nondrug measures to enhance effects
    • Duration of treatment
    • Method of storage
    • Symptoms- major adverse fx, measure to minimize
    • Major adverse drug-drug + drug-food intrxns
    • Whom to contact
  9. Condraindication vs. Precaution
    • Contraindications: pre-existing condition, avoid a particular drug under all but most desperate cirucumstances
    • Precaution: pre-existing cond'n significantly increases risk of adverse rxn to a particular drug, but not life-threatening
  10. 3 Types of Drug Names
    • Chemical: long/complex, inappropriate for every day, description w/nomenclature of chemistry
    • Generic: (nonproprietary) only one, preferable
    • Trade: (proprietary) under which drugs are marketed, easy to recall/pronounce, must be FDA approved
  11. Pharmacokinetics vs. Pharamacodynamics
    • Pharmacokinetics: how the body responds to the drug and gets it to the target site
    • Pharmacodynamics: what the drug does to the body
  12. Pharmacokinetics
    • study of drug movement throughout body
    • Absorption: from site of admin into the blood
    • Distribution: from blood into interstitial space of tissues, and from there, into cells
    • Metabolism: (biotransformation) enzymatically mediated alteration of drug structure
    • Excretion: movement of drugs/metabolites out of body

    • Application to Therapeutics: max bens/min harm, intensity of response directly r/t concentration of drug at site of axn, balance achieved by selecting appropriate route/dose/schedule
    • Three Ways to Cross Cell Membrane: (1) channels/pores, (2) transport systems, (3) direct penetration
  13. Factors Affecting Absorption
    • Rate of Dissolution: rapid means faster onset
    • Surface Area: larger = faster
    • Blood Flow: great concentration gradient = more rapid absorption
    • pH partitioning: pH plasma & pH admin site difference facilitates greater tendency to be ionized in plasma
  14. Determinants of Intensity of Response
    • Administration: dosage, time, route; poor patient adherence/staff errors (=toxicity/treatment failure); errors detract from achievement of therapeutic objective
    • Pharmacokinetics: “impact of body on drugs," how much of administered dose gets to the site of action
    • 1. Drug absorption
    • 2. Drug distribution
    • 3. Drug metabolism
    • 4. Drug excretion
    • Pharacodynamics: “Impact of drugs on body," nature/intensity of response, drug-receptor interaction followed by sequence of events
    • Individual Variation: drug interactions, physiologic variables (age, gender), pathologic variables (diminished organ fxn), genetic variables, must tailor drug therapy to individual
  15. Med Admin r/t Patient Care
    • Pre-Admin Assessment: baseline, ID high risk, capacity for self care
    • Dosage/Administration: dose depends in individual, indication, calculation
    • Evaluation/Promote Therapeutic fx: eval, promote adherence, non-drug measures
    • Minimize Adverse fx: ID high risk, forewarn of adverse fx, know your drugs
    • Minimize Adverse Interactions: drug Hx, OTC intrxn, monitor for a/e, alert for unknown intrxn
    • Making PRN Decisions: decide when/how/ehy
    • Managing Toxicity: early signs, procedure for management
  16. Med Admin r/t Patient Education
    • Must give patient drug info
    • Dosage/Admin: name, dose size, technique, duration, storage
    • Promote Ther. fx: pt knows nature & expected time course
    • Minimize A/E: knowledge
    • Minimize adverse intrxn
  17. Med Admin r/t Drug Therapy
    • PreAdmin assessment: baseline, high risk, selfcare?, contraind/precautions
    • Analysis/Nrsg Dx: judge appropriateness, ID potential health problems drug might cause, determine pt capacity for selfcare
    • Planning: define goals, set priorities, ID interventions, est. criteria for eval
    • Implementing: drug admin, pt educ, intrvn to promote ther. fx, intrvn to minimize adverse fx
    • Eval: ther. response, a/e, adherence, satisfaction
  18. New Drug Development
    • Randomized Controlled Trial (RCT): (to minimize personal bias)
    • 1. Use of controls--standard drug vs. nondrug; placebo
    • 2. Randomization--control group; experimental group
    • 3. Blinding--single (subject blind); double (researcher + subjects blind)
    • Stages of New Drug Development: preclinical; clinical (4 phases)
    • Downfalls: Little info on women or children; failure to detect all adverse fx
    • Exercising Discretion Regarding New Drugs:
    • 1. Be neither the first to adopt to new, nor the last to abandon the old
    • 2. Maximum benefit w/minimum harm
    • 3. Balance potential benefits w/inherent risks
    • 4. New drugs generally greater risks than old drugs
  19. (MEC) minimum effective concentration:
    below which therapeutic benefit will not occur
  20. Toxic Concentration:
    plasma level at which toxic levels begin
  21. Therapeutic Range:
    • between MEC and Toxic Conc.
    • objective is to maintain levels between
    • wide range: safely with ease
    • narrow range: difficult to be safe, more likely for complications
  22. Single Dose Time Course:
    • levels rise in absorp then fall in metab/excr
    • latency btwn admin and onset of fx
    • duration determined by metab/excr
  23. Drug Half Life:
    • time for amt of drug in body to decrease by 50%
    • key point: percentage not amount is lost
    • determines dosing interval
  24. Process of Plateau
    • admin 2nd dose before 1st is eliminated
    • levels increase w/each dose
    • plateau achieved when amt of drug eliminated btwn doses equals dose admin'd (levels remain constant)

    Time to Plateau: reached in approx. 4 half lifes
  25. Peak vs. Trough
    • Peak Concentration: highest level (keep below toxic concentration)
    • Trough Concentration: lowest level (keep above MEC)
  26. Loading Dose vs. Maintenance Dose
    • Loading Dose: large intial dose (small doses to maintain plateau)
    • Maintenance Dose: small doses maintain plateus after high drug level established w/loading dose
  27. Pharmacodynamics:
    (Maximum Efficacy, Relative Potency)
    • relationship btwn size of admin dose and intensity of response produced
    • graded relationship (↑dose = ↑response)
    • can be adjusted to patient needs

    • Maximum Efficacy: largest effect that a drug can produce, determined by height of D-R curve
    • Relative Potency: amt of drug must be given to elicit effects, potent is to produce fx @low doses
  28. Pharmacodynamics:
    • specific chemical in body that drugs interact with to produce fx
    • body has own receptors for endogenous compounds (hormones, NTs, etc)
    • binding usually reversible
    • drugs can mimic endogenous axn or block axn of endogenous compounds (cannot give new fxns/only alter rate)
    • selectivity offers fewer side effects but does not guarantee safety (lock + key analogy)
  29. Simple Occupancy Theory:
    • intensity of response is r/t #of receptors occupied by the drug
    • maximal response occurs when all available receptors occupied
  30. Affinity:
    • strength of intrxn/attraction btwn drug and receptor
    • ↑affinity: strong attraction; very potent; bind at low concentrations
    • ↓affinity: weak attraction; low potency; bind in high concentrations
  31. Intrinsic Activity:
    • ability of drug to activate the receptor following binding
    • ↑intrinsic activity: cause intense receptor activation; high maximal efficacy
    • ↓intrinsic activity: cause slight activiation; low maximal efficacy
  32. Agonist vs. Antagonist
    • Agonist: drug that mimic body’s own regulatory molecules, activate receptors, have affinity and intrinsic activity
    • Antagonist: drug that blocks/prevent axn of endogenous regulators, affinity for receptor but no intrinsic activity (no receptor activation), most commonly for drug overdose
    • Noncompetitive: binds irreversibly, decrease #cells receptors, reduce maximal response
    • Competitive: binds reversibly, competes w/agonist for receptor binding, higher conc. wins
  33. Partial Agonist:
    • mimic axns of regulatory molecules, but produce responses of intermediate intensity
    • only moderate intrinsic activity
    • maximal effect is lower than full agonist
    • can act as both agonist/antagonist
  34. Therapeutic Index:
    • measure of drug safety
    • ratio of LD50 to ED50
    • ↑index relatively safe
    • ↓index rel. unsafe
    • safety defined by highest dose requirex for thereapeutic fx substantially lower than lethal dose
  35. Drug-Drug Intrxn:
    • Intensified fx: potentiative, ↑ther. fx, ↑adverse fx
    • reduced fx: ↓ther. effects is detrimental, while ↓adv. fx is beneficial
    • creation of unique response:response not characterized by one of single drugs alone
  36. Drug-Food Intrxn:
    • ↑or↓absorption
    • grapefruit juice effect
    • food ↑risk toxicity
    • affect drug action
    • timing
  37. Drug-Supplement Intrxn:
    dietary suppl can interact w/conventional drugs thru pharmacokinetic/dynamic mechanisms and increase toxicity or reduce beneficial response
  38. ADRs: Factors, Identifying, Minimizing
    Factors: body weight/composition, age, pathophysiology, tolerance, placebo effect, variable absorption, genetics, gender, race, failure to take meds as prescribed

    Identifying: shortly after first used, abate when disct’d, reappear when restart, illness itself or explained fx?

    • Minimizing Adverse Rxn: Responsibility of everyone involved in drug production and use
    • --Anticipation, early detection signs
    • --Monitor fxn of target organ
    • --Individualized therapy (potential risk vs. probable benefits)
    • --Chronic disorders especially vulnerable
  39. Adverse Effect
    noxious, unintended, undesired effect that occurs at normal doses; all body systems, variable intensity
  40. Side Effect
    nearly unavoidable 2ndary drug effect produced at therapeutic doses
  41. Toxicity
    adverse drug rxn caused by excessive dosing
  42. Allergic Reaction
    prior sensitization of immune system, intensity largely independent of dosage
  43. Idiosyncratic Effect
    uncommon drug response resulting from genetic predisposition
  44. Iatrogenic
    disease produced by drugs; essentially identical to naturally occurring pathology
  45. Physical Dependence
    develop w/longterm use, body has adapted to drug exposure, abstinence sydr will result if discont; patients should be warned
  46. Carcinogenic:
    ability to cause cancers
  47. Teratogenic Effect
    drug induced birth defect
  48. Medication Errors:
    Types, Causes, Reporting, Reducing
    Types: 13 major causes, cause harm directly or indirectly, fatal errors (wrong dose, overdose, wrong route)

    • Cause: human factors, communication mistakes, name confusion (90% all errors)
    • Reporting Errors: medication error report program (MER)

    Reducing Errors: help/encourage pt to be active/informed members of HC team, give HC providers tools/info needed to prescribe/dispense/admin as safely as possible, computerized med orders, have senior pharmacist accompany on rounds, barcodes on everything, careful use of abbreviations
  49. 3 Steps to Reduce Med Errors
    • 1. Check/Double Check 6 Rights
    • 2. Appropriate Knowledge Base
    • 3. Clarify anything unsure about
Card Set
Pharm 1
Test 1