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  1. Schedule I
    High abuse potential, no accepted medical use

    LSD and Heroin
  2. Schedule II
    High abuse potential, accepted medical use

  3. Schedule III
    Less abuse potential than schedule II, moderate dependence liability

  4. Schedule IV
    Less abuse potential than schedule II drug; limited dependence liability

  5. Schedule V
    Less ause potential and very limited dependence
  6. Blinded trial
    the patients dont know
  7. Double blinded Trial
    Both the patients and the doctors dont know who received what
  8. During clinical trials:
    • •a relatively small number of patients are given the
    • drug.

    •sample size is not fully representative of patients who will actually use the drug.

    •patients takes drug for a relatively short time .
  9. Clinical testing Phase I
    healthy volunteers, evaluates drug metabolism and determines effects in humans
  10. Clinical testing Phase II and Phase III
    patients, evaluates therapeutic utility, dosage range and effectiveness. Manufacturer applies to FDA for a New Drug Application after completing phase III
  11. Clinical testing Phase IV
    –drug is released to patients for general use.

    New adverse effects are revealed, voluntary reporting of adverse effects
  12. The same generic name is never used for more than one medication.

    is this true or Flase
  13. Generic names tell the nurse the chemical ingredients of the drug

    True or False
  14. The generic name of the drug will be the same no matter which company produces the drug.

    True or False
  15. Generic names are easy to recall and pronounce.

    True or False
  16. Generic names often suggest the action of the drug.

    True or Flase
  17. Generic names of the same therapeutic class often have a similar suffix making them easier to identify.

    True or False
  18. Drug Classifications
    Drugs that share similar characteristics are grouped together as a pharmacologic group or family.
  19. •Unlike FDA approved agents, DSHEA herbal supplements:
    –Require no proof of efficacy or safety

    –No standardization or quality control

    –May stay on market until after harm has occurred
  20. Four Basic Pharmacokinetic Processes



  21. Solubility refers to
    the ability of a drug to dissolve and form a solution.
  22. Lipid solubility is essential
    •for any drug that must diffuse across the cell membrane because the membrane is partially composed of lipids
  23. Ionization
    •A molecule dissociates into ions when it dissolves in water or other liquids.

    • •In dissociating, the molecule gives up or accepts a proton, thus converting some molecules into
    • charged particles.

    •Ionized drugs are poorly absorbed, because they do not diffuse easily across lipid membranes.
  24. Non-ionized drug molecules
    are lipid soluble and easily pass through lipid membranes.
  25. pH partitioning (ion trapping) :
    A drug accumulates on the side of a membrane where the pH most favors its ionization
  26. Absoption
    •A drug moves from its site of administration into the venous or lymphatic circulation
  27. Intravenous Route
    –Bypasses GI tract and variability of absorption from other areas

    • –Many advantages
    • •Rapid onset and control

    •Use of large fluid volumes

    •Use of irritant medications

    –Highly dangerous

    •Rapid onset and irreversibility!

    •Volume overload



    –Peripheral versus central administration

    –IV push medication (bolus)
  28. Intramuscular Route
    Deltoid, Ventrogluteal, Vastus lateralis

    –Viscous or irritating medications

    –Depot preparations

    –Z track technique
  29. Absorption from stomach or small intestine

    –Factors that influence absorption
    •Gastric and intestinal pH

    •Solubility and stability of drug

    •Gastric emptying time/food in gut

    •Co-administration of other drugs
  30. Most variable route
    –Oral Drug Forms


    –Enteric coating

    –Sustained release

  31. Topical Route
    –Application to skin or mucous membranes

    –Sublingual or buccal


    –Local versus systemic effects
  32. Bioavailability
    The fraction of the administered dose that reaches the systemic circulation and produces effects

    •Preparations are equal in bioavailability if the drug they contain is absorbed at the same rate and the same extent
  33. Distribution
    The delivery of the drug into any and all body compartments it can penetrate
  34. Factors that influence Distribution
    –Cardiac output

    –Regional blood flow and capillary permeability

    –Ability of the drug to exit the vascular system

    –Ability of drugs to enter the cells

    –Volume of distribution

    –Degree of plasma protein binding

    –Drug reservoirs or storage sites

    • •Physiologic
    • barriers
  35. Blood Brain Barrier
    • •Selective mechanism that opposes the passage of most ions and large molecular compounds from the
    • blood to the brain tissue.

    • •Drugs must be lipid soluble or have a transport system to leave the blood stream and reach a site
    • of action within the brain.
  36. Placental Drug Transfer
    Membranes of the placenta do NOT constitute an absolute barrier to the passage of drugs

    Lipid soluble drugs readily cross the membrane
  37. Plasma Protein Binding
    •Drugs circulate in the plasma either bound or unbound to plasma protein, usually albumin.

    •Bound drug molecules are pharmacologically inactive and they remain that way until released from the protein.

    •By increasing levels of free drug, increased intensity of drug response may lead to possible toxicity.
  38. In addition to plasma protein binding, drugs may be distributed to
    •bone, fat, plasma proteins, or other tissues for storage.
  39. Metabolism (also known as biotransformation):
    Enzymatically mediated alteration of drug structure. The alteration or changing of a drug to more ionized or water-soluble and less lipid-soluble forms called metabolites.
  40. Metabolite
    • Chemical form of a drug that is a product of one or more biochemical metabolic reactions
    • involving the parent drug; more ionized
  41. •Hepatic Drug-Metabolizing Enzymes
    •Cytochrome P450 system: Causes changes in rate of metabolism of certain drugs requiring changes in dosage
  42. Hepatic First-Pass Phenomenon
    •Rapid hepatic inactivation of certain drugs

    • •Orally administered drugs are first absorbed through the walls of the small intestine and initially
    • travel through the portal vein to the liver, where they undergo metabolism before reaching the systemic circulation.

    •This is known as the first-pass phenomenon.
  43. Minimum effective concentration (MEC)
    •Plasma drug level below which therapeutic effects will not occur. A drug must be present at a level at or above the MEC.
  44. Plateau (steady state)
    which is the evenly distributed concentration of a drug, occurs when the administration rate equals the rate of drug elimination.

    • is achieved in approximately four
    • half-lives.
  45. Half-life
    • •is the time needed for the plasma
    • concentration of a drug to be reduced by 50%.

    determines dosing interval. Drugs with a short half life need short dosing interval.

    • •Drugs with a longer half life can have longer intervals between doses without loss of therapeutic
    • effect.
  46. Peak concentration
    the highest serum level after administration, must be kept below toxic level.
  47. Trough concentration
    the lowest serum level after administration, must be kept above MEC.
  48. by continuous infusion, and reducing dosage size and interval can limit
    Administration fluctuationsin drug levels.
  49. Loading Dose
    the initial dose

    •is given to achieve plateau more quickly, an initial large dose may be given. Loading doses are used for drugs with long half–lives.

    •Plateau is maintained via a smaller dose, known as a maintenance dose, given after a loading dose.
  50. Most of the drug in the body will be eliminated over an interval of approximately
    •four half lives (the same interval to reach plateau) .
  51. Maximal efficacy
    žthe largest effect that a drug can produce.
  52. Relative potency
    the amount of drug given to elicit an effect
  53. Two drugs can be equally effective but
    have different potency.
  54. Affinity
    žis the strength of attraction between a drug and its receptor.

    •High affinity drugs have a strong attraction for receptor sites. Drugs with high affinity are very potent.

    •Drugs with low affinity have to be present in high concentrations to elicit a response.
  55. Intrinsic Activity
    žis the ability of a drug to activate a receptor upon binding.

    ž•Drugs with high intrinsic activity have high maximal efficacy and produce an intense response.
  56. Agonist
    žActivate receptors and have high affinity and intrinsic activity

    žMimic action of endogenous regulators
  57. Antagonists
    žPrevent receptor activity and have high affinity but no intrinsic activity

    žLack of intrinsic activity prevents receptor activity.

    žEffect of antagonist is determined by how much agonist is present.

    • •Competitive antagonists: Produce receptor
    • blockade by competing with agonists.

    •Receptor is occupied by whichever agent is higher in concentration.
  58. Partial Agonists
    • žAn agonist with moderate intrinsic activity.
    • Maximal effect is lower than a full agonist.

    žCan act as agonists (if no full agonist is present) and antagonists (if a full agonist is present)
  59. Desensitization (refractoriness)
    results from continuous exposure of cell receptors to an agonist.
  60. Hypersensitivity results from
    continuous exposure of cell receptors to antagonist
  61. Average effective dose (ED50)
    Dose required to produce a defined therapeutic response in 50% of the population.

    žPatients must be evaluated individually for the proper dosing. Consider patient variables.
  62. Therapeutic index (ED50 : LD50):
    žRatio between average effective dose & average lethal dose

    žWide therapeutic index is relatively safe.

    žNarrow therapeutic index is relatively unsafe.
  63. Potentiation
    žwhen a patient is taking two drugs, one drug may intensify the effects of the other.

    •Increase the therapeutic effect of one of the drugs

    •Increase the adverse effects of one of the drug
  64. Inhibitory Interactions
    žAn inhibitory drug interaction results in the reduced effects of one drug.

    •Reduced therapeutic effect

    •Reduced adverse effects
  65. Drug- Food interactions
    žFood and drugs may interact to alter the effect of pharmacotherapy.

    • žDrug efficacy may be either diminished or enhanced nutritionally by changes in drug absorption, drug
    • metabolism, and drug excretion.
  66. Grapefruit juice Effect
    Grapefruit juice inhibits an isoenzyme responsible for intestinal metabolism of multiple drugs

    žThis inhibitory effect is dependent on the amount of juice consumed & can persist for up to 3 days

    • ž Increases amount of drug available for absorption
    • which increases the blood level of drugs

    žPatient teaching point
  67. Drug Herb Interactions
    žDrug interactions may also result from herbal supplements interacting with drugs.

    žThey can have an impact on therapeutic outcome including increased toxicity from herbal supplements and reduced therapeutic outcomes of prescribed agents.
  68. Drug Allergy
    marked by increasing reactivity on subsequent exposures to the foreign agent. It is independent of dosage.
  69. Anaphylaxis
    ža systemic reaction caused by contraction of smooth muscles and increased vascular permeability.

    žIt is characterized by dyspnea, bronchospasm, laryngeal edema, cardiac dysrhythmias, and occasionally seizures.

    • žAnaphylaxis is a medical emergency. It is the most
    • serious of allergic reactions.
  70. Idiosyncratic Responses
    ždrug response is an unusual, abnormal or peculiar response to a drug.

    žžSometimes an idiosyncratic response is referred to as a paradoxical response.

    • ž
    • Idiosyncratic responses are thought to occur because of genetic enzymatic deficiencies that alter the drug’s metabolism
  71. Iatrogenic Disease
    ža disease produced by drugs.

    • žFor example, some adverse effects of drugs produce symptoms which resemble naturally occurring
    • disease
  72. Physical Dependence
    • ža state in which the body has adapted to prolonged drug exposure in such a way that abstinence
    • syndrome will result if drug use is discontinued.

    žAbstinence syndrome varies depending on drug.

    žPatient teaching related to abrupt discontinuation
  73. Carcinogenic effect
    •Ability of certainmedications and environmental chemicals to cause cancer
  74. Teratogenic effect
    •Drug induced birth defects
  75. Neurotoxicity
    žInjury to the CNS is largely irreversible.

    žNeurotoxicity can occur after exposure to drugs and other chemicals and gases.

    žThe extreme susceptibility of neural tissue to toxicants is largely due to its high metabolic rate, high lipid content, and high circulatory requirement.

  76. Signs and Symptoms of Neurotoxicity
    changes in level of consciousness (drowsiness, restlessness)auditory and visual disturbances, nystagmus, and tonic-clonic (grand mal) seizures.
  77. Hepatotoxicity
    • The liver is highly susceptible to toxicants due to direct exposure to ingested drugs and other
    • toxicants. Primary site of drug metabolism.

    • žManifestations of hepatotoxicity include hepatitis,
    • jaundice, elevated liver enzymes [laboratory values], and fatty infiltration of the liver.
  78. Nephrotoxicity
    žHigh susceptibility due to high vascularity

    žChemically induced kidney damage is typically manifested as acute tubular necrosis.

    žžLaboratory values to assess: Blood urea nitrogen (BUN), creatinine, creatinine clearance
  79. Immunotoxicity
    žA wide variety of drugs can affect the immune system.

    žSome may cause immunosuppression (decrease ability to fight infection), whereas others may directly destroy immune system components (i.e. leukocytes)
  80. Cardiotoxicity
    • žIrregularities in cardiac rhythms and conduction and possibly heart damage may result from an
    • adverse effect known as cardiotoxicity.

    • žCause unknown
    • ž
    • žCharacteristics of cardiotoxicity include transient
    • cardiac arrhythmias and depression of myocardial function.
  81. Ototoxicity
    žMany drugs can produce ototoxicity, which affects the eight cranial nerve and result is inner ear or auditory nerve damage.

    žStructures of the inner ear that may be affected include the cochlea, vestibule and semicircular canals.

    žOtotoxicity may or may not be reversible.
  82. Body surface area is more precise than
    Body weight

    •Percentage of body fat can change drug distribution
  83. Tolerance
    decreased responsiveness to a drug as a result of repeated drug administration.

    • žPatients who are tolerant to a drug require higher doses to produce the same effects that were
    • achievable with lower doses before tolerance had developed.
  84. Pharmacodynamic Tolerance
    žoccurs when a minimum effective concentration (MEC) is abnormally high.

    žžThis is thought to result from chronic receptor occupation
  85. Metabolic Tolerance
    Results from accelerated drug metabolism brought about by the ability of certain drugs to induce synthesis of hepatic drug-metabolizing enzymes. Dosage must be increased to maintain therapeutic levels
  86. Tachyphylaxis
    • žA form of tolerance where the reduction in drug responsiveness is brought on by repeating dosing
    • over a short time (within hours) instead of days to weeks as in pharmacodynamic and metabolic
    • tolerance.
  87. Genetic Predisposition

    žPharmacogenetics is the study of genetically inherited conditions that affect the way drugs act on the body and modify the way the body acts on drugs.


    •Glucose-6-dehydrogenase deficiency (G6PD): Administration of certain drugs causes hemolytic anemia. Common in African, Middle Eastern, and South Asian peoples.
  88. Err on the side of caution:
    Any drug taken during pregnancy will reach the fetus

    žPhysiologic changes during pregnancy can alter pharmacokinetics of drugs


    –Blood volume


  89. Pregnancy Category A
    • Adequate and well-controlled studies
    • have failed to demonstrate a risk to the fetus in the first trimester of pregnancy (and there is no evidence of risk in later trimesters).
  90. Pregnancy Category B
    • Animal reproduction studies have failed to demonstrate a risk to the fetus and there are no adequate and well-controlled studies in pregnant women OR Animal studies have shown an
    • adverse effect, but adequate and well-controlled studies in pregnant women have failed to demonstrate a risk to the fetus in any trimester.
  91. Pregnancy Category C
    • Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and
    • well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks.
  92. Pregnancy Category D
    • There is positive evidence of human
    • fetal risk based on adverse reaction data from investigational or marketing experience or studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks.
  93. Pregnancy Category X
    Studies in animals or humans have demonstrated fetal abnormalities and/or there is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience, and the risks involved in use of the drug in pregnant women clearly outweigh potential benefits.
  94. Functions of the ANS
    •Involuntary System

    •Responsible for:

    –Control of smooth muscle (e.g., bronchi, blood vessels, GI tract)

    –Cardiac muscle

    –Exocrine glands (e.g., gastric, sweat, salivary)

    •Monitored by both the sympathetic and parasympathetic nervous systems
  95. The ANS works by
    •antagonism between the sympathetic and parasympathetic nervous systems.

    •To effect an action, a neurotransmitter needs to bind with an appropriate receptor site on the effector organ or tissue.

    This is accomplished by synaptic transmission.
  96. Synaptic Transmission
    •Involves the synthesis of neurotransmitters in the nerve terminal.

    •Includes storage of the neurotransmitter awaiting an action potential.

    •Involves release of the specific neurotransmitter.

    •After release, the neurotransmitter diffuses across the synaptic gap and reversibly binds to a receptor on the postsynaptic cell.
  97. Synaptic Transmission after binding
    •and exerting an effect, the neurotransmitter is dissociated from its binding site by a variety of mechanisms.

    •The neurotransmitter is now degraded or “reuptaked” for reuse.
  98. Neurotransmitters



    •Preganglionic transmission is mediated by acetylcholine.

    •Postganglionic transmission is mediated by NE.

    •Adrenal medulla stimulation to release epinephrine is mediated by acetylcholine.
  99. Adrenergic Receptors
    •Alpha-1, alpha-2, beta-1, and beta-2.

    •Drugs that stimulate the receptors are called agonists.

    •Drugs that block the receptors are called antagonists or blockers.

    •Most drugs stimulate or block more than one receptor at a time.

    •Some drugs are relatively selective in their stimulation or blockade.
  100. Stimulation of Alpha-1 Receptors
    • •Stimulation causes:
    • –Vasoconstriction
    • –Increased peripheral resistance
    • –Increased blood pressure (BP)
    • –Pupil dilation (mydriasis)
    • –Closure of the internal sphincter of the bladder

    • •Blocking causes the opposite
    • effects.
  101. Stimulation of Alpha-2 Receptors

    –Decreased release of NE, reducing sympathetic outflow from brain


    •Blocking causes the opposite effects.
  102. Stimulation of Beta-1 Receptors


    –Increased myocardial contractility

    –Increased lipolysis

    • •Blocking causes the opposite
    • effects.
  103. Stimulation of Beta-2 Receptors



    –Slightly decreased peripheral resistance

    –Increased muscle and liver glycolysis

    –Increased release of glucagon

    –Relaxation of uterine smooth muscle

    • •Blocking causes the opposite
    • effects.
  104. Epinephrine
    •Nonselective adrenergic agonist:

    –Stimulates all alpha and beta receptors

    •Many therapeutic uses, such as:

    –Cardiopulmonary arrest

    –Ventricular fibrillation

    –Anaphylactic shock


    •Adverse effects related to stimulation of all receptors are common.

    •CNS and cardiac adverse effects are the most common and may be the most serious.
  105. Phenylephrine
    •Alpha-1 stimulant

    •Potent vasoconstrictor

    • •Pharmacotherapeutics include:
    • –Vascular failure
    • –Hypotension
    • –Shock states

    •Topical pharmacotherapeutics:

    –Nasal decongestant

    Pupil dilation (mydriasis)

  106. Prazosin
    •Alpha-1 blocker.

    •Used to treat hypertension.
  107. Isoproterenol
    •Nonselective beta-2 stimulant.

    •Pharmacotherapeutics include:

    –Congestive heart failure

    –Various types of shock


    •Inhaled pharmacotherapeutics include:




    •Adverse effects are primarily related to cardiac stimulation.
  108. Propranolol
    •Nonspecific beta blocker.

    •Used primarily for cardiovascular disorders.

    •Adverse effects are due to cardiac and respiratory effects.

    •Discontinue slowly to prevent rebound tachycardia leading to angina and possibly myocardial infarction.
  109. Parasympathetic Nervous System (PSNS)
    •Acetylcholine is the preganglionic and postganglionic neurotransmitter.


    • –Muscarinic:
    • -Nicotinic
  110. Muscarinic:
    •Concentrated in the heart, smooth muscle, and exocrine glands
  111. Nicotinic:
    •Found in the central nervous system (CNS), the neuromuscular junction, autonomic ganglia, and the adrenal medulla
  112. •Drugs that stimulate the PSNS receptors:


  113. Drugs that block the PSNS receptors:


  114. Excess Cholinergic Effects
    •Decreased intraocular pressure

    •Mitosis (constriction of pupil)


    •Increased salivation

    •Increased bronchial secretions

    •Bronchial constriction

    •Increased GI tone


    •Decreased BP


    •Contraction of bladder detrusor muscle
  115. Excess Anticholinergic Effects
    •Increased intraocular pressure

    •Mydriasis (dilation of pupils)


    •Decreased sweating

    •Dry mouth

    •Decreased bronchial secretions

    •Respiratory depression

    •Decreased GI motility with possible constipation

    •Decreased BP followed by increased BP

    •Tachycardia and, possibly, palpitations

    •Urinary retention


    •Drowsiness, confusion, and agitation
  116. Anticholinergic Poisoning
    •Mad as a hatter

    •Blind as a bat

    •Red as a beet

    •Dry as a bone
  117. Pilocarpine
    •Direct-acting cholinergic

    •Topical pharmacotherapeutics:

    –Simple and acute glaucoma

    –Preoperative and postoperative elevated intraocular pressure

    Drug-induced mydriasis
  118. Nicotine
    •Stimulates the CNS

    • •Pharmacotherapeutics are limited to preparations to
    • assist in smoking cessation.

    • •Adverse effects are related to
    • its effects on the cardiovascular system and CNS
  119. Neostigmine
    •Indirect-acting cholinergic drug

    •Acts by reversibly inhibiting postsynaptic cholinesterase

    • •Used in the treatment of myasthenia gravis to minimize muscle
    • fatigue

    Most serious adverse effect: cholinergic crisis
  120. Atropine
    •Anticholinergic drug

    •Antidote to cholinergic poisoning


    –Preoperatively to dry secretions

    –Acute cardiac emergencies

    –Topically (homatropine) to treat ophthalmic disorders

    –Treatment of motion sickness and diarrhea
  121. Atropine Adverse effects
    • •Adverse effects related to loss
    • of acetylcholine stimulation on receptors

    •Most serious adverse effect: anticholinergic overdose (poisoning)
Card Set:
2011-07-10 17:45:21

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