Pharmacology Unit 3 Study Guide & Vocabs

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Pharmacology Unit 3 Study Guide & Vocabs
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Pharmacology Unit 3 Study Guide & vocabs
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  1. 1) Ø What is an agonist, an antagonist, a partial agonist
    • a) Agonist
    •   i) –a compound which increases or intensifies the activity of a receptor
    •    (1) –a “stimulator
    •     (a) (–drug that stimulates normal receptor activity)
    • b) Antagonist
    •   i) –compound which decreases the activity of the receptor or prevents an agonist from acting on a receptor
    •    (1) (–drug that inhibits normal receptor activity)
    •    (2) Competitive antagonist
    •      (a) –compound that binds to the same site of a receptor as an agonist
    •        (i) Effects are reversible by competition w/ agonist
    •      (b) Advantage: can use agonist & competitive antagonist to control exact degree of response
    •    (3) Noncompetitive antagonist
    •      (a) –compound that binds to a different part of a receptor than an agonist, but still prevents normal agonist action
    •        (i) Can’t be displaced by competition from agonist
    •     (b) Advantage: can block an effect no matter what the concentration of the agonist
    •     (c) allosteric
    • c) Partial agonist
    •   i) –compound which increases or intensifies the activity of a receptor
    •     (1) And is therefore, an agonist
    •   ii) But is less effective than other agonist
    •     (1) Can decrease their effectiveness when in competition w/ them for the same receptor sites
  2. 2) Ø What is the difference between a competitive and a non-competitive antagonist
    • a) Competitive antagonist
    •   i) –compound that binds to the same site of a receptor as an agonist
    •    (1) Effects are reversible by competition w/ agonist
    •   ii) Advantage: can use agonist & competitive antagonist to control exact degree of response
    • b) Noncompetitive antagonist
    •   i) –compound that binds to a different part of a receptor than an agonist, but still prevents normal agonist action
    •    (1) Can’t be displaced by competition from agonist
    •   ii) Advantage: can block an effect no matter what the concentration of the agonist
    •   iii) allosteric
  3. 3) Ø What is the difference between a structurally specific and a structurally nonspecific drug?
    • a) Structural specific drug
    •   i) –work by receptor theory: when the drug fits the shape of the active site of the receptor, a complex is formed which causes altered cell activity
    •    (1) Receptor – a molecule w/ which a drug interacts to produce a characteristic biological response
    •     (a) Drug-receptor complex causes biological responses such as:
    •       (i) Transport of ions or molecules
    •       (ii) Enzyme activation or deactivation
    •       (iii) Protein synthesis
    •       (iv) Release of hormones or transmitter
    •     (b) Location of receptors:
    •       (i) Cell membranes
    •       (ii) Cell components
    •          1. DNA
    •          2. Enzymes
    •       (iii) For most drugs, we don’t actually know
    •   ii) –depends upon the drug: may stimulate or inhibit normal receptor activity
    •    (1) Stimulates: agonist
    •    (2) Inhibits: antagonist
    •  b) Structural nonspecific drug
    •   i) –work by simple physical or chemical action
    •   ii) –drug actions not mediated by receptors;
    •    (1) Ex:
    •     (a) Volatile anesthetics- dissolve in membrane & decrease nerve conduction (no specific receptor)
    •     (b) Antacids
    •     (c) Emollients
    •     (d) Osmodiuretics (mannitol) –filter into tubule & pulls water w/ it
    •     (e) Some laxatives work similarly (MgSO4)
    •     (f) Complexes to remove ions or compounds - EDTA for lead poisoning
  4. 4) Ø What are the factors that influence the rate of drug passage through a membrane
    • a) Membrane Structure:
    •   i) “3 layers” chiefly a lipid bilayer w/ small amounts of protein floating in it and on other side
    •    (1) Chiefly lipids pass through main membrane
    •    (2) Pores for small water soluble substances
    •    (3) Complexes for carrier mediated transport
    • b) Main:
    •   i) Influences drug passage through membrane proper the most
    •    (1) Its lipid solubility
    •   ii) Size & shape of the molecule
    •   iii) Its degree of ionization (i.e. charge)
    •    (1) –influenced by pH
    •      (a) Acid (ex. Barbiturates)
    •        (i) Less ionized at low environmental pH (acidic environment)
    •          1. “acid in like (acid) environment is LESS ionized”
    •        (ii) More ionized at high environmental pH (works at: basic environment?)
    •          1. “acid in unlike (Base) environment is MORE ionizd”
    •        (iii) –has more H+ than OH-
    •         1. Ex:
    •            a. HCL -> H+ + Cl-
    •            b. H2CO3 -> H+ HCO3-
    •            c. HA -> H+ + A-
    •      (b) Bases (ex: morphine or quinine: endings –ine or –amine indicate alkaline drugs)
    •        (i) Less ionized at high environment pH (basic environment)
    •          1. “base in like (Base) environment is LESS ionized”
    •       (ii) More ionized at low environmental pH (works at: acidic environment?)
    •         1. “base in unlike (acid) environment is MORE ionized”
    •       (iii) –has more OH- than H+
    •         1. Ex:
    •           a. NaOH -> Na+ + OH-
    •           b. NH4)H -> NH4+ + OH-
    •           c. BOH -> B+ + OH-
    •    (2) Summary:
    •     (a) In SIMILAR environment: drugs are LESS ionized (not Charged)
    •       (i) acid in acid
    •       (ii) base in base
    •     (b) In OPPOSITE environments drugs are MORE ionized (Charged: split into + & -)
    •       (i) Acid in Base
    •       (ii) Base in Acid
    •    (3) The form of drug moves through membranes more readily: is Not Ionized!
    •     (a) Ionized particles are “trapped” by membranes
    •     (b) Ionization influences reabsorption
    •       (i) Ex: nephron (pH: 4-8 depends on drugs or food/liquid intake)
    •         1. Want to eliminate acidic drug in the nephron
    •           a. Trap it in tubules: ionize the tubules
    •             i. Less likely to move & reabsorbed
    •           b. Make tubular fluid’s pH to more alkaline
    •   iv) The pH of the surrounding medium
  5. 5) Ø Understand ionization and how it influences drug movement
    • a) Its degree of ionization (i.e. charge)
    •   i) –influenced by pH
    •    (1) Acid (ex. Barbiturates)
    •      (a) Less ionized at low environmental pH (acidic environment)
    •        (i) “acid in like (acid) environment is LESS ionized”
    •      (b) More ionized at high environmental pH (works at: basic environment?)
    •        (i) “acid in unlike (Base) environment is MORE ionizd”
    •      (c) –has more H+ than OH-
    •        (i) Ex:
    •          1. HCL -> H+ + Cl-
    •          2. H2CO3 -> H+ HCO3-
    •          3. HA -> H+ + A-
    •    (2) Bases (ex: morphine or quinine: endings –ine or –amine indicate alkaline drugs)
    •      (a) Less ionized at high environment pH (basic environment)
    •        (i) “base in like (Base) environment is LESS ionized”
    •      (b) More ionized at low environmental pH (works at: acidic environment?)
    •        (i) “base in unlike (acid) environment is MORE ionized”
    •      (c) –has more OH- than H+
    •        (i) Ex:
    •          1. NaOH -> Na+ + OH-
    •          2. NH4)H -> NH4+ + OH-
    •          3. BOH -> B+ + OH-
    •   ii) Summary:
    •    (1) In SIMILAR environment: drugs are LESS ionized (not Charged)
    •      (a) acid in acid
    •      (b) base in base
    •    (2) In OPPOSITE environments drugs are MORE ionized (Charged: split into + & -)
    •      (a) Acid in Base
    •      (b) Base in Acid
    •   iii) The form of drug moves through membranes more readily: is Not Ionized!
    •    (1) Ionized particles are “trapped” by membranes
    •    (2) Ionization influences reabsorption
    •      (a) Ex: nephron (pH: 4-8 depends on drugs or food/liquid intake)
    •        (i) Want to eliminate acidic drug in the nephron
    •          1. Trap it in tubules: ionize the tubules
    •             a. Less likely to move & reabsorbed
    •          2. Make tubular fluid’s pH to more alkaline
  6. 6) Ø What factors affect drug absorption
    • a) absorptiontransfer of drug molecules from place deposited to circulating fluids
    •   i) route of administration
    •    (1) changes place deposited so changes absorption
    •      (a) oral
    •      (b) subcutaneous or intramuscular
    •      (c) IV
    •    (2) Do all absorb at the same rate?
    • b) –affects concentration at active site
    •   i) Route of administrationinjections usually more rapid absorption than oral route
    •    (1) (Contrast plot of drug plasma concentration vs time for oral route and IV administration)
    •   ii) Local conditions at site fo administration
    •    (1) Injection: amount of circulation to area
    •      (a) Patient in shock
    •      (b) Tourniquet or cooling
    •    (2) Oral
    •      (a) pH
    •      (b) presence of food
    •   iii) chemical properties of drug
    •    (1) lipid solubility vs water solubility
    •    (2) size & shape of molecule
    •    (3) ionization (if water soluble)
    • iv) forms of medication
    •    (1) oral: enteric coating, time release
    •    (2) injection: suspension ang gels can delay absorption of a given drug
    •      (a) these factors are in addition to Dosage, frequency
  7. 7) Ø How the presence of food (or timing of drug dosage around meals) alter drug absorption
    • a) Before meal
    •   i) much more quick absorption
    • b) After meal
    •   i) Slower transit time & slower absorption
  8. 8) Ø In terms of distribution of a drug, how does the blood brain barrier differ from the placental barrier
    • a) From blood stream to?
    • b) Relative perfusion and permeability of area
    •   i) Blood brain barrier
    •    (1) Glial cells plug capillary
    •    (2) Pores themselves are smaller
    •    (3) Interstitial space minimal(/less) – packed glial cells
    •      (a) Lipid soluble drugs penertrate
    •   ii) Placental “barrier”Almost no barrier at all
    •    (1) Low perfusion – explains anesthetic
    •    (2) Some proteins and even viruses cross
    •      (a) Microbleeds even permit some RBC passage
    •    (3) Lipid soluble drugs pass readily (alcohol, tretracyline)
    •   iii) Bindings to non-receptor sites like plasma proteins
    •    (1) Can affect onset, intensity, and duration
    •      (a) Doesn’t affect absorption …why?
    •    (2) Usually weak binding so effect not severe
    •    (3) Sometimes use priming dose then smaller maintenance
    •   iv) Other storage sites (fat, muscle, liver, kidney, bone)
    •    (1) Often requires more drug (see volume of Distribution)
    •    (2) May redistribute to and from storage
    •      (a) Relative perfusion may be an issue
    •    (3) (low vascularity of adipose causes it to saturate more slowly… may pull drug form brain, etc.)
    •   v) Body weight
    •    (1) Dose per Kg body weight
    •  vi) Sex
    •    (1) Relates to both size and fat distribution
  9. 9) Ø What is the effect of plasma protein binding on drug distribution
    • a) Apparent Volume of Distribution (Vd): A calculated Value
    •   i) Vd = 3 liters
    •    (1) Plasma only
    •   ii) Vd= 16 liters
    •    (1) Extracellular distribution (plasma + interstitial)
    •   iii) Vd= 40 liters
    •    (1) Both intra and extracellular distribution
    •   iv) Vd > 40 liters
    •    (1) Storage Depots present
  10. 10) Ø Where are drugs metabolized
    • a) Metabolism (biotransformation): the chemical alternations of a drug by the body
    •   i) Usually liver (also blood enzymes, intestinal mucosa, etc)
    •   ii) Usually changed to less active chemical
    •    (1) If more active, more metabolized again
    •   iii) More ionized so more readily eliminated
    • b) CYTP450 system
    •   i) –most common group of enzymes found in liver microsomal fraction (also called CYP)
    •    (1) Inducible
    •    (2) Inhibition
    •      (a) Competitive binding rarely clinically significant
    •      (b) Covalent binding to enzyme – permanent
    •        (i) Degree of inhibition often more input, than mech
    •   ii) Ex include CYP ____:
    •    (1) 1A2, 2C9, 2D6, 3A4 etc
    •    (2) These participate in the metabolism of most drugs
    •    (3) CYP3A4 alone helps metabolize 50% of prescribed meds
    •   iii) FDA suggests in vitro testing to predict interactions
    • c) Special patient considerations
    •   i) Pathology – hepatic, renal, cardiovascular
    •   ii) Age – infants and elderly
    •   iii) Genetic – inherited errors of metabolism
    •   iv) Drug exposure – may depress or activate liver
    •    (1) Other prescribed medications
    •    (2) Non-prescribed “drugs” (Alcohol, tobacco induced P450)
    •    (3) “metabolic” Tolerance – require more to maintain effect
    •      (a) Eliminate more drug so less reaches Active Site
  11. 11) Ø What is the significance of induction and inhibition of the CYTP450 system
    • a) –most common group of enzymes found in liver microsomal fraction (also called CYP)
    •   i) Inducible – (induces Cytochrome P450
    •    (1) Increase the rate of metabolism of that drug
    •      (a) As well as any drug metabolize by CYTP450)
    •   ii) Inhibition
    •    (1) (decrease metabolism of drugs metabolize by it)
    •    (2) Competitive binding rarely clinically significant
    •    (3) Covalent binding to enzyme – permanent
    •      (a) Degree of inhibition often more input, than mech
    • b) Ex include CYP ____:
    •   i) 1A2, 2C9, 2D6, 3A4 etc
    •   ii) These participate in the metabolism of most drugs
    •  iii) CYP3A4 alone helps metabolize 50% of prescribed meds
    • c) FDA suggests in vitro testing to predict interactions
  12. Excretion
    • a) –drug elimination from the body
    •  i) Routes:
    •    (1) Kidney
    •    (2) Liver –Bile to feces
    •      (a) Enterohepatic circulation possible
    •    (3) Sweat glands
    •    (4) Saliva
    •    (5) Lungs
    •    (6) Mothers milk (traps alkaline drugs)
    •   ii) Excretion RATE important
    •    (1) Avoid cumulative effects
    •   iii) Rate – For kidney (nephron) depends upon:
    •    (1) Filtration
    •      (a) Circulation – GFR (glomerular filtration rate)
    •      (b) Concentration of drug not bound by plasma protein
    •    (2) Secretions
    •      (a) Drug characteristic
    •      (b) Active transport (infants and elderly)
    •    (3) Reabsorption
    •      (a) Fats vs water soluble
    •      (b) Size and shape of water soluble molecules
    •      (c) pH& ionization
    •   iv) Clearance – ml/min or L/hr (calculate volume)
    •    (1) –volume of fluid that would be completely cleared of a drug in a minute, if all were removed from that volume and none were removed from remaining fluid in body
    •      (a) Compensate for plasma concentration
    •    (2) Physiologist & Clinicians refer to “renal” clearance
    •      (a) Clinicians use “renal clearance” in general to estimate individual patient renal function (Usually test creatinine clearance)
    •    (3) Research Pharmacologist refers to “total” drug clearance
    •      (a) Includes metabolism and excretion by all routes
    •      (b) Incorporated into the concept of a drug’s effective half-life in the body
  13. b) Intensity of Response: to given dose of a drug
    • i) Concentration at Active Site
    •   (1) Pharmacokinetics
    • ii) Ability of Active Site to Respond
    •   (1) Physiological State
    •     (a) (sleeping pills
    •     (b) or hormones)
    •   (2) Pathological State
    •     (a) (digitalis or aspirin)
    •   (3) Tolerance (2nd Kind) – “Receptor” or “Cellular”
    •     (a) Receptor number may change
    •     (b) Internal response may change
    •       (i) Perhaps in 2nd Messenger systems
    •       (ii) Leads to physical dependence on the drug
    • iii) Individual Patient Differences
    •   (1) Age (enzyme, blood brain barrier, circulation)
    •     (a) Very old & very young: enzymatic issues
    •      (i) Infants: immature enzyme, immature liver & kidney, blood brain barrier incomplete, gastrointestinal motility is inconsistent
    •      (ii) Old: worn out enzyme, circulatory dysfunction
    •   (2) Weight
    •     (a) (sometimes use surface area)
    •     (b) Dosage differs per size/weight
    •   (3) Sex
    •     (a) Size body composition, pregnancy, and nursing
    •       (i) Category: Chart for pregnant women
    •         1. A: Controlled Human Trials = no risk shown
    •         2. B: Possible Animal risk but limited human trials = no risk shown
    •         3. C: Animal test may show some damage = human risk unknown
    •         4. D: Evidence of human fetal risk: life threatening only
    •         5. X: Contraindicated = No possible benefit for risk to fetus
    •   (4) Environment
    •     (a) Physical
    •       (i) Temperature – affect circulation
    •         1. Hot- vasodilation
    •         2. Cold - vasoconstriction
    •       (ii) Altitude –oxygen carrying capacity changes
    •     (b) Psychosocial
    •       (i) Sensory distraction
    •         1. Person’s state of mind affect
    •           a. Miserable respond poorly to treatments/drugs & heal poorly
    •       (ii) Placebo
    •         1. Effective 30% of the time
    •       (iii) Compliance –largest barrier of drug therapy
    •         1. Ease of use
    •         2. Cost (affordable)
    •         3. Patient responsibility
    • iv) Physiology, pharmacology, or pathology
    •   (1) Physiology
    •     (a) Diurnal rhythms
    •     (b) Hormones
    •     (c) Fluids, electrolytes, acid-base balance
    •   (2) Pharmacology
    •     (a) Other meds, drug abuse history, tobacco or alcohol (P450)
    •   (3) Pathology
    •     (a) Hepatic, renal, cardiovascular
    •       (i) Disease makes it work not so well
    •     (b) Special Cases
    •       (i) Fever + aspirin
    •         1. Risk of hay fever?
    •         2. In kids: increase chance to get Ray syndrome
    •      (ii) Infection + insulin
    •         1. Increase prone to infection
    •      (iii) Pulmonary disease + anesthetics
    •         1. Anesthetics increase prone to pulmonary disease
    •           a. Bronchi spasm
    •              i. Respiratory distress
    •   (4) Genetics
    •     (a) Metabolism – deficiencies or excessive in enzyme
    •       (i) Sulfonamides – can’t metabolize – toxic
    •       (ii) Seizure medications may be metabolized 4% faster in some individuals
    •     (b) Receptors
    •       (i) Insulin receptors defective in some type II diabetics
    •   (5) Assess pre-drug status of the individual –baseline state (ex: history: Kidney problems?)
    •     (a) Especially note areas affected by drug (either + or -)
    •     (b) Monitor BOTH
    •       (i) Effectiveness
    •       (ii) And toxicities
  14. c) Adverse Responses to Drugs:
    • i) Those specific to drug (may harmful effects)
    •   (1) Blood abnormalities
    •   (2) Liver or Kidney damage
    •   (3) Teratogenic effects
    •   (4) Dermatologic Effects
    • ii) Drug Idiosyncracy
    •   (1) (abnormal reaction to drug)
    •   (2) Non-allergic abnormal response – genetic?
    •     (a) (can’t be predicted)
    •     (b) (patient specific? Genetic?)
    • iii) Drug Allergy (don’t use “hypersensitivity”)
    •   (1) (reaction to drug, due to previous exposure)
    •   (2) Responses to Histamine (Local-hive/rash? Systemic-drop blood pressure/ swelling of throat/etc?)
    •     (a) Predictable
  15. d) Drug Interactions
    • i) Due to simultaneous administration of 2 or more drugs
    •   (1) May INCREASE therapeutic or toxic effect
    •     (a) Additive
    •     (b) Synergistic
    •     (c) Potentiation
    •   (2) May Decrease therapeutic or toxic effect
    •     (a) Antagonism
  16. e) Mechanism of Drug Interactions
    • i) Alter Pharmacodynamics
    •   (1) Binding to receptor site modified (other antagonists or agonists)
    •   (2) Increase or decrease rate of different portions of pathway
    • ii) Alter Pharmacokinetics
    •   (1) Absorption
    •     (a) Antacids in GI, vasoconstriction, physical incompatibility at site of admin
    •   (2) Distribution
    •     (a) Competition for plasma proteins or other storage
    •   (3) Metabolism
    •     (a) Stimulate (“induce”) or depress (“bind to”) liver enzymes
    •     (b) Binding to plasma protein
    •   (4) Excretion
    •     (a) Diuretics
    •     (b) Competition for plasma protein
  17. f) Competition for Plasma Proteins
    • i) (Plasma Proteins:
    •   (1) One of ways we distribute water soluble drugs through blood
    •   (2) Plasma protein binding:
    •     (a) It can decrease the availability of free drug to active site
    •     (b) Slow distribution down
    •     (c) Slow ultimate elimination from the body)
    •   (3) (bound to same location: the drug plasma protein like more
    •     (a) will have higher concentration in blood)
    • ii) Ex: Drug A is bound to plasma protein in same position that Drug B binds
    •   (1) What will happen when B is added:
    •     (a) If B binds more tightly than A
    •       (i) Receptor receives drug A not drug B
    •       (ii) (“A” already in blood stream: bump off by higher affinity B = drug A is released and free to attach to active site)
    •     (b) If A binds more tightly than B
    •       (i) Receptor gets more of B than expected
    •       (ii) Will not be as much need for a priming dose
    • iii) Q: what would you change for each drug to make both meds more safe & effective?
    •   (1) [think about 2 receptor factors: plasma protein binding- blood stream; & receptor binding- active site]
  18. 13) Ø Review the individual patient differences that may affect absorption, distribution, metabolism and excretion of drugs. (p 70)
    • a) Age (enzyme, blood brain barrier, circulation)
    •   i) Very old & very young: enzymatic issues
    •    (1) Infants: immature enzyme, immature liver & kidney, blood brain barrier incomplete, gastrointestinal motility is inconsistent
    •    (2) Old: worn out enzyme, circulatory dysfunction
    • b) Weight
    •   i) (sometimes use surface area)
    •   ii) Dosage differs per size/weight
    • c) Sex
    •   i) Size body composition, pregnancy, and nursing
    •    (1) Category: Chart for pregnant women
    •      (a) A: Controlled Human Trials = no risk shown
    •      (b) B: Possible Animal risk but limited human trials = no risk shown
    •      (c) C: Animal test may show some damage = human risk unknown
    •      (d) D: Evidence of human fetal risk: life threatening only
    •      (e) X: Contraindicated = No possible benefit for risk to fetus
    • d) Environment
    •   i) Physical
    •    (1) Temperature – affect circulation
    •      (a) Hot- vasodilation
    •      (b) Cold - vasoconstriction
    •    (2) Altitude –oxygen carrying capacity changes
    •  ii) Psychosocial
    •    (1) Sensory distraction
    •      (a) Person’s state of mind affect
    •        (i) Miserable respond poorly to treatments/drugs & heal poorly
    •    (2) Placebo
    •      (a) Effective 30% of the time
    •    (3) Compliance –largest barrier of drug therapy
    •      (a) Ease of use
    •      (b) Cost (affordable)
    •      (c) Patient responsibility
    • e) Physiology, pharmacology, or pathology
    •   i) Physiology
    •    (1) Diurnal rhythms
    •    (2) Hormones
    •    (3) Fluids, electrolytes, acid-base balance
    •   ii) Pharmacology
    •    (1) Other meds, drug abuse history, tobacco or alcohol (P450)
    •   iii) Pathology
    •    (1) Hepatic, renal, cardiovascular
    •      (a) Disease makes it work not so well
    •    (2) Special Cases
    •      (a) Fever + aspirin
    •        (i) Risk of hay fever?
    •        (ii) In kids: increase chance to get Ray syndrome
    •      (b) Infection + insulin
    •        (i) Increase prone to infection
    •      (c) Pulmonary disease + anesthetics
    •        (i) Anesthetics increase prone to pulmonary disease
    •          1. Bronchi spasm
    •            a. Respiratory distress
    •   iv) Genetics
    •    (1) Metabolism – deficiencies or excessive in enzyme
    •      (a) Sulfonamides – can’t metabolize – toxic
    •      (b) Seizure medications may be metabolized 4% faster in some individuals
    •    (2) Receptors
    •      (a) Insulin receptors defective in some type II diabetics
    •   v) Assess pre-drug status of the individual –baseline state (ex: history: Kidney problems?)
    •    (1) Especially note areas affected by drug (either + or -)
    •    (2) Monitor BOTH
    •      (a) Effectiveness
    •      (b) And toxicities
  19. 14) What is the difference between a drug idiosyncracy and a drug allergy
    • a) Drug Idiosyncracy
    •   i) (abnormal reaction to drug)
    •   ii) Non-allergic abnormal responsegenetic?
    •    (1) (can’t be predicted)
    •    (2) (patient specific? Genetic?)
    • b) Drug Allergy (don’t use “hypersensitivity”)
    •   i) (reaction to drug, due to previous exposure)
    •   ii) Responses to Histamine (Local-hive/rash? Sytemic-drop blood pressure/ swelling of throat/etc?)
    •     (1) predictable
  20. Define: Agonist
    •   i) –a compound which increases or intensifies the activity of a receptor
    •    (1) –a “stimulator
    •     (a) (–drug that stimulates normal receptor activity)
  21. Define: Antagonist
    •   i) –compound which decreases the activity of the receptor or prevents an agonist from acting on a receptor
    •    (1) (–drug that inhibits normal receptor activity)
    •    (2) Competitive antagonist
    •      (a) –compound that binds to the same site of a receptor as an agonist
    •        (i) Effects are reversible by competition w/ agonist
    •      (b) Advantage: can use agonist & competitive antagonist to control exact degree of response
    •    (3) Noncompetitive antagonist
    •      (a) –compound that binds to a different part of a receptor than an agonist, but still prevents normal agonist action
    •        (i) Can’t be displaced by competition from agonist
    •     (b) Advantage: can block an effect no matter what the concentration of the agonist
    •     (c) allosteric
  22. Define: Partial Agonist
    •   i) –compound which increases or intensifies the activity of a receptor
    •     (1) And is therefore, an agonist
    •   ii) But is less effective than other agonist
    •     (1) Can decrease their effectiveness when in competition w/ them for the same receptor sites
  23. Define: Competitive antagonist
    • i) –compound that binds to the same site of a receptor as an agonist
    •    (1) Effects are reversible by competition w/ agonist
    •   ii) Advantage: can use agonist & competitive antagonist to control exact degree of response
  24. Define: Non-competitive antagonist
    • i) –compound that binds to a different part of a receptor than an agonist, but still prevents normal agonist action
    •    (1) Can’t be displaced by competition from agonist
    •   ii) Advantage: can block an effect no matter what the concentration of the agonist
    •   iii) allosteric
  25. Define: Structurally specific drug
    • i) –work by receptor theory: when the drug fits the shape of the active site of the receptor, a complex is formed which causes altered cell activity
    •    (1) Receptor – a molecule w/ which a drug interacts to produce a characteristic biological response
    •     (a) Drug-receptor complex causes biological responses such as:
    •       (i) Transport of ions or molecules
    •       (ii) Enzyme activation or deactivation
    •       (iii) Protein synthesis
    •       (iv) Release of hormones or transmitter
    •     (b) Location of receptors:
    •       (i) Cell membranes
    •       (ii) Cell components
    •          1. DNA
    •          2. Enzymes
    •       (iii) For most drugs, we don’t actually know
    •   ii) –depends upon the drug: may stimulate or inhibit normal receptor activity
    •    (1) Stimulates: agonist
    •    (2) Inhibits: antagonist
  26. Define: Structurally nonspecific drug
    • i) –work by simple physical or chemical action
    •   ii) –drug actions not mediated by receptors;
    •    (1) Ex:
    •     (a) Volatile anesthetics- dissolve in membrane & decrease nerve conduction (no specific receptor)
    •     (b) Antacids
    •     (c) Emollients
    •     (d) Osmodiuretics (mannitol) –filter into tubule & pulls water w/ it
    •     (e) Some laxatives work similarly (MgSO4)
    •     (f) Complexes to remove ions or compounds - EDTA for lead poisoning
  27. Define: Drug Idiosyncracy
    •   i) (-abnormal reaction to drug)
    •   ii) Non-allergic abnormal responsegenetic?
    •    (1) (can’t be predicted)
    •    (2) (patient specific? Genetic?)
  28. Define: Drug Allergy
    • (don’t use “hypersensitivity”)
    •   i) (reaction to drug, due to previous exposure)
    •   ii) Responses to Histamine (Local-hive/rash? Sytemic-drop blood pressure/ swelling of throat/etc?)
    •     (1) predictable

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