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Flashcards

Pharmacology

johanna_hillbrick 3rd Year Semester 2 English 92 cards

Cards in this deck (92)

  1. 1Clinical PharmacologyUsing pharmacodynamic and pharmacokinetic data and applying that knowledge in a clinical setting to understand and explain the in vivo behaviour of (radio)pharmaceuticals.
  2. 2Pharmacodynamics'what the drug does to the body'
    -relationship between administration of a drug and its influence on molecular, biochemical and physiological processes within the body.
  3. 3Pharmacokinetics'What the body does to the drug'
    - relationship between absorption, distribution, metabolism and excretion of a drug from the body over time.
  4. 4Radiopharmacokineticsthe study over time of a radiopharmaceutical's absorption, biodistribution and elimination following introduction to the body.
  5. 5Why do most radiopharmaceuticals not elicit a clinical pharmacodynamic response?only trace amount of the active ingredient is used so when the RP is administered it is not in a great enough concentration to cause a response.
  6. 6Pharmacokinetics in NM-New development of RPs with desirable properties.
    -Dosimetry calculations
    -PK of radiopharmaceuticals can be visualised in NM studies.
  7. 7Receptora specific macromolecule that selective naturally occurring substances or selective drugs can bind to.
    This binding may instigate, alter or cease a biochemical response in the body
  8. 8Receptor Binding-ability of a substance to bind to a receptor is related to the substance's chemical structure.
    -substances classified as agonists or antagonists.
  9. 9AgonistA substance that stimulates or activates a receptor to produce a physiological response.
  10. 10Partial Agonista substance that activates a receptor but to a limited extent compared to a full agonist.
  11. 11Antagonist-A substance that prevents action of an agonist at a receptor site.
    -It has affinity and binds to receptor sites but does not instigate change in function.
    -binding can be reversible or irreversible.
  12. 12AffinityHow tightly the substance binds
  13. 13Intrinsic Activitymeasure of the ability of the substance, once bound to cause physiological effects.
    full agonists: A=1
    partial agonists: A<1
    antagonists: A=0
  14. 14Observed physiological effects vary with:-The substrate concentration
    and
    -its affinity to the receptor.
  15. 15Receptor Binding: -Reversible Binding-Substrate may freely interact or dissociate from the receptor
    [S]+[R] -> <- [SR]
    -equilibrium may occur
    -Has the potential for competitive binding.
  16. 16Receptor Binding: -Competitive Binding-a substrate may compete with naturally occurring substances or drugs for the same receptor site
    -the substance in the receptor site may be displaced by the second substance.
  17. 17Receptor Binding: -Irreversible Binding-substance forms a covalent bond with receptor.
    -binding is permanent and this receptor will not be available for use for the rest of its life.
  18. 18Drugs and Binding-Drugs are usually agonists or antagonists.
    -receptor binding will activate or deactivate a secondary messenger system which in turn instigates or prevents a response.
  19. 19Sites of action:Tissue
    Ion channels
    Enzymes
    Carrier proteins
  20. 20Concentration-Effect Relationship-An increase in response is seen with increase in drug concentration
    -As drug concentration increases, saturation of receptor binding occurs and a maximal effect is reached.
  21. 21E-maxThe maximal effect at which the drug concentration is great enough to occupy all receptors.
  22. 22EC 50The drug concentration at which half of the maximum drug effect is seen.
  23. 23The range of ideal therapeutic response for most therapeutically active drugsbetween 20-80%
  24. 24The 3 Pharmacokinetic Principles-Absorption
    -Distribution
    -Elimination (metabolism and excretion)
  25. 25AbsorptionThe movement of a drug from its administered site to the vascular compartment or site of action.
  26. 26Drug Administration Methodsoral, IV, IA, subcutaneous, intramuscular, sublingual, transdermal, rectal, intravaginal, intranasal, inhalation, aural, optical, intrathecal, intraperitoneal
  27. 27Bioavailability (F)The fraction of dose of an intact rug that is absorbed into the systemic circulation.
    Oral admin- F= 0-1
    IV admin- F=1
  28. 28First Pass MetabolismThe extent of drug metabolism by the liver that occurs following GI absorption of a drug.
    -occurs on many orally absorbed drugs and reduces bioavailability.
  29. 29Oral absorption formulation factors-balance of water and lipid solubility
    -Drug pH
  30. 30Oral Administration dosage forms:-Solid (tablet or capsule)
    -Liquid (suspension or solution)
    *rate limiting steps for absorption are dissolution and disintergration
  31. 31Formulation Factors for Orally Administered Drugs-Surface area/particles size
    -drug stability
    -complexation
  32. 32Physiological Factors for Orally Administered Drugs-food and fluid
    -gastric emptying rate
    -metabolism
    -physical activity
    -posture
  33. 33Oral Absorption Advantages-simple, non invasive method
    -good for long acting drugs
    -less risk of overdose
  34. 34Oral Absorption Disadvantages-first pass metabolism
    -bioavailiability influenced by formulation and physiological factors.
  35. 35IV Absorption-direct introduction of the drug into the systemic circulation
    -rapid distribution through the body
  36. 36IV Absorption Advantages-rapid effect
    -drugs are not effected by first pass metabolism resulting in 100% bioavailiability
    -precise dose given
  37. 37IV Absorption Disadvantages-phlebitis and pain
    -extravasation
    -vein access issues
    -toxicity and overdose
    -drug precipitation
  38. 38Intramuscular and Subcutaneous Absorption-Intramuscular injections are injections of drugs directly into muscle tissue
    -Subcutaneous injections are given directly underneath the epidermal layer and above muscle tissue.
  39. 39Intramuscular and Subcutaneous Absorption AdvantagesSimilar to IV but:
    -good for poor venous access
    -slower acting (less risk of overdose and toxicity)
    -longer acting
  40. 40Intramuscular and Subcutaneous Absorption Disadvantages-Drug solubility issues
    -Variable absorption rates
    -absorption can be influenced by local tissue vascularity, disease state, drug solubility and drug vehicle.
  41. 41local tissue vascularityDrug absorption from a site is related to the extend of vascular perfusion to the area.
    muscle > subcutaneous perfusion
  42. 42Disease StateDisease states or injuries that restrict the peripheral vasculature will alter the rate of absorption from IM or SC sites.
    -Shock, AMI, CCF
  43. 43Drug solubility and drug vehicle-Lipid soluble drugs are usually absorbed rapidly
    -Water soluble drugs are usually absorbed slowly
  44. 44Intradermal AbsorptionPatches or creams on the skin
    -absorption by the penetration of the stratum corneum via passive diffusion
    or via hair follicles.
  45. 45Intradermal Absorption Advantages-No first pass metabolism
    -Bioavailiability not influenced by factors affecting oral absorption
    -constant and continuous rate of drug delivery
    -can cease drug admin immediately
  46. 46Intradermal Absorption Disadvantages-physicochemical properties of the drug can alter absorption
    -not effective for large drug molecules
    -effected by skin and age variations
  47. 47Absorption via InhalationUsed to achieve local effects within the respiratory system. With drugs acting directly on the cells within the lung tissue adjacent to the airways.
  48. 48Absorption via Inhalation advantages-Drugs exert local effects and decrease risk of systemic side effects
    -can also get systemic absorption from lungs which bypass hepatic first pass effect.
  49. 49Absorption via Inhalation disadvantages-Deposition of drug dependent on particle size.
    -possible metabolism of drug in the lungs causing a reduction in bioavailiability
  50. 50Radiopharmaceutical distributionMost initially bio-distribute within the vascular compartment via dilution along the concentration gradient. Further movement into other compartments may then occur.
  51. 51Aerosol Inhalation-liquid/solid particles suspended in liquid
    -lung penetration varies with droplet size
  52. 52Gaseous Exchange-Inert gases inhaled and exchanged into the vascular compartment via alveoli
    -Distributed from blood into adipose or diffusion back into lungs
  53. 53Ion Exchange-electrolytes in vascular compartment
    -simple exchange with salts
  54. 54Passive Transport-cross membranes via simple diffusion or mediated diffusion
    -lipophilic agents (HMPAO)
  55. 55Active TransportUse of cellular mechanisms/membrane transport systems to move RPs from the vascular compartment into the cells, or to cross a cellular barrier (BBB) through the expenditure of energy.
  56. 56Endocytosis-Process through which a substance gains entry into a cell, without passing through the cell membrane, via formation of intracellular vesicles.
  57. 573 Types of Endocytosis-Phagocytosis -solid particles
    -Pinocytosis - dissolved materials
    -Receptor mediated endocytosis- specific molecules
  58. 58Phagocytosis-Chemotaxis towards foreign materials
    -Vesicle formation and foreign material ingestion.
  59. 59Autologous Product-Product isolated from the body, labelled, and re-administered
    -Bio-distribution varies with cell damage
    -e.g. WBCs or RBCs
  60. 60Single Compartment Modelconsidering for drugs that-following absorption, distribute from the systemic circulation
    e.g. 99m-Tc DTPA
  61. 61Two Compartment Modelfor drugs that following absorption, distribute to a peripheral compartment.
    e.g. 99m-Tc MAG-3, sestamibi
  62. 62Multi Compartment Modelfor drugs that following absorption, distribute to greater than one peripheral compartment
    e.g. 99m-Tc MDP
  63. 63apparent volume of distribution (Vd)-The apparent volume of fluid that a radiopharmaceutical distributes into.
    -This value is based on the total amount of RP introduced into the body and the measured concentration of the RP in the plasma.
  64. 64Uses for Vd-calculating the biological half life of a drug
    -calculating the clearance of a drug
    -calculating loading doses for therapeutically active drugs to achieve steady plasma drug concentrations
  65. 65factors that may influence Vd-Protein binding
    -tissue binding
    -blood flow,
    -lipid solubility
  66. 66Protein Binding-binding of radiopharmaceuticals to plasma proteins
    -Drug protein binding is a reversible process with an equilibrium forming between bound and non bound drugs.
  67. 67Tissue BindingFree drug can also bind to tissue once it has left the vascular compartment
  68. 68Blood flow to tissue-variance in localised blood flow depending upon the tissue type
    -changes in regional blood flow can alter Vd
  69. 69Lipid SolubilityThe greater the lipid solubility of a drug the greater the Vd, as the drug will be able to permeate through cellular membranes readily, distribute into fat and cross the BBB from the central vascular compartment.
  70. 70ClearanceThe irreversible elimination of a pharmaceutical from the systemic circulation.
    -volume of blood cleared of drug per unit time (mL/min)
    Cl= rate of elimination/plasma concentration
  71. 71Half LifeHalf like is the time taken for half of the amount of drug within the body to be cleared.
    -relates to both the Vd of the radiopharmaceutical and its clearance (Cl)
  72. 72excretion, metabolism and eliminationExcretion is when the drug leaves the body unchanged while metabolism is the changing of the drug into a different chemical form. Elimination is the broad term for both.
  73. 73What does the half life determine?-the duration of drug action following a single dose
    -the time taken for a drug to reach steady state
    -the frequency with which doses can be given
  74. 74Hepatic clearanceDrugs can be metabolised or excreted unchanged via the hepatic system into the GIT
  75. 75Metabolism-The termination of biologically active chemical compounds via the alteration of their chemical structure.
    -The new chemical structure is generally more polar allowing efficient removal from the body.
  76. 76Active MetabolitesNew compounds produced by metabolism which have their own pharmaceutical action (same or different from the original drug)
  77. 77Hepatic First Pass Metabolism-The extent of drug metabolism by the liver that occurs following absorption of a drug from the GIT
    -the intact drug enters the circulation
    -metabolised drug is generally eliminated
  78. 78Phase 1 Metabolism-chemical compound undergoes an oxidation reaction to produce a more polar compound.
    -Other types of reactions may also occur
    -Enzymes in the ER assist in metabolism
    -CYP enzymes
  79. 79Phase 2 Metabolism-The oxidised compound undergoes a conjugation reaction.
    -Which increases the polarity and alters the molecular shape.
    -They are then excreted.
  80. 80Factors Affecting Hepatic Clearance-age, genetics, drug interactions, drug concentration, hepatic function, hepatic extraction ratio, hepatic blood flow, plasma protein binding.
  81. 81hepatic extraction ratioThe fraction of drug that enters the liver via the blood that is extracted during one pass of the blood through the liver.
  82. 82Kidney Clearance Methodsglomerular filtration and proximal tubular secretion
  83. 83Factors Effecting Renal Clearance of a RPTubular Reabsorption, urine pH, urine flow rate, renal impairment, plasma protein binding
  84. 84Breast Milk ExcretionExcretion of drugs or metabolites into breast milk depends on:
    -Lipid solubility,
    -plasma protein binding
    -pH partitioning
  85. 85Salivary ExcretionActive drug or metabolites may be actively excreted from the salivary glands into the upper GIT.
    Excretion depends on:
    -Lipid solubility,
    -plasma protein binding
    -pH partitioning
  86. 86Therapeutic Drug MonitoringThe individualisation of a drug dose achieved through patient monitoring- depending upon the response of the individual to the drug
  87. 87Cardiac Drugs: AdenosineClass: Antiarrhythmic
    Use: Acute treatment of SVT
    Pharmacology: causes peripheral and coronary arterial vasodilation (depresses sinus node activity)
  88. 88Cardiac Drugs: Adenosine -contraindications and adverse effectscontraindications:
    -asthma, heart block
    adverse effects:
    flushing, chest pain, SOB, headache, hypotension, arrhythmias
  89. 89Cardiac Drugs: DipyridamoleClass: anti-platelet drug
    Name: dipyridamole (Persantin)
    Indication: prevention of stroke and TIA and cardiac stress testing
    Pharmacology: increases circulating adenosine levels
  90. 90Cardiac Drugs: Dipyridamole -contraindications and adverse effectscontraindications: asthma, acute MI, unstable angina, severe aortic stenosis, uncontrolled heart failure and arrhythmia.
    adverse effects: headache, hot flushes, tachycardia, hypotension, nausea, bronchospasm (rare) and SOB (rare).
  91. 91Cardiac Drugs: RegadenosonClass: selective A2a adenosine receptor agonist
    Indications: pharmacologic stress agent for radionuclide myocardial perfusion imaging in patients unable to undergo exercise stress
  92. 92Cardiac Drugs: Regadenoson -contraindications and adverse effectscontraindications: 2nd or 3rd degree heart block, sinus node dysfunction
    adverse effects: (less likely than the other 2) SOB, headache, flushing, dizziness, angina and nausea

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3rd Year Semester 2 Flashcards on Pharmacology, created by johanna_hillbrick on 30/09/2014.
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