Intro to Pharm

  1. What is a Drug
    Something that causes physioological changes in an organism when administered
  2. What kind of a mixture are most drugs
  3. What is pharmacokinetics
    This is what the body does with the drug (absortion, distribution, biotransformation, and elimination)
  4. What are three ways that a drug can be classified
    • Main effect
    • Clinical and therapeudic use
    • Mechanism of action
  5. What are the different routes for drug administration
    Enteral and parenteral
  6. What is the enteral route of a drug
    This is when the drug enters the body through the GI tract is some way
  7. What is the parenteral route of a drug into the body
    This is when the drug enter the body by any route but the GI tract
  8. What is used for the quantatative measurement of a drug
    The volume of drug distribution VD
  9. What are the two ways that a drug is removed from the body
    • Biotransformation
    • Excretion
  10. What is the most important route for drug excretion
    Renal excretion
  11. Metabolism or biotrasformation of a drug means
    The conversion of a drug into a different substance, This can activate the drug, deactivate the drug, or maintain the drugs activity
  12. What is the most important organ involved in drug metabolism
  13. What is a major enzyme of drug metabolism found in the smooth ER of the liver
    cytochrome P450 (CYP) enzymes
  14. What is pharmacodynamics
    What the drug does to the body
  15. The molecular target for a drug is called
    Drugs receptor
  16. Most of the drug receptors in the body are
    Macromolecules which are proteins most of the time
  17. Some examples of drug receptors that are proteins are
    Regulatory proteins, ion channels, enzymes, carrier proteins, and structural proteins
  18. A single drug may have more then one
    Receptor and can therfore effect them in different ways and degrees
  19. What are the different classes of drugs based on effect and function on a receptor
    • Agonist (Either initiates or decreases the activity)
    • Antagonist (Prevents any activation of the receptor)
  20. What is a pharmacological action
    The observed effect which has been produced by the drug
  21. Theoretically drugs can be divided into what two groups of pharmacological effects
    • Drugs targeting self
    • Drugs targeting non-self (like bacteria, viruses, ect)
  22. What is Toxicology
    The study of the adverse affects of drugs
  23. What is Contraindictions
    A condition that makes the drug inadvisable
  24. What is an Autacoid
    Any chemical substance that is able to transmit signals between cells
  25. What are the three main classes of Autocoids
    • Hormones
    • Neurotransmitters
    • Autocoids
  26. What are the general effects of a hormone
    • They are secreted directly into the circulation by endocrine organs
    • They target distal organs, tissues or cells
    • They are typically slow acting
  27. What are the characteristics of a neurotransmitter
    • They are released by neurons
    • They target adjacent cells
    • Rapid acting
  28. What are the characteristics of the subclass of Autocoids
    • They are local factors (paracrine factors)
    • They act in a short range on adjacent cells
    • Rapid acting
  29. What are the major classes of the subclass of Autocoids
    • Histamine
    • Serotonin
    • Endergeneous peptides (Vaso active)
    • Eicosinoids (Prostaglandins and leukotrienes)
    • Cytokines
  30. What are the two most important H-1 receptor antagonists up to this point
    • 1st generation
    • Dimenhydrinate (Dramamine)
    • Diphenhydramine (Benedryl)
    • 2nd Generation
    • Cetirizine (Zyrtec)
    • Loratadine (Claritin)
  31. What are the affects of the 1st generation H-1 receptor antagonists Dimenhydrinate and Diphenhydramine
    • They have strong sedative effects
    • They block autonomic receptors
  32. What are the affects of the 2nd generation H-1 receptor antagonists Cetirizine and Loratadine
    Less sedation then first generation
  33. What are the pharmacokinetics of H-1 receptor antagonists
    • They are rapidly absorbed after administration (2-3hrs)
    • Widely distributed to all the body
    • Effects the body for 4-6 hrs in most cases
    • They are reversible competitive inhibitors of Histamine receptors
  34. Why are 1st generation H-1 receptor antagonists better sedatives
    They pass the Blood Brain Barrier
  35. Several 2nd generation H-1 antagonists are metabolized by
    The CYP3A4 system
  36. What kind of receptors do the H-1 antagonist inhibit
    G proteins that are stimulated by histamine and that stimulate IP3 DAG2nd receptors
  37. 1st Generation H-1 antagonists besides blocking Histamine receptors can effect
    Muscarinic cholinoreceptors, alpha adrenoreceptors, and serotonin receptors
  38. 2nd generation H-1 antagonist, beyond general histamine receptors also inhibit
    Histamine receptors specifically in the mast cells and basophils
  39. What are the pharmacological effects of the H-1 antagonist
    Inhibition of Adema, Itching, antinausea, histamine induced hypotension, inhibition of bronchiolar and GI constriction
  40. Why should caution be taken when trying to sedate a child with 1st generation H-1 antagonists
    It has the opposite effect on them
  41. Which 1st generation H-2 receptor can be a potent local anesthetic when given in high doses
  42. What is prophylactic
    Using a drug prior to issue emerging
  43. What are the mild adverse effects of 1st generation H-1 receptors
    Dizziness, fatigue, nausea/vomiting, constipation, diarrhea
  44. What effects could overdose of H-1 Antagonists have
    Hallucinations, convulsions, tachycardia, coma, cardiorespiratory collapse, death
  45. What are the two H-2 receptor antagonists to remember at this point
    • Cimetidine
    • Famotidine
  46. What are the only two routes into the body for Cimitidine and Famotidine (H-2 Antagonists)
    Oral and Parenteral (injection)
  47. What is bioavailability of Cimetidine and Famotidine
    50% percent because it is matobolized in the liver
  48. Does Cimetidine and famotidine pass the BBB
    Yes, it circulates to the whole system
  49. How is Cimetidine and famotidine cleared
    Through the combination of hepatic metabolism, glomerular filtration, and renal tubule secretion. For this reason, patients with renal or hepatic issues should be monitored close
  50. Cimetidine and famotidineneed is to to be used with caution on the elderly because
    The clearance of the drug is dimished by 50% as well as the distribution
  51. H-2 antagonitsts have what pharmacodynamics
    They are competetive inhibitors of histamine in the stomach parietal cells, as well as cardiac muscle, mast cells, and the brain
  52. What specific receptors in the in the cascade are affected by H-2 antagonists
    GPCR's which stimulate production of cAMP
  53. What kind of clinical uses are the H-2 antagonists used for
    Gastric reflux disease (GERD), Sour stomach (Dyspesia), and peptic ulcers.
  54. Ulcers caused by H. Pylori should not be treated with
    H-2 Antagonists
  55. What are the adverse affects of Famotidine and Cinetidine
    There are none, only mild affects such as diarrhea, headache, fatigue, ect
  56. Cimetidine can have an effect on
    Dihydrotesterone blockage causing gynecomastia, galactorrhea (sponateous milk production in women), loss of labido, and impotence
  57. What are the contraindications of H-2 Antagonists
    Antacids, cimetidine with drugs that are metabolized by the P450 system (since it will inhibit the effects), use of alcohol
  58. What is the Triptan Drug to remember and what does it affect
    Sumatriptan, serotonin
  59. Sumatriptan is administered how and has what reaction time
    Oral, nasal, parenteral 1-3 hours
  60. What is the mechanism of action of sumatriptan
    It is an agonist for serotonin 5-HT and they mediate vasoconstriction in the brain
  61. What are the pharmacological uses of Sumatriptan
    Migraine headaches (Cluster headaches)
  62. What is the toxicity of Sumatriptan
    • It can alter sensations (tingling, warmth, ect.)
    • Dizziness
    • Weakness
    • Neck pain
    • Injection site reactions
    • Chest discomfort
  63. What are the contraindications or Sumatriptan
    • Not to be taken with any cardiovascular disease
    • Use of other 5H-T agonists
  64. How are Eicosanoids derived
    They are lipid derived autacoids
  65. What are the two main groups of Eicosanoids
    • Prostanoids
    • Leukotrienes
  66. Prostanoids, a class of Eicosanoids have what two sub classes
    • Prostaglandins
    • Thromboxanes
  67. Arachidonic acid (AA) is a poly unsaturated fat that is significant because
    • We can't make them
    • They are the precursors to Eicosanoids
  68. The Arachidonic Acid can be synthesized to Eicosanoids by what two important routes
    • Cyclooxygenase (COX) pathway
    • Lipoxygenase (LOX) pathway
  69. What are the two main enzymes in the COX pathway
    • COX-1 (The body requires these)
    • COX-2 (These are for special needs)
  70. The LOX pathway is specifically for
  71. What are the pharmacodynamics of Eicosanoids
    • They are used as Autocoids (Paracrine/ autocrine secretion)
    • They bind to G proteins to activate or inhibit cAMP, IP3/DAG, phospholipase C, and Rho GTPase pathways
  72. What are the pharmacological effects of Eicosanoids
    • Increase the synthesis and release of Prostaglandins which affect a rise in body temperature and the hypothalmic set point
    • Potent anteriole vasodialators in vascular beds
    • Constrictors in pulmonary beds (Bronchioles)
  73. Eicosanoids are also used in the female and male reproduction system for
    • Women- Uterine contractions,
    • Men- Enhance penile erection by relaxing smooth muscle in the corpora cavernosa
  74. Prostaglandis E and F are used in the eye for
    Lowering intraocular pressure
  75. What are the clinical uses of Alprostadil (Eicosanoid)
    • Penile injections
    • Keeps the ductus arteriosus in neonates open for corrective surgery later
  76. What are the clinical uses of Dinoprostone (Eicosanoid)
    • Synthetic preparation of PGE2
    • Stimulate Uterine contractions
    • Abortion in 2nd trimester (1/4 are incomplete)
    • Labor induction
  77. What are the clinical uses of Latanoprost (Eicosanoid)
    • Eyes drops
    • Gluacoma
    • Irreversible brown pigmentation of iris and eyelashes
  78. What are the clinical uses of Eicosanoid inhibitors
    • Asthma
    • Organ transplant rejection
  79. What is unique about Latanoprost
    It requires metabolism to activate it
  80. What are the two Eicosanoid Inhibitors
    • Glucocorticoids
    • NSAID's
Card Set
Intro to Pharm
Intro to Pharm