pharmacology

Card Set Information

Author:
lacey0133
ID:
62866
Filename:
pharmacology
Updated:
2011-02-07 14:18:35
Tags:
exam
Folders:

Description:
pharm dr murphy
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user lacey0133 on FreezingBlue Flashcards. What would you like to do?


  1. Drug
    any chemical that can affect living processes
  2. Pharmacology
    the study of drugs and their interactions with living systems
  3. Clinical pharmacology
    the study of drugs in patients and healthy volunteers (humans)
  4. Pharmacotherapeutics
    drugs to diagnose, prevent, or treat medical conditions or prevent pregnancy
  5. Pharmacy
    The practice of preparing and dispensing drugs
  6. Properties of an ideal drug
    • Effectiveness, Safety, Selectivity
    • -reversible action, predictability, ease of administration, no drug-drug interactions, low cost, chemical stability, possession of a simple generic name
  7. What determines how an individual responds to pharmacotherapy
    • Prescribed dose: medication errors, patient compliance
    • Administered dose: pharmacokinetics: absorption, distribution, metabolism, escretion
    • concentration at sites of action: pharmacodynamics: drug receptor interaction, patients functional state, placebo effects
    • intensity of response
  8. pharmacokinetics
    impact of the body on the drug
  9. pharmacodynamics
    impact of drug on the body
  10. six rights
    dose, drug, patient, route, time, documentation
  11. Preclinical testing
    evaluated for toxicities, pharmacokinetic properties, potentially useful biologic effect, 1-5 years
  12. Clinical testing (4 phases)
    • 2-10 years
    • phase I: normal volunteers, evaluation of drug metabolism, effects on humans
    • phase II &III: tested in 500-5000 patients, determin therapeutic effects, dosage ranges, patient safety, 3-6 months per phase
    • phase IV: postmarketing surveillance
    • with conditional approval form FDA
    • usage is for the general population, new side effects may be discovered, voluntary reporting by health professionals is essential
  13. Absorption (1)
    • movement of a drug from its site of administration into the blood
    • factors: rate of absorption (dissolution), surface area, blood flow, lipid solubility, pH partioning
  14. Distribution (2)
    • the movement of drugs throughout the body
    • many drugs bind reversibly to albumin, while bound to albumin drug molecules cannot leave the vascular system
  15. Metabolism (3)
    • the enzymatic alteration of drug structure
    • most drug metaboliosm takes place in the liver and is catalyzed by the cyochrome p450 system of enzymes
    • most inportant consequence is promotion of renal drug excretion by converting lipid soluble drugs into morepolar forms
    • conversion of drugs to less active or inactive forms, conversion of drugs to more active forms, conversion of prodrugs to their active forms, and conversion of drugs to more toxic or less toxic forms
    • first pass effect is the rapid inactivation of oral drugs before being able to reach body
  16. Excretion (4)
    • most drugs excreted by the kidneys: glomerular filtration, passive tubular reabsorption, and active tuular secretion
    • Drugs that are highly lipid soluble undergoe extensive tubular reabsorption and therefore cannot be excreted until they are converted by the liver to more polar forms
    • Bile is an important route of excretion for certain drugs, which may undergo reabsorption back into the portal blood by the intestine, called enterohepatic recirculation
  17. plateau
    4 half lives
  18. time for all of drug to be excreted
    4 half lives
  19. Pharmacodynamics
    is the study of the biochemical and physiologic effects of drugs and the molecular mechanisms by which those effects are produced
  20. maximal efficacy
    the biggest effect a drug can produce
  21. potency
    high potency- a drug that produces its effects at low doses
  22. receptor
    • any functional macromolecule in a cell to which a drug binds to produce its effects.
    • reversible
    • all drugs can do i s mimic or block the action of the bodys own regulatory molecules
    • cel membrane embedded enzymes
    • ligand gated ion channels
    • g protein coupled receptor systems
    • transcription factors
  23. affinity
    • the strength of attraction betwen a drug and its receptor
    • high affinity= high potency
  24. intrinsic activity
    • the ability of a drug to activate receptors
    • high intrinsic activity= high maximal efficacy
  25. agonists
    • molecules that activate receptors
    • affinity allows them to bind to receptors, and intrinsic activity allows them to activate the receptor after binding
  26. antagonists
    • prevent receptor activation by endogenous regulatory molecules and by other drugs
    • they have affinity but lack of intrinsic activity
    • no observable effects in absence of agonists
    • noncompetitive: bind irreversibly to receptors
    • competitive: bind reversibly to receptors
  27. partial agonists
    • has moderate intrinsic activity
    • can act as agonists (if there is no full agonist present), and as antagonists (if a full agonist is present)
  28. continuous exposure to agonists/antagonists
    • desensitization/down regulation
    • hypersensitivity
  29. Therapeutic index
    • LD50/ED50 is a measure of a drugs safety
    • higher=safer
  30. pharmacodynamic interactions
    • interactions in which the interacting drugs act at the same site
    • interactions in which the interacting drugs act at separate sites
    • may be potentiative or inhibitory
  31. on an empty stomach
    1 hour before a meal, or 2 hours after
  32. childs dose
    body surface area of the child* adult dose/ 1.73 m^2
  33. Neuropharmacology
    • the study of drugs that alter processes controlled by the nervous system (produce effects equivalent to those produced by excitation or suppression of neuronal activity
    • most act by altering synaptic transmission
    • some alter axonal conduction
  34. Synaptic transmission 5 steps
    • transmitter synthesis
    • transmitter storage
    • transmitter release
    • binding of transmitter to its receptors
    • termination of transmitter action by dissociation of transmitter from the receptor followed by tranmitter reuptake or degradation
  35. Somatic nervous system
    controls movements of voluntary muscles
  36. Autonomic nervous system
    the sympathetic nervous system and the parasympathetic nervous system
  37. Parasympathetic nervous system
    • slows HR
    • increases gastric secretions and salivation
    • empties the bladder and bowel (gi motility)
    • focuses eye for near vision and constrics the pupil (miosis)
    • contracts bronchial smooth muscle
    • increase in pulmonary secretions
    • increase in glycogen synthesis (liver)
    • erection
  38. Sympathetic Nervous system
    • increase HR
    • decrease gastric secretions and salivation
    • decrease bladder voiding, and bowels (GI motility)
    • Pupil relaxation (far vision mydriasis)
    • bronchodilation
    • ejaculation
    • renin release
    • adrenal gland secretions
    • basal metabolism
    • lipolysis
    • glycogenolysis (skeletal muscle)
    • regulation of body temp (sweating)
    • implementation of fight or flight response
  39. autonomic feedback loop Reflex
    a sensor, a effector, and neurons connecting the sensor to the effector
  40. Dominant tone
    • parasympathetic
    • Sympathetic in blood vessels
  41. adrenal medulla
    functional equivalent of a postganglionic sympathetic neuron
  42. Acetylcholine
    • released by:
    • all preganglionic neurons of the sympathetic and parasympathetic nervous systems
    • all postganglionic neurons of the parasympathtic nervous system and sympathetic nervous system (that go to sweat glands)
    • All motor neurons
  43. Norepinephrine
    the transmitter released by most postganglionic neurons of the sympathetic nervous system except those that go to sweat glands
  44. Epinephrine
    the transmitter released by the adrenal medulla
  45. subtypes of cholinergic receptors
    • (acetylcholine receptors)
    • nicotinic N
    • nicotinic M
    • muscarinic
  46. four major subtypes of adrenergic receptors
    • alpha 1
    • alpha 2
    • beta 1
    • beta 2
  47. nicotinic N
    • promotes transmission at all autonomic ganglia (stimulation of postganglionic nerves)
    • promotes release of epinephrine from the adreanl medulla
  48. nicotinic M
    contraction of skeletal muscle
  49. muscarinic
    • Eye: miosis (contract ciliary & iris sphincter muscles)
    • Heart: decreased HR
    • Lung: increased secretions, and bronchoconstriction
    • Bladder: increase voiding (contract detrusor and relax trigone)
    • GI: increase salivation, secretion, motility and bowels
    • erection
    • increase sweating
    • blood: vasodilation
  50. alpha 1
    • Eye: mydriasis (contracts iris radial muscle)
    • constricts veins and arterioles
    • promotes ejaculation
    • prevents bladder voiding: by contracting smooth muscle in the prostatic capsule and bladder (trigone and sphincter)
  51. alpha 2
    • regulate neurotransmitter release
    • located on nerve terminals
    • referred to as presynaptic or prejunctional
  52. beta 1
    • increase HR
    • increase force of myocardial contraction
    • increase conduction velocity through the av node
    • promotes release of renin by kidney (increase in BP)
  53. beta 2
    • bronchodilation
    • relaxes uterine smooth muscle
    • increases liver glycogenolysis
    • enhances contraction and glycogenolysis of skeletal muscle
    • dilates arterioles in the heart lungs and skeletal muscle
  54. Dopamine
    dilates blood vessels in the kidney
  55. who binds to what receptors
    • acetylcholine: nicotinic N, nicotinic M, muscarinic
    • Epinephrine: alpha 1, alpha 2, beta 1, beta 2
    • Norepinephrine: alpha 1, alpha 2, beta 1
    • dopamine: alpha 1, beta 1, dopamine
  56. termination of neurotransmission at cholinergic junctions
    by degradation of acetylcholine, by acetylcholinesterase
  57. termination of neurotransmission at adrenergic junctions
    • by reuptake of intact norepinephrine into nerve terminals
    • following reuptake it may be stored in vesicles for reuse or destroyed by monoamine oxidase
  58. Muscarinic agonists
    • bind to muscarinic receptors and cause receptor activation
    • since nearly all muscarinic receptors are associated with the parasympathetic nervous system they resemble those produced by stimulation of parasympathetic nerves
    • cause: bradycardia, increased secretion from sweat salivary, bronchial and gastric glands, contraction of intestinal and bronchial smooth muscle, voiding, miosis
  59. Muscarinic antagonists
    • (parasympatholytic drugs, antimuscarinic drugs, muscarinic blockers, anticholinergic drugs)
    • blocks ACh at muscarinic cholinergic receptors causing: increased HR, reduceed secretionf rom sweat salivary, bonchial and gastric glands, relaxed intestinal and bronchial smooth muscle, urinary retention, mydriasis, excitation (delirium, hallucinations)
  60. cholinersterase inhibitors
    • reversible & irreversible
    • inhibit cholinersterase so that acetylcholine is unable to be broken down, so it accumulates
    • increased glandular secretions, increased tone and motility of GI smooth muscle, urinary urgency, bradycardia, bronchial constriction, miosis
    • Myasthenia Gravis: muscle strength
  61. blockage of nicotinic cholinergic receptors
    • neuromuscular blockers: nM at NMJ, muscle relaxation during surgery (do not reduce consciousness or pain) respiratory deppression
    • nondepolarizing, and depolarizing
  62. adrenergic agonists
    • (sympathomimetics)
    • Most act by direct activation of adrenergic receptors
    • alpha 1 causes vasoconstriction and mydriasis and is used for hemostasis, nasal decongestion, elevation of BP, and as adjuncts to local anesthetics
    • alpha 2 used for HTN and severe pain
    • beta 1Increase HR, contraction force, conduction through AV node, used to treat heart failure, AV block and cardiac arrest
    • beta 2 used to treat asthma and delay preterm labor
  63. alpha adrenergic blocking agents
    • alpha 1 used for treating HTN and BPH, dilation of arterioles and veins, and relaxation of smooth muscle in the bladder neck, and prostate
    • adverse effects: orthostatic hypotension, reflex tachycardia, nasal congestion, inhibition of ejaculation
  64. beta-adrenergic blocking agents
    • Beta 1: reducing HR, force of contraction, and AV conduction ... surpress secretion of renin
    • Beta II: bronchoconstriction, vasoconstriction, reduced glycogenolysis
    • Indications: htn, angina pectoris, heart failure, supraventricular tachydysrhythmias, MI
    • adverse effects beta 1: bradycardia, reduced CO, AV block, precipitation of heart failure
    • adverse effects of beta 2: bronchoconstriction, reduced glycogenolysis
  65. Drugs affecting ACh
    • (primarily parasympathetic and somatic)
    • muscarinic receptor agonist and antagonist
    • cholinesterase inhibitor
    • neuromuscular blockers
  66. Drugs affecting Epi and NE
    • (primarily sympathetic)
    • alpha 1, beta 1, and beta 2 adrenergic aganosts and antagonists
    • alpha 2 adrenergic agonist
  67. Bethanechol (urecholine)
    • Class: muscarinic receptor agonist
    • mechanism of action: reversibly activates mAChR, acts on parasymp NS, sweat glands (symp NS), and vascular smooth muscle (contains mAChR, but not innervated by PNS)
    • Therapeutic use: used in tx of urinary retention (post op and postpartum), muscarinic activation in bladder results in emptying
  68. Atropine (AtroPen)
    • Class: muscarinic receptor antagonist, reffered to as anticholinergic drugs
    • mechanism of action: reversibly inhibits activation of mAChR by Ach, acts at mAChR at therapeutic doses, at sufficiently high doses can act on nAChR
    • Therapeutic uses: Use in eye exams for mydriasis, used to increase HR, to decrease GI tone motility, as antidote to muscarinic agonist poisoning
  69. Neostigmine (prostigmin)
    • Class: Cholinesterase inhibitor
    • mechanism of action: reversibly inhibits EChE, at therapeutic levels, only effects mAChR and nAChR of NMJ (force of contraction)
    • Therapeutic use: tx of myasthenia gravis (by increase of ACh at NMJ leads to increase in muscle strength), reverse effects of tubocurarine
  70. Tubocurarine
    • Class: competitive neuromuscular blocker (non-depolarizing)
    • Mechanism of action: competitively inhibts ACh from binding to nicotinic M receptors which prevents ACh from stimulating muscle contractions, positively charged molecule which cannot cross blood brain barrier
    • Therapeutic use: increase of muscle relaxation (flaccid paralysis), used during surgery, mechanical ventilation, and endotracheal intubation
  71. Succinylcholine (Anectine)
    • Class: Depolarizing neuromuscular blocker
    • Mechanism of action: ultra short acting drug, binds to nM receptors (and initially activates receptor which leads to initial transient muscle contractions but does not readily release from nAChr, thus preventing ACh from binding; prevents subsequent contractions), positively charged molecule that cant cross blood brain barrier
    • Therapeutic use: muscle relaxation, used during short procedures (endotracheal intubation, endoscopy)
  72. Epinephrine
    • Class: adrenergic receptor agonist
    • Mechanism of action: sympathetic acting drug, activates alpha 1, alpha 2, beta 1, and beta 2 receptors
    • therapeutic use: alpha 1(vasoconstriction, slows absorption of local anesthetic, decreases superficial bleeding, decreases nasal decongestion, increases Bp), beta 1 (restores cardiac function in pts in cardiac arrest), beta 2 (bronchodilation in pts with asthma), tx for anaphylactic shock
  73. prazosin
    • Class: alpha 1 adrenergic receptor antagonist
    • mechanism of action: competitive antagonist of alpha 1 adrenergic receptor which leads to dilation of arterioles and veins; relaxation of smooth muscle in bladder
    • Therapeutic use: HTN mainly, benign prostatic hyperplasia ( because of muscle relaxation effects in bladder)
  74. propanolol (inderal)
    • Class: beta 1 and beta 2 andrenergic receptor antagonist
    • Mechanism of action: competitive antagonist of beta 1 in heart (decrease HR, force of contractility, CO), kidney (decrease renin, BP), and of beta 2 in the lungs (bronchoconstriction), blood vessels (vasoconstriction), liver & skeletal muscles (decrease in glycogenolysis)
    • Therapeutic use: tx HTN, angina pectoris, dysrhythmias, MI (based on antagonism of beta 1)
  75. metaprolol (lopressor)
    • Class: beta 1 (Selective) adrenergic receptor antagonist, referred to as cardioselective beta AR antagonist
    • Mechanism of Action: Preferentially blocks beta 1 ARs (located in heart and kidney), result of blocking beta 1 AR in heart (decreased HR, decreased force of contraction, and decreased AV conduction velocity), Result of blocking beta1 AR in kidney (decrease renin secretion)
    • Therapeutic use: HTN mainly, angina pectoris

What would you like to do?

Home > Flashcards > Print Preview