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150 Cards in this Set
- Front
- Back
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What is pharmacology and when did it originate?
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Originated in the 19th century. Is the study of how substances interact with living systems.
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Pharmacology encompasses the study of drug: (5)
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Compositions and properties
Effects Interactions Therapeutic applications Toxicology |
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What is pharmacotherapeutics?
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The use of drugs to diagnose, prevent, treat disease or prevent pregnancy.
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What is a drug?
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Any chemical that can affect living processes.
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What are properties of an ideal drug? (4 including others)
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Effectiveness, Safety, Selectivity
Other: Reversible Action, Predictability, Ease of administration, Lack of drug interactions, Low cost, Chemical stability, Simple generic and trade name. |
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What are sources of drugs? (4)
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Plant, Animal, Inorganic, Synthetic sources.
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Is selective toxicity of a drug the same as the therapeutic index of a drug?
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No
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What is drug selective toxicity?
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Administration of a drug that will have a negative effect on pathogenic organisms while having a minimum effect on the host.
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What is a drug's therapeutic index?
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The ratio between the drug dose which produces an undesired effect to the drug dose which causes the desired therapeutic effects.
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What drug was produced post WWII to control diarrhea?
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Donnagel
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What drug produced early 21st century control cholesterol? Give both the trade and generic name. For the generic name explain how the name came about.
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Vytorin (Ezetimibesimvastatin)
Ezetimibe (Zetia) + Simvastatin (Zocor) |
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Vioxx (Rofecoxib) was withdrawn from the market was an issue of what?
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Production efficiency vs Safety
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What is clinical pharmacology?
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The study of drugs in humans.
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What is therapeutics?
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The medical use of drugs.
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How can we prevent adverse drug effects? (3)
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Patient education, caregiver vigilance, correct script and monitoring.
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What is the ultimate diagnostic tool?
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Whatever the patient tells you and whatever you can hear and see.
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What is the effectiveness of a drug?
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If the drug elicits a correct response that it is marked for.
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What is drug safety?
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There is no such thing as a safe drug, we can only give drugs safely.
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What is a drugs selectivity?
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Selectivity varies with each drug and no drug is truly selective.
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What is the therapeutic objective of a drug?
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To provide maximum benefit with minimum harm.
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What are the four factors that determine the intensity of drug responses.
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Administration
Pharmacokinectics Pharmacodynamics sources of individual variation |
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Drug Intensity:
What factors affect drug intensity with administration? |
Medication Errors
Patient Adherence |
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Drug Intensity:
What factors will affect intensity with pharmacokinetics? |
Absorption
Distribution Metabolism Excretion |
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Drug intensity:
What factors will affect intensity with pharmacodynamics? |
Drug - receptor interaction
Patient's functional state Placebo effects |
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Drug intensity:
What are factors that affect intensity with individual variations? |
Physiologic, genetic, pathologic variables, and drug interactions
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What was the first legislation to regulate drug safety? What did it do?
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Food and Drug cosmetic act 1938. It checked for toxicity but not effectiveness.
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Which legislation actually tested for effectiveness of the drug since the Food and Drug cosmetic act of 1938 did not check it.
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Harris Kefauver Amendment 1962
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Which act made rules for the manufacture and distribution of drugs who have the potential for abuse? (Schedule 1-4)
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Controlled Substance Act 1970
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What act allowed for drugs to be released quickly?
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Accelerated approval of drugs 1992
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Explain the FDA Modernization Act of 1992.
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- Fast track drug approval
- Drug manufacturers will be notified 6 months prior to their drug being taken off the market. - Money for incentive to conduct research on pediatric patients. - Clinical trial database - Off label use of drugs |
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Act to promote research on effectiveness and safety of drugs in children since no testing was done prior to this.
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Best pharmaceuticals for children act 2002.
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Which act allowed the FDA to require drug manufacturers to conduct drug trials on children?
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Pediatric Research Equity Act 2003.
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What are the stages of new drug development?
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Preclinical testing
Clinical Testing - Phase 1 - normal volunteers (Metabolism and biological effects) - Phase 2/3 - Patients (Therapeutic dosage and dosage range. Conditional approval - New Drug Application) - Phase 4 - Post marketing surveillance |
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What are the components of a randomized clinical trial for new drug development?
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1. Use of controls
2. Randomization 3. Blinded - single and double |
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Bypasses the arrival of AP to the exocytosis of Ach.
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Guanidine
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Muscarinic Agonists
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Methacholine
Bethanechol |
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Nictonic Agonist
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Nicotine
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Anticholinesterase
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Physostigime, DFP, Neostigime
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Block loading of Ach into vesicles
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Vesamicol
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Prevent reuptake of Ach.
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Hemicholinium
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Prevent Ach Vesicles from fusing.
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Botulinum Toxin
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Nn Antagonists
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Macamylamine
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Nm Antagonists (Depolarizing)
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Acturanium
Tubocurarine |
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Nm Agonists (Depolarizing)
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Succynilcholine
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Muscarinic Antagonists
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Atropine
Scopolamine |
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What is myasthenia Gravis?
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Degredation of Nm receptors
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Bypass the arrival of AP to exocytosis of NE.
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Tyramine
Amphetamines |
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Non selective Adrenergic agonists
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Epinephrine
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Selective alpha 1 agonist
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Phenylephrine
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Selective B1/B2 agonist
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Isoproterenol
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Nonselective A1/A2 Antagonist
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Phenoxybenzmine
Phentolamine |
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B1 Agonist
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Dobutamine
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B2 Agonist
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Terbutaline
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Selective A2 Autoreceptor antagonist
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Yohimbine
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Prevents reuptake of NE
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Cocaine
TCA |
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Increase [NE] for vesicle exocytosis
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MAOI (Pargyline)
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Selective A2 Autoreceptor Agonist
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Clonidine
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Nonselective A1/A2 Antagonist
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Phenoxybenzmine
Phentolamine |
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Selective A1 Antagonist
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Prazosin
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Nonselective B Antagonist
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Propanolol
Carteolol |
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Selective B1 Antagonist
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Atenolol
Metoprolol Betaxolol |
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Pseudotransmitter made from this. Fools tyrosine enzyme
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Alpha - Methyl Tyrosine
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Reverse [NE] in cytoplasm and vesicles
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Resperine
Guanthidine (give some extra info on this) |
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In what enviroment will acidic drugs accumulate? Basic drugs?
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Acidic drugs will accumulate in a basic environment. Basic drugs will accumulate in an acidic environment.
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Barriers of absorption to IV admin?
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None
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Absorption pattern of IV drugs.
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Instantaneous and complete.
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Advantages of IV Drugs. (4)
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Rapid Onset
Control over plasma drugs levels Allows use of large fluid volumes Allows administration of irritant drugs |
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Disadvantages of IV drugs. (6)
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Difficulty, cost and inconvienence
Irreversibility Risk of fluid overload Infection Embolism Drug must be completely dissolved |
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Barriers of absorption for IM drugs.
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None
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Absorption pattern of IM drugs. (2 factors)
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Water solubility of drug
Blood flow to area |
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IM drug advantages. Disadvantages?
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Administer poorly soluble drugs
Depot administration Discomfort and inconvenience. |
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Barriers of absorption of oral drugs.
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GI layer of cells
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Rate of absorption of oral drugs.
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Highly variable
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Disadvantages to oral drugs.
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High Variablity
Inactivation of drugs Patient cooperation Local irritation |
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Consequences of drug metabolism
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Increase renal excretion of drugs
Inactivation or increased activity of drugs Activation of prodrugs Increased or decreased toxicity |
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What drug inhibits the active tubular secretion in the kidneys?
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Probenicid
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Dose-response relationship of administering a competitive antagonist.
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Moves the curve to the right. (lowers protency of the agonist)
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Dose-relationship of administering a noncompetitive antagonist.
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Moves the curve downward. (lowers efficacy of agonist)
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Guanidine
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Bypasses AP and exocytosis to release Ach.
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Methacholine
Bethanecol |
Muscarinic Agonists
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Nicotine
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Non selective Nicotinic agonists
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Physostigime, Neostigime, DFP
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Anticholinesterase
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PAM (Pralidoxime)
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Binds to DFP to reverse the anticholinesterase effect.
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Vesamicol
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Prevent Ach packaging.
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Botulinum Toxin
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Prevent vesicle fusion.
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Hemicholium
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Prevent reuptake of Ach.
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Macamylamine
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Nn Antagonist
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Atracurium, Tubocurarine, Parconium
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Nm antagonist causing a NMB.
Non depolarizing. |
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Succinylcholine
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Nm agonist causing fatigue of muscle ctx. leading to NMB.
Depolarizing Short acting |
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Atropine, Scopolamine
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Muscarinic Antagonist
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Tyramine, Amphetamine
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Bypass AP to exocytosis to release NE.
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Epinephrine
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Non selective adrenergic agonist.
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Phenylephrine
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Alpha 1 agonist
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Isoproterenol
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B1/B2 Agonist
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Phenoxybenzmine, Phentolamine
(To increase transmission) |
Alpha antagonist, mostly alpha 1.
Increases transmission of Betas |
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Dobutamine
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B1 agonist
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Terbutaline
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B2 Agonist
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Yohimbine
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A2 Antagonist
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Cocaine; TCA
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Inhibit reuptake of NE which causes negative feedback loop to produce more EL DOPA!!
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Pargyline (MAOI)
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Inhibit MAO to prevent breakdown of NE.
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Clonidine
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A2 Agonist
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Phenoxybenzmine, Phentolamine
(To decrease transmission) |
Alpha antagonist (blocks a2)
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Prazosin
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A1 Antagonist
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Propranolol, carteolol
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Non selective B Antagonist
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Metoprolol, Betaxolol, Atenolol
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B1 Antagonist
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Alpha - Methyl Tyrosine
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Prevents uptake of tyrosine to make NE. It tricks the tyrosinimase to think its tyrosine.
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Resperine Guanthidine
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Reverse [NE] so it stays in the cytosol.
Reserpine can freely enter the cell. Guanthidine will enter through NE reuptake channels. So initially there will be more NE but eventually there will be less. |
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Stages of Anesthesia
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Induction
Excitement Operative Danger |
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Drugs that cause amnesia.
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Benzo
- Diazepam (Valium) - Midazolam (Versed) They are sedatives/tranqs |
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Drugs that cause Analgesia.
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Narcotics
- Morphine - Fentanyl NSAIDS |
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Drugs that cause anethesia.
Induction and maintenance. |
Induction
- Thiopental (Pentohal) - Etomidate - Ketamine - Propofol - Benzo's, Narcotics Maintenance - Inhalants - Narcotics - Benzo |
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Drugs that cause muscle relaxation.
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Atracurium, Tubocurarine
Succinylcholine |
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How do inhalants work?
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GABA activation, since it is the principal inhibitory transmitter.
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How are inhalants excreted?
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Expiration of lungs.
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Specific Toxicities of Inhalants
Methoxyflurane Enflurane Halothane (also explain halothane hepatitis) Sevoflurane |
Methoxy - fluoride metabolite > DI
Enflurane - fluoride metabolite > Nephrotoxcity Halothane - Hepatoxicity Sevoflurane - both Renal/Nephrotoxicty |
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Side effects of Inhalants (4)
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Respiratory/Cardiac depression
Sensitivity to catecholamines - halothane and methoxyflurane (Dysarythmias) MH Aspiration of Gastric contents |
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How does MH happen?
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Halothane (or other inhalants) + Succinylcholine causes Ca2+ to be released at the sacroplasmic reticulum. Or the Ryanodine R1 receptors are abnormal.
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Four things that happen in MH.
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- Hypermetabolic state (CO2 increase, Increase in O2 consumption causing acidosis)
- Increased sympathetic activity - Muscle spasm (hyperkalemia) - Hyperthermia |
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How do you treat MH?
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- Sodium Dantrolene/Bicarbonate
- Stop inhalants (consider all IV), NMB |
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Potential toxicity to OR staff
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- Headaces, Drowsiness
- Spontaneous abortion - Methionine synthetase inhibited by NO |
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Preanesthetic medications
- Reduce Anxiety - Amnesia - Relief of periop. pain Suppress adverse responses: - Excessive salivation - Excessive bronchial secretion - Coughing - Bradycardia - Vomiting |
- Benzo - reduced anxiety; amnesia;
- Antacids - Anticholinergic - to prevent severe bradycardia |
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Toxicities of Local Anesthesia
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- CNS (Seizures; drowsiness > unconsciousness; Death from resp. dep.)
- CV - Vasodilation - Cardiac Depression - Bradycardia - AV block - Hypotension - Cardiac arrest |
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Local anesthetic structures and activity relationship
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Hydrophillic group - secondary or tertiary amine
Hydrophobic group - aromatic moiety Increased hydrophobicity increases potency (because it can cross membranes) |
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How do tetrodotoxin and Saxitoxin work?
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Blocks Na+ channels so you can't depolarize.
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What is Neuroleptic Malignant syndrome?
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Muscle rigidity evidence by increased CPK.
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What can reduce muscle rigidity in NMS?
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Lorazepam
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What drugs are contraindicated in NMS?
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Anticholinergics
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What causes TD?
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Hypersensitivity to D2 receptors from prolonged blockage.
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What are antipsychotics not indicated for?
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Anxiety and Insomnia
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What are side effects of Atypicals from blockage of receptors other than DA.
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Alpha, M, H, 5-HT (reuptake)
Weight gain, hyperglycemia, Anticholinergic effects, QTc prolongation |
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What are other side effects of Antipsychotics?
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Cardiac Effects
Dermatological Opthamalogical Poikilothermia |
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Clozapine Side effects
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Myocarditis
Tachycardia Seizures Agranulocytosis Sialorrhea |
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Drug interactions with Antipsychotics. (5)
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Increased sedation
- Alcohol - Anesthetics - Anthistamines - Hypnotics - Opiates Increased hypotensive effects - A/B blockers Increased antipsychotic effects - Antidepressants Clozapine + Carbamazepene = Very low WBC P450 enzyme interaction |
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Sudden cessation of antipsychotics cause what?
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Withdrawal dyskinesias
Insomnia GI (Diarrhea, Cramping) |
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What medications do we use to treat Acute mania in Bipolar disorder?
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Anticonvulsants (Divalproex and Carbamazepine)
Antipsychotics Lithium/Valproic Acid |
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What medications are used for mood stabilizing in Bipolar disorder?
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Lithium
Anticonvulsants Antipsychotics |
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What treatment can be used for refractory patients with Bipolar disorder?
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ECT
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Side effects of Lithium
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Thyroid abnormalities
Nephrogenic DI (From chronic tx) -Inhibits ADH effect - Competes for Na Reuptake Direct effect on 5-HT, DA, NE, Ach Receptors Cardiac Effects (T wave flattening) Leukocytosis Allergic rxn Cognitive Effects Edema Weight Gain Dermatologic abnormalities |
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How is lithium elminated?
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Urine mostly
Breast milk Saliva Sweat |
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Therapeutic ranges of lithium.
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1.0 - 1.2 mg/dl - acute tx
0.7 - 1.0 mg/dl - Chronic tx |
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Toxicity in Lithium
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depends on levels
1.2-2.0 2.0-3.0 >3.0 |
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How can toxicity increase for lithium?
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Dehydration
Na Depletion Excessive Dose Medications |
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Valproic Acid (Divalproex; Depakote) therapeutic ranges.
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45-125 mg/dl
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Side effects of Valproic acid
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Sedation
Weight Gain Nausea Alopecia Heptatis/Pancreatitis Thrombocytopenia NTD |
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Drug interactions with valproic acid.
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Increase antidepressant + Antipsychotic
Increase anticoagulant drugs Interactions with other anticonvulsants |
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What does Lamotrigine do?
How does it work? Side effects? Drug interactions? |
Bipolar Depression
Affect release of glutamate or Ion channels Fatal Rash Valproic acid |
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Side effects of SSRI
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GI probs
Insomnia Anxiety/Restlessness Sexual dysfunction Bruxism Withdrawal |
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Side effects of TCA
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Sedation
Anticholinergic Effects Postural Hypotension Sinus Tachycardia EKG changes Seizures Sexual Dysfunction |
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Side effects of St. John's Wort
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Dry mouth
Dizziness GI probs Serotonin syndrome, Induction of mania |
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Side Effects of MAOI
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Serotonin syndrome
Hypertensive crisis |
