respiratory pharmacology. pharmacology the study of substances that interact with living systems...
TRANSCRIPT
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Respiratory Pharmacology
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Pharmacology
• The study of substances that interact with living systems through chemical processes
• Especially by binding to regulatory molecules and activating or inhibiting normal body processes
• Basically manipulating normal human chemical mechanisms for a desired effect
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Pharmacology
• We will focus on respiratory therapy drugs, but must first learn basic general terms and regulatory systems
• Medical pharmacology is the science of substances used to prevent, diagnose and treat disease
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Toxicology
• Not covered in this class, but must be able to differentiate between pharmacology and toxicology which is:
• The branch of pharmacology that studies the harmful effects of chemicals on living systems
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Drug
• Any substance that interacts with a molecule or protein that plays a regulatory role in living systems.
• Includes oxygen and other therapeutic gases along with our inhaled aerosolized medications.
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Definitions
• Endogenous: Substances made inside body
• Exogenous: substances made outside the body
• Hormones: are endogenous drugs• Toxin: poisons of biologic origin
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Definitions
• Receptors: Specific molecule, usually a protein, that interacts with a specific chemical that then causes a change in the specific molecule, causing a change in regulatory function
• BETA 2 = Epinephrine• Musucarinic= AcH• Lock that a key fits into; ex:• Lock receptor and epinephrine the key to
opening the lock
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Definitions
• Agonist: any drug that binds to a receptor and activates the receptor
• Drug that fits into a receptor, will then activate and a chemical reaction occurs within the cell. When agonist leaves the binding site it deactivates the receptor.
• SABA: Short acting Beta Adrenergic– Ex: Albuterol, Xopenex (for quick relief)
• LABA: Long acting Beta Adrenergic– Ex: Serevent, Foradil, Brovana
(preventative)
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Definitions
• Antagonist: any drug that binds to a receptor and prevents the activation of the receptor
• Can be called competitive antagonist; competes with the agonist for binding site.
• RT’s antagonist drug= Atrovent (short acting), Spiriva (long acting)
• Blocks Ach from attaching to Musacarinic receptors
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Definitions
• Chemical Antagonist: binds directly with an agonist, instead of the receptor site, to prevent the agonist from reaching the receptor. Ex: Heparin
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Definitions
• Absorbed: drug must be able to absorb into the body to work
• Delivery: Must be able to get to intended site to work; gut, intestines, liver, blood…then to site of action
• Elimination: drugs must be eliminated at a reasonable rate. Affected by kidney or liver problems
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Terminology
• Names of a drug
– Chemical name
– Generic name (assigned by US
Pharmacopoeia)
– Proprietary name
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Drug Name
• The chemical name is assigned according to rules of nomenclature of chemical compounds
• The brand name is always capitalized and is selected by the manufacturer.
• The generic name refers to a common established name irrespective of its manufacturer.
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Example
• The chemical name for albuterol sulfate (albuterol sulfate inhalation solution) is α1 [(tert-butylamino) methyl]-4-hydroxy-m-xylene-α, α'-diol sulfate (2:1) (salt), and its established chemical structure is as follows:
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• Chemical Name- not responsible for knowing
• Code name- not responsible for knowing
• Generic Name/Official name: Zafirlukast
• Trade/Brand: Accolate (manufactures chosen name)
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Sources of drugs
• Animal– Thyroid hormone, insulin, pancreatic
disease• Plant
– Khellin, atropine, digitalis, reserpine, eucalyptus oil, pine, anise
• Mineral– Copper sulfate, magnesium sulfate,
mineral oil
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FDA
• When a drug is approved by the Food and Drug Administration (FDA—the government agency responsible for ensuring that drugs marketed in the United States are safe and effective), it is given a generic (official) name and a trade (proprietary or brand) name. The trade name is developed by the company requesting approval for the drug and identifies it as the exclusive property of that company.
• When a drug is under patent protection, the company markets it under its trade name. When the drug is off-patent (no longer protected by patent), the company may market its product under either the generic name or trade name. Other companies that file for approval to market the off-patent drug must use the same generic name but can create their own trade name. As a result, the same generic drug may be sold under either the generic name or one of many trade names.
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Terminology
• General terms
– Action (mode of action, intended drug effect)
– Side effect (not intended effect,
nausea/tachycardia…)
– Half life time required for concentration of a drug in the
body to decrease by 50%. Half-life also represents the time
necessary to reach steady state or to decline from steady
state after a change
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Terminology
• General terms
– Tolerance decrease in susceptibility to the effects of a
drug due to its continued administration.
– Tachyphylaxis rapid decrease in response to a drug after
administration of a few doses. Initial drug response cannot be
restored by an increase in dose
– Potentiation The action of a substance, at a dose
that does not itself have an adverse action, in
enhancing the effect of another substance
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Terminology• General terms
– Synergism the interaction of elements that when
combined produce a total effect that is greater than the
sum of the individual elements, contributions, etc.
– Agonist is a chemical that binds to a receptor of a cell
and triggers a response by that cell. Agonists often mimic
the action of a naturally occurring substance. Whereas
an agonist causes an action, an antagonist blocks the
action of the agonist and an inverse agonist causes an
action opposite to that of the agonist.
– Antagonist: blocks reaction of a agonist
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Terminology
• Anticholinergic actions• inhibition of parasympathetic response manifested by dry mouth,
decreased peristalsis, constipation, blurred vision, and urinary retention.
• Bioavailability• fraction of active drug that reaches its action sites after
administration by any route. Following an IV dose, bioavailability is 100%; however, such factors as first-pass effect, enterohepatic cycling, and biotransformation reduce bioavailability of an orally administered drug.
• cholinergic response• stimulation of the parasympathetic response manifested by
diaphoresis, salivation, abdominal cramps, diarrhea, nausea, bronchoconstriction and vomiting
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Phases of Action
• Pharmaceutical phase
– Refers to method by which a drug is
administered and the form in which it is
administered
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Routes of Administration
• Intravenous (IV) (RT will never give IV drugs, most
common route of systemic meds)
• Inhaled (Aerosol) RT route of administration
• Intramuscular (IM) (includes diabetes meds,
vaccines, boosters…)
• Subcutaneous (SubQ) (Xylocain administration,
numbing agent)
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Routes of Administration
• Sublingual
• Rectal
• Oral (most common route outside of
hospital)
• Topical
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Pharmacokinetic Phase
• Describes the time course and disposition of a
drug in the body based upon absorption,
distribution, metabolism, and elimination and the
effects and routes of excretion of the
metabolites of the drug
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Pharmacokinetic Phase
• Ionized drugs have minimal side effects
generally; non-ionized drugs have
greater side effects
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Pharmacodynamic Phase
• Describes the mechanism of action of a
drug (how it actually works in the
patients body)
• Effects are caused by combining a drug
with a matching receptor
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Neurotransmission
• Neuron: basic cell of the nervous system, provide instant method of cellular communication
• Don’t confuse nerve with neuron, nerve is a collection of neuron axon fibers
• The signals in nerves can run both ways– Efferent (out)– Afferent (in)
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Neurotransmission
• Hormones such as epinephrine and AcH are stored in packets in the neuron; action potential causes these stored transmitters to release into organs, muscles…
• AcH: made by mitochondria as part of energy transfer (Kreb cycle) along with lecithin that contains choline.
• AcH is in the neuromuscular junction. Voluntary muscle movement, stimulated at nicotinic receptors to cause muscle contraction
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Neurotransmission
• Myasthenia Gravis antibodies block the nicotinic receptors in the neuromuscular junction from getting AcH.
• AcH is also used by the autonomic nervous system in the control of
• Parasympathetic smooth muscle movement (lungs, heart). The receptor here is called muscarinic
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Neurotransmission• AcH also found in the CNS, and
affect brain and spinal cord transmissions.
• Catecholamines (Dopamine, norepinephrine, epinephrine):
• Made from the amino acid tyrosine. Located in the autonomic nervous system signals sympathetic smooth muscle movement and organ is epinephrine and norepinephrine. The receptors are alpha and beta
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Neurotransmission
• AcH esterase breaks down AcH in the synapse. (cholinesterase)
• So, if we block AcH esterase, we end up with more AcH in the synapse
• MG patients are on cholinesterase inhibitors
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• Ach is a natural hormone.• AcH in the lungs causes bronchospasm• AcH in the lungs attaches to M1-M3 recptors which are on
the smooth muscle cell• Cholinesterase is a naturally occurring enzyme that breaks
down AcH. • Cholinesterase attaches to M2 receptors to get into the
smooth muscle cell• ATROVENT and SPIRIVA are used to block Ach from
attaching to M receptors. However, they are non specific and inadvertently block M2 as well
• AcH also attaches to Nicotinic receptors on skeletal muscle to cause contraction.
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Second messenger activation
• drugs cause a reaction once it attaches to a receptor site, or blocks a receptor site.
• Second messenger activation allows complex chemical reactions to occur
• Drugs that affect smooth muscle use 2nd messengers
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Second messenger activation
• When a neurotransmitter attaches to a receptor it then activates a G protein within the cell.
• This then stimulates a enzyme called adenylyl cyclase to actively convert ATP to cAMP
• ATP is energy source that makes cAMP; increase cAMP activates many different regulatory proteins
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Second messenger activation
• cAMP regulates calcium within the bronchial smooth muscle cells to cause bronchodilation
• Cyclic AMP is made from ATP and is a second messenger.
• Phoshodiesterase (PDE) removes cAMP
• Phosphodiesterase is inhibited by caffeine (Xanthines)
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Second messenger activation
• Caffeine can increase cAMP• Weak bronchodilator• Second messenger drugs such as
all of those we use as RT’s have gradual and long lasting effects. As opposed to drugs which work directly through ion channels.
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Neurotransmission
• Epinephrine used by the sympathetic nervous system.
• Also in the CNS
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Review of basic Pharm
• http://www.youtube.com/watch?v=OawHxPiGBio
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Neurotransmitter
• http://www.youtube.com/watch?v=haNoq8UbSyc
• http://www.youtube.com/watch?v=X0Iz2FTSe2M
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Agonist/Antagonists
• http://www.youtube.com/watch?v=oD12QHE-4WY&feature=related