Restrictive Diseases - Respiratory Therapy Files

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Transcript Restrictive Diseases - Respiratory Therapy Files

Respiratory Pharmacology
Week 1
HOMEWORK/Reading
• Read RAU’s Pharmacology
• Ch. 1-3
• Do workbook chapters for each
Objectives
• Syllabus and Course Outline
• Discuss what Pharmacology is
• Process of naming Drugs
• Abbreviations and Symbols
• Routes of Administration
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
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
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
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.
Definitions
• Endogenous: Substances made
inside body
• Exogenous: substances made
outside the body
• Hormones: are endogenous drugs
• Toxin: poisons of biologic origin
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
• Lock that a key fits into; ex:
• Lock receptor and epinephrine the
key to opening the lock
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.
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.
Definitions
• Chemical Antagonist: binds directly
with an agonist, instead of the
receptor site, to prevent the agonist
from reaching the receptor. Ex:
Heparin
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
Terminology
• Names of a drug
– Chemical name
– Generic name (assigned by US
Pharmacopoeia)
– Proprietary name
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.
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:
• Chemical Name- not responsible for
knowing
• Code name- not responsible for
knowing
• Generic Name/Official name:
Zafirlukast
• Trade/Brand: Accolate
(manufactures chosen name)
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
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 offpatent (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.
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
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
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
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
Phases of Action
• Pharmaceutical phase
– Refers to method by which a drug is
administered and the form in which it is
administered
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)
Routes of Administration
• Sublingual
• Rectal
• Oral (most common route outside of
hospital)
• Topical
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
Pharmacokinetic Phase
• Ionized drugs have minimal side effects
generally; non-ionized drugs have
greater side effects
Ionized vs. Nonionized
•
•
Ionized
Some drugs are made up of several elements combined to make
the drug which has no charge (neither plus or minus). If these
drugs can be ionized, they can split into two parts. One of the
parts carries a plus charge (+) while the other part has a negative
charge (-). A simple example is table salt or sodium chloride
(NaCl) which can become ionized in water. NaCl is an inorganic
compound.
NaCl = Na+ + Cl[the pluses and minuses should be positioned higher like the
number for a footnote]
•
Nonionized
Other types of drugs such as organic compounds don't ionize.
The molecules in their structures are stuck together in such a
way that they do not separate into parts. An example of a
nonionized compound is benzene.
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
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)
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
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
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
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
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
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
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)
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.
Neurotransmission
• Epinephrine used by the
sympathetic nervous system.
• Also in the CNS
Review of basic Pharm
• http://www.youtube.com/watch?v=O
awHxPiGBio
Neurotransmitter
• http://www.youtube.com/watch?v=ha
Noq8UbSyc
• http://www.youtube.com/watch?v=X
0Iz2FTSe2M
Agonist/Antagonists
• http://www.youtube.com/watch?v=o
D12QHE-4WY&feature=related