1. Respiratory Pharmacology

2. 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

3. 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

4. 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

5. 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.

6. Definitions Endogenous: Substances made inside body
Exogenous: substances made outside the body
Hormones: are endogenous drugs
Toxin: poisons of biologic origin

7. 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

8. Definitions SABA: Short acting Beta Adrenergic
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)

9. 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

10. Definitions
Chemical Antagonist: binds directly with an agonist, instead of the receptor site, to prevent the agonist from reaching the receptor. Ex: Heparin

11. 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

12. Terminology Names of a drug Chemical name
Generic name (assigned by US Pharmacopoeia)
Proprietary name

13. 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.

14. 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:

15. Chemical Name- not responsible for knowing
Code name- not responsible for knowing
Generic Name/Official name: Zafirlukast
Trade/Brand: Accolate (manufactures chosen name)

16. Sources of drugs Animal Plant Mineral
Thyroid hormone, insulin, pancreatic disease
Plant
Khellin, atropine, digitalis, reserpine, eucalyptus oil, pine, anise
Mineral
Copper sulfate, magnesium sulfate, mineral oil

17. 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.

18. 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

19. 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

20. 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

21. Terminology Anticholinergic actions Bioavailability
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

22. Phases of Action Pharmaceutical phase
Refers to method by which a drug is administered and the form in which it is administered

24. 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)

25. Routes of Administration
Sublingual
Rectal
Oral (most common route outside of hospital)
Topical

26. 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

27. Pharmacokinetic Phase
Ionized drugs have minimal side effects generally; non-ionized drugs have greater side effects

28. 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

29. 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)

30. 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

31. 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

32. 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

33. 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

34. 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.

35. 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

36. 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

37. 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)

38. 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.

39. Neurotransmission Epinephrine used by the sympathetic nervous system.
Also in the CNS

40. Review of basic Pharm

41. Neurotransmitter http://www.youtube.com/watch?v=haNoq8UbSyc

42. Agonist/Antagonists