Pharmacology
1. Pharmacology: the study of drugs
-Toxicology (study of environmental toxins)
-therapeutics: 2 subtypes--> (use a drug to treat a disease)
1.pharmacodynamics (what a drug does to the body)
2.pharmacokinetics (what the body does to a drug, absorb, distribute etc)
2.what is a drug: any chemical that changes the processes of living
3.Drug Nomenclature: Chemical name: N-Acetyl-p-aminophenol (development stage)
Generic Name: Acetominophen (easier to pronounce and remember) *only 1 generic name. They all have the same suffix.
Trade name: Tylenol (can be numerous trade names)
4.Drug Resources: 1. physicians desk reference (PDR)
2.Nursing drug guides (mosby's' et al.)
3.Online resources (epocrates.com)
5. What is a receptor? 5 components: 1. some component on or inside a cell that substances can bind
2.Most drugs and endogenous substances bind receptors
3.Most protein based
4.Lock and key (structurally match up to receptor)
5.Receptor Subtypes (ex: ACH-nicotinic receptor: recognizes both autonomic ganglion and skeletal muscle, but can make one that
only recognizes on area)
6.Types of Receptors: 1. Receptors located on the cell surface
2. Intracellular Receptors
-Cytosolic receptors
-Nuclear receptors
7.Why have receptors on the cell surface?: Majority of hormones are not have able to cross the membrane through diffusion, so
they have to bind to a receptor on the surface to get into the cell.
,They are not lipid soluble.
most hormones and neurostransmitters are lipid INSOLUBLE, so they need receptors to bring them into the cell.
8.Receptors on the cell surface
Communication of hormones and receptors.: 1. Receptors are linked to ion channels. They
control the opening of it. (Ex: acetylcholine is able to get Na+ into the cell by initiating opening of ion channels when it binds)
2.receptors linked to enzymes (ex: insulin or GH, bind to receptor on surface and causes the enzymatic portion to produce
changes within the cell. *Picture ^)
3.Receptors linked to second messengers
(Both use G proteins: Adenylate Cyclase System, IP3 system)
9. Second Messenger System
Adenylate Cyclase steps: 1. hormone binds to the specific receptor (1st messenger) *The receptor must be COUPLED to the G
protein to work.
2.Causes GTP to bind to protien
3.Causes G protein to move away from receptor through the membrane until it encounters an enzyme
4.the enzyme is adylte. cyclase
5.ad cly. takesATP and convert it to cyclic ATP 6 .CYClic ATP is our second messenger.
7. Cyclic ATP activates an enzyme and triggers responses of the target cell.
10. Second messenger system
Phospholipase C Mechanism (IP3 system) Steps: 1. hormone binds to receptor
2.receptor coupled to g protein
3.G protein moves away from receptor into the membrane
4.moves through membrane and encounters enzyme phospholipase C
5.Phospholipase C causes the production of 2 products (BAG and IP3)
6.It allows the signals to become amplified.
Ex: Every step of the way the response gets bigger. 2 --> 4 --> 8 -->16
11. Intracellular Receptors (2)
, Pharmacology
LIPID SOLUBLE substances: 1. Cytosolic (cytoplasm) ex: thyroid hormone 2. Nuclear (goes into
nucleus)
12. Non receptor mechanisms: - Nitrates- reduced to NO, bind guanylate cyclase
Ex: vasodilators
-Some chemotherapeutic agents become incorporated into cellular components and block metabolic reactions
13. agonist
antagonist: ag: drug that binds a receptor and produces a biochemical response
Ant: binds the receptor but doesn't produce a biochemical response. "it's a blank" No second messenger is produced.
*So why have it? tumor causing too much epinephrine binding, so antagonist drug competes with epinephrine for that receptor
and blocks its ability to bind and cause the heart to contract too much.
14. Affinity: high vs low.
Specificity= selectivity (dose-dependent)
* You want highly selective/specific drugs. So you don't produce side-affects: A: attraction between a drug and a receptor
High affinity: drug will bind, even when the drug is in extremely low concentration Low affinity:
won't bind drug until there is a high concentration of it.
S: How specific the drug is for a particular type of receptor.
Drugs that are highly selective, ONLY bind to that one receptor.
As the dose is increased, it may become less and less selective.
*this causes side-affects to go up.
15. Efficacy
Intrinsic Activity ~ efficacy: E: Does the drug to what it was intended. Effectiveness of the drug.
*more important than potency
IA: More effective response even by stimulating it just a little bit.
16. Potency Tolerance
Additive/synergistic drug interactions: P: how concentrated a drug is.
T: need for a higher dose of a drug to produce the standard effect
, Ex: oxycotin for pain, after 2 week, the oxycotin won't produce the same pain modulating affects as before.
Add/syn: more than one drug can produce one type of response.
Ex: NE and E increases HR.
Giving both at the same time, and 20 bpm happened, the drugs were additive. 10 bpm from NE, and 10 bpm from E.
BUT if a 30 bpm happens, its a synergistic interaction.
The SUM is greater than it's parts.
17. Drug Receptor interactions: Occupancy Theory: if 1mg dose was given, a certain percent of receptors would be blinded.
But if you give a 10mg dose, you'd bind more receptors and so on. Bigger responses based on # of receptors bound.
*BUT you don't have to bind all the receptors to get 100% of the response you wanted.
These are called "spare receptors"
18. Rate Theory: The act of binding of a drug produces the response downstream.
Some drugs bind and start the reaction and then let go. Then they bind again to start the reaction again.
19. receptor states theory: agonist will bind to a receptor and some receptors will be active and inactive. when binds to
active, it changes the ratio and makes other receptors active.
antagonist would bind to the active and inactive receptors, but keep them at their initial state. (don't create more active receptors
by binding)
20. Agonist Graded Dose Response Curves: Add a little bit of a drug, and record the response, then
add a little more and record until you reach that desired intensity. ("Graded")
-Threshold:
-Efficacy:
-Maximal efficacy: maximum response. drug doesn't cause any more activity.
-Potency
21. Full Agonist: Some dose that is so low that it doesn't create a response. Then if the dose is increased, a THRESHOLD is hit.
Efficacy is the Greater and Greater responses as the dose increases. until the maximal effect range is hit.
Increase the dose, decrease that selectivity. So you want to get your patient to get the dose that is at the maximal efficacy range
and NOT over it. Otherwise, their chance for side-affects is a lot worse. The higher dosage won't change the response.
1. Pharmacology: the study of drugs
-Toxicology (study of environmental toxins)
-therapeutics: 2 subtypes--> (use a drug to treat a disease)
1.pharmacodynamics (what a drug does to the body)
2.pharmacokinetics (what the body does to a drug, absorb, distribute etc)
2.what is a drug: any chemical that changes the processes of living
3.Drug Nomenclature: Chemical name: N-Acetyl-p-aminophenol (development stage)
Generic Name: Acetominophen (easier to pronounce and remember) *only 1 generic name. They all have the same suffix.
Trade name: Tylenol (can be numerous trade names)
4.Drug Resources: 1. physicians desk reference (PDR)
2.Nursing drug guides (mosby's' et al.)
3.Online resources (epocrates.com)
5. What is a receptor? 5 components: 1. some component on or inside a cell that substances can bind
2.Most drugs and endogenous substances bind receptors
3.Most protein based
4.Lock and key (structurally match up to receptor)
5.Receptor Subtypes (ex: ACH-nicotinic receptor: recognizes both autonomic ganglion and skeletal muscle, but can make one that
only recognizes on area)
6.Types of Receptors: 1. Receptors located on the cell surface
2. Intracellular Receptors
-Cytosolic receptors
-Nuclear receptors
7.Why have receptors on the cell surface?: Majority of hormones are not have able to cross the membrane through diffusion, so
they have to bind to a receptor on the surface to get into the cell.
,They are not lipid soluble.
most hormones and neurostransmitters are lipid INSOLUBLE, so they need receptors to bring them into the cell.
8.Receptors on the cell surface
Communication of hormones and receptors.: 1. Receptors are linked to ion channels. They
control the opening of it. (Ex: acetylcholine is able to get Na+ into the cell by initiating opening of ion channels when it binds)
2.receptors linked to enzymes (ex: insulin or GH, bind to receptor on surface and causes the enzymatic portion to produce
changes within the cell. *Picture ^)
3.Receptors linked to second messengers
(Both use G proteins: Adenylate Cyclase System, IP3 system)
9. Second Messenger System
Adenylate Cyclase steps: 1. hormone binds to the specific receptor (1st messenger) *The receptor must be COUPLED to the G
protein to work.
2.Causes GTP to bind to protien
3.Causes G protein to move away from receptor through the membrane until it encounters an enzyme
4.the enzyme is adylte. cyclase
5.ad cly. takesATP and convert it to cyclic ATP 6 .CYClic ATP is our second messenger.
7. Cyclic ATP activates an enzyme and triggers responses of the target cell.
10. Second messenger system
Phospholipase C Mechanism (IP3 system) Steps: 1. hormone binds to receptor
2.receptor coupled to g protein
3.G protein moves away from receptor into the membrane
4.moves through membrane and encounters enzyme phospholipase C
5.Phospholipase C causes the production of 2 products (BAG and IP3)
6.It allows the signals to become amplified.
Ex: Every step of the way the response gets bigger. 2 --> 4 --> 8 -->16
11. Intracellular Receptors (2)
, Pharmacology
LIPID SOLUBLE substances: 1. Cytosolic (cytoplasm) ex: thyroid hormone 2. Nuclear (goes into
nucleus)
12. Non receptor mechanisms: - Nitrates- reduced to NO, bind guanylate cyclase
Ex: vasodilators
-Some chemotherapeutic agents become incorporated into cellular components and block metabolic reactions
13. agonist
antagonist: ag: drug that binds a receptor and produces a biochemical response
Ant: binds the receptor but doesn't produce a biochemical response. "it's a blank" No second messenger is produced.
*So why have it? tumor causing too much epinephrine binding, so antagonist drug competes with epinephrine for that receptor
and blocks its ability to bind and cause the heart to contract too much.
14. Affinity: high vs low.
Specificity= selectivity (dose-dependent)
* You want highly selective/specific drugs. So you don't produce side-affects: A: attraction between a drug and a receptor
High affinity: drug will bind, even when the drug is in extremely low concentration Low affinity:
won't bind drug until there is a high concentration of it.
S: How specific the drug is for a particular type of receptor.
Drugs that are highly selective, ONLY bind to that one receptor.
As the dose is increased, it may become less and less selective.
*this causes side-affects to go up.
15. Efficacy
Intrinsic Activity ~ efficacy: E: Does the drug to what it was intended. Effectiveness of the drug.
*more important than potency
IA: More effective response even by stimulating it just a little bit.
16. Potency Tolerance
Additive/synergistic drug interactions: P: how concentrated a drug is.
T: need for a higher dose of a drug to produce the standard effect
, Ex: oxycotin for pain, after 2 week, the oxycotin won't produce the same pain modulating affects as before.
Add/syn: more than one drug can produce one type of response.
Ex: NE and E increases HR.
Giving both at the same time, and 20 bpm happened, the drugs were additive. 10 bpm from NE, and 10 bpm from E.
BUT if a 30 bpm happens, its a synergistic interaction.
The SUM is greater than it's parts.
17. Drug Receptor interactions: Occupancy Theory: if 1mg dose was given, a certain percent of receptors would be blinded.
But if you give a 10mg dose, you'd bind more receptors and so on. Bigger responses based on # of receptors bound.
*BUT you don't have to bind all the receptors to get 100% of the response you wanted.
These are called "spare receptors"
18. Rate Theory: The act of binding of a drug produces the response downstream.
Some drugs bind and start the reaction and then let go. Then they bind again to start the reaction again.
19. receptor states theory: agonist will bind to a receptor and some receptors will be active and inactive. when binds to
active, it changes the ratio and makes other receptors active.
antagonist would bind to the active and inactive receptors, but keep them at their initial state. (don't create more active receptors
by binding)
20. Agonist Graded Dose Response Curves: Add a little bit of a drug, and record the response, then
add a little more and record until you reach that desired intensity. ("Graded")
-Threshold:
-Efficacy:
-Maximal efficacy: maximum response. drug doesn't cause any more activity.
-Potency
21. Full Agonist: Some dose that is so low that it doesn't create a response. Then if the dose is increased, a THRESHOLD is hit.
Efficacy is the Greater and Greater responses as the dose increases. until the maximal effect range is hit.
Increase the dose, decrease that selectivity. So you want to get your patient to get the dose that is at the maximal efficacy range
and NOT over it. Otherwise, their chance for side-affects is a lot worse. The higher dosage won't change the response.
