Pharmacology Made Easy 4.0 -
Introduction to 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). 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 and 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-
effects
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-effects 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.
Introduction to 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). 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 and 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-
effects
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-effects 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.
