Basic pharmacology

Dr aysha
Pharmacology Basics
 Drug Nomenclature
• Chemical-Scientific Name
• Generic name
– NOT CAPITALIZED
• Official Name
• Brand or Trade name
– Symbol R with a circle around it
– Name capitalized
 Drug Classifications
• Body system
• Therapeutic or clinical use
• Chemical action
• Prescription vs non-prescription
• Illegal or recreational
 Pregnancy Categories
• A-no risk
• B-minimal risk or no studies done
• C-risk identified
• D-well studied definite risk-benefit may out do
risk
• X-positive evidence fetal anormalities-not
used
 PRACTICE EXAMPLES
• Use your drug book
• Find 5 Medications
• Tell us the scientific, trade and generic names
 What are drugs made of?
• Minerals
• Plant
• Animal
• Synthesis
• Microorganisms
 Drug Preparations

• Solid Preparations
– Capsule
– Tablet
– Pill
– Lozenge
 Drug Preparations
• Solid Preparations
– Suppository
– Ointment
– Powder

• Tablets or pills may be “scored”

 Drug Preparations
• Fluid preparations
– Oral parenteral or injectable or IV
• Gaseous preparation
 PHARMACOKINETICS
• Study of the metabolism and action of
drugs
• Particularly emphasizes the following:
1. Absorption
2. Distribution
3. Biotransformation
4. Excretion
 ABSORPTION

• The movement of a drug from its point

of entry into the body into systemic
circulation
 Slow Absorption

• Orally (swallowed)

• through Mucus Membranes

– Oral Mucosa (e.g. sublingual)
– Nasal Mucosa (e.g. insufflated)

• Topical/Transdermal
(through skin)

• Rectally (suppository)
 Faster Absorption

• Parenterally (injection)
– Intravenous (IV)
– Intramuscular (IM)
– Subcutaneous (SC)
– Intraperitoneal (IP)

• Inhaled (through lungs)

 Fastest Absorption

• Directly into brain

– Intracerebral (into brain tissue)
– Intracerebroventricular (into brain ventricles)

General Principle: The faster the absorption, the quicker the

onset, the higher the addictiveness, but the shorter the duration
 Absorption: Solubility
• Water-soluble
– Ionized (have electrical charge)
– Crosses through pores in capillaries, but not cell membranes

• Lipid(fat)-soluble
– Non-ionized (no electrical charge)
– Crosses pores, cell membranes, blood-brain-barrier

Dissociation constant or pKa  indicates the pH where 50% of the drug is ionized
(water soluble) and 50% non-ionized (lipid soluble);
pKeq = pH + log [X]ionized/[X]non-ionized

This affects a drug's solubility, permeability, binding, and other characteristics.

 DISTRIBUTION

• The manner in which a drug is

transported from the site of
absorption to the site of action
Distribution: Depends on Blood Flow and
Blood Brain Barrier
 Bioavailability

• The fraction of an administered dose of drug that reaches the blood

stream.
• What determines bioavailability?
– Physical properties of the drug (hydrophobicity, pKa, solubility)
– The drug formulation (immediate release, delayed release, etc.)
– If the drug is administered in a fed or fasted state
– Gastric emptying rate
– Circadian differences
– Interactions with other drugs
– Age
– Diet
– Gender
– Disease state
 Depot Binding
(accumulation in fatty tissue)
• Drugs bind to “depot sites” or “silent receptors” (fat, muscle,
organs, bones, etc)

• Depot binding reduces bioavailability, slows elimination,

• Depot-bound drugs can be released during sudden weight

loss – may account for flashback experiences?
 BIOTRANSFORMATION

• The process by which drugs are

inactivated and transformed into a form
that can be eliminated from the body
 EXCRETION
• The process of eliminating drugs from
the body
• Primarily accomplished through the
kidneys but may also involve
• liver,
• lungs,
• intestines,
• sweat
• mammary glands
 Metabolism and Elimination (cont.)
• Half-lives and Kinetics
– Half-life:
• Plasma half-life: Time it takes for plasma concentration of a
drug to drop to 50% of initial level.
• Whole body half-life: Time it takes to eliminate half of the
body content of a drug.
– Factors affecting half-life
• age
• renal excretion
• liver metabolism
• protein binding
 PHARMACODYNAMICS

How a drug works and how we can

expect the body to respond to
the administration of a drug
 Pharmacodynamics

• Receptor
– target/site of drug action (e.g. genetically-coded proteins
embedded in neural membrane)

• Lock and key or induced-fit models

– drug acts as key, receptor as lock, combination yields response
– dynamic and flexible interaction
 Pharmacodynamics (cont.)

• Affinity
– propensity of a drug to bind with a receptor

• Selectivity
– specific affinity for certain receptors (vs. others)
 Agonism and Antagonism

Agonists facilitate receptor

response

Antagonists inhibit receptor

response

(direct ant/agonists)
 Modes of Action
• Agonism • Antagonism
– A compound that does the – A compound inhibits an
job of a natural substance. enzyme from doing its job.
– Does not effect the rate of – Slows down an
an enzyme catalyzed enzymatically catalyzed
reaction. reaction.
• Up/down regulation
– Tolerance/sensitivity at the
cellular level may be due to
a change in # of receptors
(without the appropriate
subunit) due to changes in
stimulation
 Agonists/Antagonists

• Full A single drug can bind to a single

receptor and cause a mix of effects
(agonist, partial agonist, inverse agonist,
• Partial antagonist)

Functional Selectivity Hypothesis:

• Direct/Competitive Conformational change induced by a
ligand-receptor interaction may cause
differential functional activation
• Indirect/Noncompetitive
depending on the G-protein and other
proteins associated with the target
• Inverse receptor
 Agonists/Antagonists

• Full A single drug can bind to a single

receptor and cause a mix of effects
(agonist, partial agonist, inverse agonist,
• Partial antagonist)

Functional Selectivity Hypothesis:

• Direct/Competitive Conformational change induced by a
ligand-receptor interaction may cause
differential functional activation
• Indirect/Noncompetitive
depending on the G-protein and other
proteins associated with the target
• Inverse receptor
 Important implications of
drug-receptor interaction

• drugs can potentially alter rate of any bodily/brain function

• drugs cannot impart entirely new functions to cells

• drugs do not create effects, only modify ongoing ones

• drugs can allow for effects outside of normal physiological range

IMPORTANT PHARMACOLOGICAL TERMS

• Antagonism
– The opposition between 2 or more medications ex.
narcotics and Naloxone
• Bolus
– A single, often large dose of a drug. Often the initial dose
• Cumulative action
– An increased effect caused by multiple doses of the same
drug. Caused by buildup in the blood.
• Hypersensitivity
– A reaction to a drug that is more profound than expected
and which often results in an exaggerated immune
response
• Idiosyncrasy
– A reaction to a drug that is significantly different from
what is expected
• Indication
– The medical condition for which the drug has proven
therapeutic value
• Parenteral
– Any route of administration other than the digestive tract
• Pharmacodynamics
– Study of the mechanisms by which drugs act to produce
biochemical or physiological changes in the body
• Pharmacokinetics
– Study of how drugs enter the body, reach their site of
action and are eliminated from the body
• Therapeutic Action
– The intended action of a drug given in an appropriate
medical setting
• Therapeutic Threshold
– The minimum amount of a drug that is required to cause
the desired response
• Therapeutic Index
– The difference between the therapeutic threshold and the
amount of the drug considered to be toxic
– Often referred to as Safe and Effective range
• Potentiation
– The enhancement of a drug’s effect by another drug
– Eg. promethazine may enhance the effect of morphine;
also alcohol and barbiturates
• Refractory
– The failure of a patient to respond as expected to a certain
medication
• Synergism
– The combined action of 2 or more drugs that is greater
than the sum of the 2 drugs acting independently
• Therapeutic Action
– The intended action of a drug given in an appropriate
medical setting
• Therapeutic Threshold
– The minimum amount of a drug that is required to cause
the desired response
• Therapeutic Index
– The difference between the therapeutic threshold and the
amount of the drug considered to be toxic
– Often referred to as Safe and Effective range
• Tolerance
– The decreased sensitivity or response to a drug
that occurs after repeated doses
– Increased doses are required to achieve the
desired effect
• Untoward Effect
– A side effect of a drug that is harmful to the
patient
 Factors Influencing Drug Action
• Age
• Body Weight
• Metabolic Rate
• Illness
• Psychological Aspects
– Placebo effect
• Tolerance/Dependence
• Cumulative effect
 Drug Action
• Each drug has a DESIRED effect
• Can also cause undesirable effects-known as
side effects

LOOK IN DRUG BOOK- find desired action, list of

side effects
 Adverse Reactions

• Allergic Reactions
– Hives
– Itching
– Eddema
• Anaphylactic reaction
– Respiratory distress
– Cardiovascular collapse
 Risks With Drugs
• Carcinogenicity
• Teratogen
 Drug Interactions
• Drugs can “mix” or interact with other things
– Drugs
– Foods
– Juices
 Common Abbreviations
• Daily
• BID=twice daily**
• PRN=as needed
• Ad lib=as much as needed
• Mg=milligram
• Ml=milliliter
• C=with
 Common Abbreviations
• Tid=three times a day**
• Stat=NOW
• NGT=via nasogastric tube
• Gr=grain
• Gtt=drops
• Od=right eye
• Os=left eye
• Ou=both eyes
• Pc=after eating
• Ac=before eating
• Q=every
• Qh=every hour
Six Rights of Medication Administration

• Right Drug
• Right Time
• Right Dose
• Right Patient
• Right Route
• Right Documentation
 Neuropharmacology
• Study of drugs that alter processes controlled
by the nervous system
• Division of neuropharmacological agents
– Peripheral Nervous system drugs
– Central Nervous system drugs
How Neurons Regulate Physiology

• General process
– Transmission of impulse down axon
– Release of neurotransmitter from axon terminal
– Binding of neurotransmitter to receptor on post-
synaptic cell
– Post-synaptic cell changes action
• Muscle relaxes or contracts
• Glands secrete or stop secreting
• Neurons fire more often or less often
1
 Ways we can interfere
• Alter axonal conduction
– Local anesthetics
• Alter synaptic Transmission
• Affect receptors

• If drug causes same effect as natural process:

receptor activation
• If drug reduces or causes opposite: receptor
deactivation
 Transmitter Synthesis
• Drugs can
– Increase transmitter synthesis
– Decrease transmitter synthesis
– Cause synthesis of different transmitter that is
more effective than the natural
– Theoretical: cause synthesis of ineffective
transmitter
 Steps of Synaptic Transmission
• Transmitter synthesis
• Transmitter Storage (vesicles)
• Release of Transmitter
– Only small number of vesicles release
• Receptor Binding (reversible)
• Termination of Transmission
– Reuptake
– Enzymatic degradation
– Diffusion(slow, usually doesn’t happen in vivo)
 Storage and Release
• Storage: drugs can interfere with storage
– Less transmitter stored  less released

• Transmitter release: drugs can

– Promote release
– Inhibit release
 Receptor Binding
• Drug can
– Bind directly to receptors and activate them
• Agonists
– Bind to receptors and block them
• Antagonists
– Bind to receptor and enhance activation by
natural transmitter
• No special name
 Termination of Transmitter
• Block Reuptake
– Reuptake inhibitors
• Inhibition of enzymatic degradation
• Both cause more increased transmitter action
 Receptor types and Selectivity
• Drug Selectivity: selectivity of drug for
effected receptor
– Does drug bind to only α1 receptors or does it also
bind to β1 and β2 receptors?
• Physiologic Selectivity: does the receptor do
more than one thing? (Is it present in multiple
tissues?)
– β1 receptors control heart rate, conductivity, and
contraction as well as renin release from kidney