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PHARMACOLOGY 1 *Maintenance dose: lower dose than loading

which is given in order to maintain the drug
I. INTRODUCTION concentration at steady state

A. Rational Drug Therapy Onset vs, Duration of Action

- understanding and choosing the appropriate *Onset: the time required for the drug before a
drug therapy to a specific patient basing on the pharmacologic response is elicited or seen
given patient-related conditions (i.e other *Duration of action: the span of time where
complications, age, race, etc.) pharmacologic effect is elicited

B. Terminologies
1) PHARMACOLOGY: study of substances 1) Single dose: eg. IV bolus
that interact with living systems “Peak plasma concentration”
2) TOXICOLOGY: undesirable effects/side -Drug plasma conc rises until peak plasma conc
effects is reached and then falls as the drug is
3) PHARMACOKINETICS: “what does the distributed, metabolized and excreted
body does to the drug” – LADMER system
(liberation, absorption, distribution,
metabolism, excretion, reabsorption)
4) PHARMACODYNAMICS: “what does the
drug does to the body” – mechanism of
action of drugs, how drugs act on the body
5) DRUGS
- any substance that may alter the
physiologic and biochemical processes of
the body
- any substance used for diagnosis,
2) Continuous Infusion
mitigation, treatment, prevention and cure of
“Steady State”
illnesses
-equilibrium concentration between the plasma
and tissues
C. Drug formulation
(Review the different dosage forms and routes
of drug administration)
*Dosage forms: the form or structure of the drug
available in the market (e.g. tablet, capsule,
solution, syrup, etc.)
*Route of administration: the way a drug is
inserted or administered through the body (e.g.
intravenous-IV, subcutaneous-SC/SQ, oral, etc.)

II. DOSING REGIMENS

Half-life (t1/2): time at which the concentration

3) Intermittent Doses
of the drug in the body has reached 50% upon
Peaks and Troughs
excretion
*Peaks: high points of fluctuation
*Troughs: low points of fluctuation
Loading Dose vs. Maintenance Dose
*Loading Dose: first dose given to a patient in
order to achieve the plasma drug concentration
that will give a pharmacologic effect

Pharmacology 1 Notes
mawiRPh 2016
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e. Endocytosis: uptake of molecules into

the cell
Exocytosis: movement of molecules
from the cell to the outside

B. DISTRIBUTION: movement of drug molecules

from the blood to the different tissues/part of the
body

1) Factors

a. Membrane Permeability: ability/capacity of

III. PHARMACOKINETICS the membrane to accept molecules
- increase memb permeability increases drug
A. ABSORPTION: process where drug is absorbed distribution
into the plasma/blood b. Blood flow:
-increase blood flow into an organ, increase
1) Factors Affecting Absorption distribution into that organ
c. Protein binding: process wherein drug
a. Blood flow in absorption site molecules are bound into different available
-increase blood flow increases drug proteins in plasma
absorption - acidic drugs bind to albumin
b. Surface Area - basic drugs bind to alpha-acid-glycoprotein
-increase surface area in the absorption site -increase protein binding decreases
increases drug absorption distribution
c. Contact Time d. Depot Storage: process of storage of
-increase contact time of drug to the absorbed drugs into fatty tissues
absorption site increases drug absorption -increase depot storage decreases
d. pH distribution
-acidic drugs have higher absorption in an
acidic medium 2) Volume of Distribution: theoretical value of
-basic drugs have higher absorption in a body fluid that already has a drug concentration;
basic medium approximates the extent of drug distribution in
the body
2) Transport Mechanisms: processes on how
substances are transferred from the plasma C. METABOLISM: process where drug molecules
to the cells of tissues are converted into their inactive, readily
excretable form
a. Passive Transport: no use of energy
(ATP), no carrier; diffusion of lipid 1) Phase I and Phase II Metabolism
soluble substances into the cell -both processes aims to make the drug to
membrane make more water soluble or readily
b. Active Transport: uses carrier and excretable
energy -Phase I aka functionalization
c. Transcellular: susbtance passes -Phase II aka conjugation
THROUGH the cell
Paracellular: substance passes WITHIN
the cell 2) Enzyme induction and Enzyme inhibition
d. Pore Transport: small water pores in *Enzymes are biomolecules responsible for
between the cell membrane facilitates metabolizing different substances in the
transfer of water soluble drugs body
Pharmacology 1 Notes
mawiRPh 2016
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- enzyme induction = increases enzyme

activity = increase metabolism = decrease ***Mechanisms of Antagonism:
drug concentration in the body a) Physiologic antagonism: involves drug receptor
- enzyme inhibition = decreases enzyme binding
activity = decreases metabolism = increases b) Chemical antagonism: involves chemical
drug concentration in the body reaction
c) Antagonism by neutralization: Two drugs are
D. EXCRETION: process of removing/eliminating combined and they cancel each other’s effects
drug molecules out of the body through neutralization process
*more water soluble drugs are readily excreted
*more lipid soluble drugs undergo process of ***Types of Antagonism
reabsorption a) Competitive: antagonist bind on the same
receptor the agonist bind
a. Glomerular Filtration: occurs in the glomerulus - surmountable: as you increase the conc of
b. Tubular secretion agonist, antagonism is inhibited or stopped
c. Tubular reabsorption
b) Noncompetitive: antagonist bind to extra site
called allosteric site other than where the agonist
DRUG CLEARANCE: estimates the volume of bind; non-surmountable
body fluid that has already cleared out of drug c) Irreversible: the reversibility of drug binding
molecules occurs in a longer duration, or when the drug
binds to the receptor, the receptor is permanently
IV. PHARMACODYNAMICS damaged thus malfunctions

A. At cellular level B. At Organism level

MAIN REACTION in the body: POTENCY: amount of drug required to produce

Drug + Receptor  Drug receptor complex = 50% of the maximal response of the drug
pharmacologic effect - the lower the amount of drug to produce 50%
of the maximum response, the more potent the
Theories: drug is
1) Clark’s: Drug response increases as there is
an increase in drug receptor binding EFFICACY: degree to which the drug is able to
2) Stephenson’s: almost the same with clark, produce its maximal effects
it’s just that, pharmacologic effect/response
is also variable or dependent to drug affinity ***potency is a dose to reach half of the efficacy
*Affinity: ability or strength of binding of drug molecule
to a specific receptor C. At population level:
- ED50 (effective dose 50%): dose where 50%
4 BASIC MECHANISM OF DRUG RECEPTOR of the population gave a pharmacologic response
BINDING: - LD50 (Lethal dose 50%): Dose where 50% of
1) Opens/close an ion channel population died
2) Activation of biochemical messenger - TD50(Toxic dose 50%): dose where 50% of
3) Normal cellular function is stimulated or population gave toxic response
activated
4) Normal cellular function is inhibited DRUG INTERACTIONS:

*Agonist: mimics the normal physiologic functions 1 + 1 = 2 --- Additive: two drugs given together gave a
*Antagonist: blocks the normal physiologic functions higher effect compared to just one drug
e.g. if the normal physiologic function is vasodilation,
and the drug is an antagonist, the subsequent effect now
will be vasoconstriction
Pharmacology 1 Notes
mawiRPh 2016
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1 + 1 = 3 --- Synergism: two drugs given together

produces effects that is even greater than the effect of the
combined two drugs

1 + 1 = 0 --- Antagonism: two drugs given together

cancel each other’s effects

1 + 1 >/= 2 --- Potentiation: one drug with a

pharmacologic effect added with another drug with no
pharmacologic effect produces an effect greater than one
drug only

Pharmacology 1 Notes
mawiRPh 2016